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  • 1995-1999  (441)
  • 1990-1994
  • 1997  (441)
  • Cell & Developmental Biology  (441)
  • Nuclear reactions
  • 101
    Electronic Resource
    Electronic Resource
    Regulation of adenylyl cyclase isoforms by N-alkanols (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 450-456 
    Details
    ISSN: 0730-2312
    Keywords: type II adenylyl cyclase ; type V adenylyl cyclase ; insect cells ; Gsα ; solubilization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We examined the effect of n-alkanols on adenylyl cyclase isoforms (types II and V) overexpressed in insect cells. Ethanol stimulated the type II isoform but not the type V isoform. Ethanol stimulated type II adenylyl cyclase greater than GTPγS, and the treatment of the membrane with GDPβS or cholera toxin did not affect this stimulation. Other n-alkanols inhibited type V adenylyl cyclase activity in proportion to their lipophilic potency. In contrast, type II adenylyl cyclase was stimulated by weakly lipophilic n-alkanols and inhibited by strongly lipophilic n-alkanols. When solubilized membranes and purified preparations were used, all the n-alkanols inhibited type II adenylyl cyclase. Our data suggest that n-alkanols regulated adenylyl cyclase isoform-dependently. Stimulation of the type II isoform was independent from the interaction with Gsα but required the presence of an intact membrane structure. Our study may provide another step to understanding how membrane protein subtypes are differentially regulated by n-alkanols. J. Cell. Biochem. 66:450-456, 1997. © 1997 Wiley-Liss, Inc.
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  • 102
    Electronic Resource
    Electronic Resource
    Substance P stimulates vascular endothelial cellular reducing capacity in the presence of insulin and human plasma factors (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 471-481 
    Details
    ISSN: 0730-2312
    Keywords: substance P ; cell cycle ; cell growth ; endothelial cell ; tachykinin ; nitric oxide ; insulin ; plasma ; MTT ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Substance P (SP) is an important tachykinin in vascular wall biology. In previous studies [Villablanca et al. (1994): Circ Res 75:1113-1120], the authors have demonstrated that SP is a stimulus for endothelial cell growth and proliferation in serum-free culture conditions with cells quiescent in the G0-G1 phase of the cell cycle. As mitogenic and metabolic activity may interrelate, the purpose of this study was to determine the effects of the vasoactive perivascular neuropeptide SP on changes in the metabolic function of endothelial cells, and to characterize the response, by studying cellular reducing capacity in aortic vascular endothelial cells. In addition, interactions between SP and other growth factors (insulin and non-platelet plasma factors) were investigated and compared to the responses to SP alone. Metabolic effects were determined by evaluating cellular reducing capacity by the conversion of (3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide) to formazan (the MTT assay). The findings demonstrated that SP alone (10 pg/ml-25 μg/ml) inhibited cellular reducing capacity in vascular endothelial cells. In contrast, SP in the presence of insulin (10 μg/ml) stimulated endothelial reducing capacity, as compared to SP alone, by twofold on average. The effect of SP and insulin was additive at ≤0.001 μg/ml SP, and synergistic at SP concentrations ranging within 0.01-1.0 μg/ml. SP in the presence of human platelet-poor plasma (HPPP, 5%) stimulated endothelial reducing capacity, as compared to SP alone, by threefold on average. The effect of SP and HPPP was additive at ≤0.01 μg/ml SP and synergistic at SP concentrations of 0.1-25 μg/ml. Lastly, SP in the presence of insulin and HPPP stimulated endothelial metabolic activity, as compared to SP alone, by 14-fold on average. An additive response to SP, insulin, and HPPP was observed at the lowest SP concentration studied (10 pg/ml). At all other SP concentrations studied (0.0001-25 μg/ml), the responses to insulin, HPPP, and SP were synergistic. Our studies indicate that the vasoactive neuropeptide substance P may synergize with insulin and HPPP in regulating endothelial cell metabolism. In addition, our findings suggest that the mechanisms by which SP stimulates cellular metabolism are different from the mechanisms by which it stimulates cell growth. J. Cell. Biochem. 66:471-481, 1997. © 1997 Wiley-Liss, Inc.
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  • 103
    Electronic Resource
    Electronic Resource
    Intracellular distribution of heat-induced stress glycoproteins (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 98-111 
    Details
    ISSN: 0730-2312
    Keywords: hyperthermia ; thermotolerance ; protein glycosylation ; subcellular distribution ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cellular heat stress results in elevated heat-shock protein (HSP) synthesis and in thermotolerance development. Recently, we demonstrated that protein glycosylation is also an integral part of the stress response with the identification of two major stress glycoproteins, GP50, associated with thermotolerance, and P-SG67, the “prompt” stress glycoprotein induced immediately during acute heat stress. In the present study, we characterized the subcellular location and redistribution of these proteins during the cellular injury and recovery phase. In unheated and heated CHO cells, both stress glycoproteins were present in each subcellular fraction isolated by differential centrifugation. However, the subcellular redistribution in the course of cellular recovery after heat stress was specific for each stress glycoprotein. GP50 was present in all subcellular fractions before heat stress, but showed relatively little redistribution after heat stress. By 24 h of recovery following stress, GP50 showed partial depletion from lysosomes and microsomes, and was mainly present in the mitochondria. Glycosylated P-SG67 was redistributed in a more complex fashion. It was seen predominantly in the lysosomes and microsomes immediately following heat-stress, but after 6 h of recovery following heat stress, it largely disappeared from the microsomes and was present mainly in the cytosol. By 24 h of recovery following heat stress, it was found predominantly in the nucleus-rich fraction and mitochondria. The localization of GP50 and P-SG67 by subcellular fractionation is consistent with immunolocalization studies and contrasts with the translocation of HSP70 after heat stress from cytosol to nuclei and nucleoli. These results reflect a characteristic distribution for each stress glycoprotein; their presence in virtually all subcellular fractions suggests multifunctional roles for the various stress glycoproteins in the cellular heat stress response. J. Cell. Biochem. 66:98-111, 1997. © 1997 Wiley-Liss, Inc.
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  • 104
    Electronic Resource
    Electronic Resource
    Partial purification of HLAMP-1 provides direct evidence for the multicomponent nature of the particulate matrix associated with cardiac mesenchyme formation (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 112-122 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: H-LAMP-1 is a 283 kDa protein that is involved in the transformation of endothelial cells into mesenchyme within the AV canal and proximal outflow tract of the heart. This protein is part of the particulate matrix that has been suggested to be composed of multicomponent complexes that have been termed cardiac adherons. However, to date no direct evidence has been provided that these proteins are complexed into an adheron-like particle. This report provides the first such evidence by showing that purification of hLAMP-1, under gentle conditions, results in the isolation of multiple bands of similar molecular weight within the fractions that contain anti-hLAMP-1 activity. J. Cell. Biochem. 66:112-122, 1997. © 1997 Wiley-Liss, Inc.
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  • 105
    Electronic Resource
    Electronic Resource
    Post-proliferative cyclin E-associated kinase activity in differentiated osteoblasts: Inhibition by proliferating osteoblasts and osteosarcoma cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 141-152 
    Details
    ISSN: 0730-2312
    Keywords: differentiation ; osteoblasts ; cyclin E-associated kinase ; cyclin dependent kinase inhibitors ; RB related proteins ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Spontaneous differentiation of normal diploid osteoblasts in culture is accompanied by increased cyclin E associated kinase activity on (1) the retinoblastoma susceptibility protein pRB, (2) the p107 RB related protein, and (3) two endogenous cyclin E-associated substrates of 78 and 105 kD. Activity of the differentiation-related cyclin E complexes (diff.ECx) is not recovered in cdc2 or cdk2 immunoprecipitates. Phosphorylation of both the 105 kD endogenous substrate and the p107 exogenous substrate is sensitive to inhibitory activity (diff.ECx-i) present in proliferating osteoblasts. This inhibitory activity is readily recruited by the cyclin E complexes of differentiated osteoblasts but is not found in cyclin E immunoprecipitates of the proliferating cells themselves. Strong inhibitory activity on diff.ECx kinase activity is excerted by proliferating ROS 17/2.8 osteosarcoma cells. However, unlike the normal diploid cells, the diff.ECx-i activity of proliferating ROS 17/2.8 cells is recovered by cyclin E immunoprecipitation. The cyclin-dependent kinase inhibitor p21CIP1/WAF1 inhibits diff.ECx kinase activity. Thus, our results suggest the existence of a unique regulatory system, possibly involving p21CIP1/WAF1, in which inhibitory activity residing in proliferating cells is preferentially targeted towards differentiation-related cyclin E-associated kinase activity. J. Cell. Biochem. 66:141-152, 1997. © 1997 Wiley-Liss, Inc.
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  • 106
    Electronic Resource
    Electronic Resource
    Analysis of the phosphorylation of human heat shock transcription factor-1 by MAP kinase family members (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 43-54 
    Details
    ISSN: 0730-2312
    Keywords: HSF-1 ; heat shock ; ERK1, phosphorylation ; MAP kinases ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The activation of heat shock transcription factor-1 (HSF-1) after treatment of mammalian cells with stresses such as heat shock, heavy metals, or ethanol induces the synthesis of heat shock proteins. HSF-1 is phosphorylated at normal growth temperature and is hyperphosphorylated upon stress. We recently presented evidence that HSF-1 can be phosphorylated by the mitogen activated protein kinase, ERK1, and that such phosphorylation appears to negatively regulate the activity of HSF-1. In this report, we have tested the ability of ERK1 to phosphorylate various HSF-1 deletion mutants. Our results show that ERK1 phosphorylation is dependent on a region of HSF-1 extending from amino acids 280 to 308. This region contains three serine residues that are potential ERK1 phosphorylation sites. The region falls within a previously defined regulatory domain of HSF-1. The possibility of protein kinases other than ERK1 phosphorylating HSF-1 was also examined using in-gel kinase assays. The results show that HSF-1 can be phosphorylated in a ras-dependent manner by other members of the MAP kinase family such as JNK and p38 protein kinases and possibly others. J. Cell. Biochem. 67:43-54, 1997. © 1997 Wiley-Liss, Inc.
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  • 107
    Electronic Resource
    Electronic Resource
    Decorin inhibits cell attachment to thrombospondin-1 by binding to a KKTR-dependent cell adhesive site present within the N-terminal domain of thrombospondin-1 (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 75-83 
    Details
    ISSN: 0730-2312
    Keywords: decorin ; thrombospondin-1 ; cell attachment ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Skin decorin (DCN) is an antiadhesive dermatan sulfate-rich proteoglycan that interacts with thrombospondin-1 (TSP) and inhibits fibroblast adhesion to TSP [Winnemöller et al., 1992]. Molecular mechanisms by which DCN interacts with TSP and inhibits cell adhesion to TSP are unknown. In the present study, we showed that skin DCN and bone DCN (chondroitin sulfate-rich proteoglycan) were quantitatively identical with respect to their ability to interact with TSP. Using a series of fusion proteins corresponding to the different structural domains of TSP, binding of [125I]DCN to TSP was found to be dependent of the N-terminal domain and, to a lesser extent, of the type 1 repeats and the C-terminal domain of TSP. In addition, heparan sulfate drastically inhibited [125I]DCN binding to solid-phase adsorbed TSP (80% inhibition), suggesting that DCN could bind to the N-terminal domain of TSP through interaction with heparin-binding sequences. To address this question, a series of synthetic peptides, overlapping heparin-binding sequences ARKGSGRR (residues 22-29), KKTR (residues 80-83) and RLRIAKGGVNDN (residues 178-189), were synthesized and tested for their ability to interact with DCN. [125I]DCN interacted only with peptides VDAVRTEKGFLLLASLRQMKKTRGT and KKTRGTLLALERKDHS containing the heparin-binding consensus sequence KKTR. These peptides contained glycosaminoglycan-dependent and -independent binding sites because [125I]DCN binding to VDAVRTEKGFLLLASLRQMKKTRGT and KKTRGTLLALERKDHS was partially reduced upon removal of the glycosaminoglycan chain (65% and 46% inhibition, respectively). [125I]DCN poorly bound to subpeptide MKKTRG and did not bind at all to subpeptides VDAVRTEKGFLLLASLRQ and TLLALERKDHS, suggesting that heparin-binding sequence MKKTRG constituted a DCN binding site when flanked with peptides VDAVRTEKGFLLLASLRQ and TLLALERKDHS. The sequence VDAVRTEKGFLLLASLRQMKKTRGTLLALERKDHS constitutes a cell adhesive active site in the N-terminal domain of TSP [Clezardin et al., 1997], and DCN inhibited the attachment of fibroblastic and osteoblastic cells to peptides VDAVRTEKGFLLLASLRQMKKTRGT and KKTRGTLLALERKDHS by about 50 and 80%, respectively. Although fibroblastic cells also attached to type 3 repeats and the C-terminal domain of TSP, DCN only inhibited cell attachment to the C-terminal domain. Overall, these data indicate that modulation by steric exclusion of cell adhesion to a KKTR-dependent cell adhesive site present within the N-terminal domain of TSP could explain the antiadhesive properties of DCN. J. Cell. Biochem. 67:75-83, 1997. © 1997 Wiley-Liss, Inc.
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  • 108
    Electronic Resource
    Electronic Resource
    Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 131-135 
    Details
    ISSN: 0730-2312
    Keywords: Ehrlich ascites tumor ; glucose transporter ; mRNA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no GLUT2, GLUT4, or GLUT5. The mRNA levels of GLUT1 and GLUT3 increased progressively in the tumour during development; however, there were no changes observable in mRNA levels of glucose transporters of all types in brain, liver, and heart of the host mice. These findings suggest that Ehrlich ascites tumor augments its glucose transport mechanism relative to other tissues in response to its unique growth needs. J. Cell. Biochem. 67:131-135, 1997. © 1997 Wiley-Liss, Inc.
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  • 109
    Electronic Resource
    Electronic Resource
    Prolidase activity in fibroblasts is regulated by interaction of extracellular matrix with cell surface integrin receptors This article is a US Government work and, as such, is in the public domain in the United States of America. (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 166-175 
    Details
    ISSN: 0730-2312
    Keywords: prolidase ; fibroblasts ; collagen ; integrins ; extracellular matrix-cell interaction ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Prolidase (EC 3.4.13.9) is a ubiquitously distributed imidodipeptidase that catalyzes the hydrolysis of C-terminal proline or hydroxyproline containing dipeptides. The enzyme plays an important role in the recycling of proline for collagen synthesis and cell growth. An increase in enzyme activity is correlated with increased rates of collagen turnover indicative of extracellular matrix (ECM) remodeling, but the mechanism linking prolidase activity and ECM is poorly understood. Thus, the effect of ECM-cell interaction on intracellular prolidase activity is of special interest. In cultured human skin fibroblasts, the interaction with ECM and, more specifically, type I collagen mediated by the β1 integrin receptor regulates cellular prolidase activity. Supporting evidence comes from the following observations: 1) in sparse cells with a low amount of ECM collagen or in confluent cells in which ECM collagen was removed by collagenase (but not by trypsin or elastase) treatment, prolidase activity was decreased; 2) this effect was reversed by the addition of type I collagen or β1 integrin antibody (agonist for β1 integrin receptor); 3) sparse cells (with typically low prolidase activity) showed increased prolidase activity when grown on plates coated with type I collagen or on type IV collagen and laminin, constituents of basement membrane; 4) the relative differences in prolidase activity due to collagenase treatment and subsequent recovery of the activity by β1 integrin antibody or type I collagen treatment were accompanied by parallel differences in the amount of the enzyme protein recovered from these cells, as shown by Western immunoblot analysis. Thus, we conclude that prolidase activity responded to ECM metabolism (tissue remodeling) through signals mediated by the integrin receptor. J. Cell. Biochem. 67:166-175, 1997. Published 1997 Wiley-Liss, Inc.
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  • 110
    Electronic Resource
    Electronic Resource
    Detection and cloning of epidermal zinc-α2-glycoprotein cDNA and expression in normal human skin and in tumors (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 216-222 
    Details
    ISSN: 0730-2312
    Keywords: stratified epithelia ; carcinomas ; cell differentiation ; gene expression ; keratinocytes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Zinc-α2-glycoprotein (Znα2gp) is almost ubiquitous in body fluids, and its antibody labels the corresponding secretory epithelia. We have found that Znα2gp is also expressed in human epidermis. We cloned the Znα2gp cDNA by screening our cDNA library, derived from epidermal keratinocytes, with a probe for prostate Znα2gp. It had complete nucleic acid sequence homology with that from prostate, including the signal peptide. Just as Znα2gp expression is higher in more differentiated breast tumors, so in skin tumors the highest mRNA levels occurred in the normal controls, the lowest in basal cell carcinomas (the least differentiated epidermal tumor type), and intermediate levels in squamous cell carcinomas and Merkel cell carcinomas. A similar increase in Znα2gp gene expression with differentiation was observed when epidermal keratinocytes were cultured in media that varied in cellular maturation potential. J. Cell. Biochem. 67:216-222, 1997. © 1997 Wiley-Liss, Inc.
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  • 111
    Electronic Resource
    Electronic Resource
    Purification and characterization of a silica-induced bronchoalveolar lavage protein with fibroblast growth-promoting activity (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 257-264 
    Details
    ISSN: 0730-2312
    Keywords: silicosis ; bronchoalveolar lavage protein ; fibroblast proliferation-promoting factor ; inducible macrophage factor ; fibrosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Experimentally induced silicosis provides a good model for chronic interstitial pulmonary inflammation and fibrosis. In the present study, a specific single polypeptide with an apparent molecular mass of 58,000 and a pI of 4.5 was purified and characterized from the bronchoalveolar lavage fluid of silicotic rats. The same protein was also isolated from both the extract and conditioned medium of alveolar macrophages of silicotic rats. Therefore, this protein was termed an inducible silicotic (rat) bronchoalveolar lavage protein-p58 (iSBLP58) or an inducible silicotic (rat) pulmonary macrophage factor (iSPMF-p58). iSBLP58 has been purified to homogeneity by a combination of gel permeation, Mono Q ion exchange, and reverse-phase high performance liquid chromatography. This polypeptide displayed a potent fibroblast growth-promoting activity in vitro. The sequence of the first 15 NH2-terminal amino acids was determined and was found to have high sequence homology with members of the mammalian chitinase-like protein family, which includes human cartilage gp39, mammalian oviduct-specific glycoprotein, and a secretory protein from activated mouse macrophages. J. Cell. Biochem. 67:257-264, 1997. © 1997 Wiley-Liss, Inc.
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  • 112
    Electronic Resource
    Electronic Resource
    Different mechanisms are involved in intracellular calcium increase by insulin-like growth factors 1 and 2 in articular chondrocytes: Voltage-gated calcium channels, and/or phospholipase C coupled to a pertussis-sensitive G-protein (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 414-422 
    Details
    ISSN: 0730-2312
    Keywords: IGF-1 ; IGF-2 ; type 1 IGF receptor ; intracellular calcium ; phospholipase C ; chondrocytes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This study describes the mechanisms involved in the IGF-1 and IGF-2-induced increases in intracellular calcium concentration [Ca2+]i in cultured chondrocytes and the involvement of type 1 IGF receptors. It shows that IGF-1, IGF-2, and insulin increased the cytosolic free calcium concentration [Ca2+]i in a dose-dependent manner, with a plateau from 25 to 100 ng/ml for both IGF-1 and IGF-2 and from 1 to 2 μg/ml for insulin. The effect of IGF-1 was twice as great as the one of IGF-2, and the effect of insulin was 40% lower than IGF-1 effect. Two different mechanisms are involved in the intracellular [Ca2+]i increase. 1) IGF-1 and insulin but not IGF-2 involved a Ca2+ influx through voltage-gated calcium channels: pretreatment of the cells by EGTA and verapamil diminished the IGF-1 or insulin-induced[Ca2+]i but did not block the effect of IGF-2.2)IGF-1, IGF-2, and insulin also induced a Ca2+ mobilization from the endoplasmic reticulum: phospholipase C (PLC) inhihitors, neomycin, or U-73122 partially blocked the intracellular [Ca2+]i increase induced by IGF-1 and insulin and totally inhibited the effect of IGF-2. This Ca2+ mobilization was pertussis toxin (PTX) dependent, suggesting an activation of a PLC coupled to a PTX-sensitive G-protein. Lastly, preincubation of the cells with IGF1 receptor antibodies diminished the IGF-1-induced Ca2+ spike and totally abolished the Ca2+ influx, but did not modify the effect of IGF-2. These results suggest that IGF-1 action on Ca2+ influx involves the IGF1 receptor, while part of IGF-1 and all of IGF-2 Ca2+ mobilization do not implicate this receptor. J. Cell. Biochem. 64:414-422. © 1997 Wiley-Liss, Inc.
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  • 113
    Electronic Resource
    Electronic Resource
    Retinoic acid abolishes the calcitonin gene-related peptide autocrine system in F9 teratocarcinoma cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 447-457 
    Details
    ISSN: 0730-2312
    Keywords: retinoic acid ; teratocarcinoma cells ; calcitonin gene-related peptide ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Calcitonin gene-related peptide (CGRP), expressed predominantly in F9 embryonal carcinoma cells, is both a potent chemotactic agent and an autocrine growth factor for these cells. We analyzed the effect of retinoic acid (RA)-induced differentiation of F9 cells into primitive parietal endoderm-like cells, on CGRP production and the CGRP responsiveness of these cells. Poly(A) RNA extracted from F9 cells and analysed by Northern blotting and hybridization with a CGRP probe showed a specific band of about 1200 bases corresponding to mature CGRP mRNA. This band was not detected in F9 cells treated for 6 days with RA (differentiated primitive parietal endoderm-like cells) or in PYS cells (established parietal endoderm-like cell line). During RA-induced differentiation of F9 cells, CGRP mRNA levels fell within 24 h after treatment and were almost undetectable after 2 days. RA treatment also reduced CGRP secretion by F9 cells; the effect was maximal at 3 days and remained stable thereafter. Similarly, RA rapidly reduced adenylate cyclase responsiveness to chicken CGRP (cCGRP) and human CGRP (hCGRP). An 80% fall in cAMP release into the culture medium in the presence of CGRP was observed after 24 h of RA treatment. These results demonstrate that RA rapidly abolishes the CGRP autocrine system involved in the proliferation of F9 cells, at the same time inducing their differentiation into primitive parietal endoderm. They point to the interaction between retinoic acid and growth factors in the regulation of cell proliferation and differentiation. J. Cell. Biochem. 64:447-457. © 1997 Wiley-Liss, Inc.
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  • 114
    Electronic Resource
    Electronic Resource
    Expression and localization of epitope-tagged protein kinase CK2 (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 525-537 
    Details
    ISSN: 0730-2312
    Keywords: protein kinase ; protein kinase CK2 ; casein kinase II ; casein kinase 2 ; nuclear localization ; epitope tag ; expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Protein kinase CK2, formerly known as casein kinase II, is a ubiquitous protein serine/threonine kinase. The enzyme exists in tetrameric complexes composed of two catalytic (CK2α and/or CK2α′) subunits and two subunits (CK2β) that appear to have a role in modulating the activity of the catalytic subunits. With the exception of their unrelated carboxy-terminal domains, the two isozymic forms of mammalian CK2 display extensive sequence identity. Furthermore, CK2α and CK2α′ exhibit remarkable conservation between species, suggesting that they may have unique functions. In the present study, the cDNAs encoding CK2α and CK2α′ were modified by addition of the hemagglutinin tag of the influenza virus at the amino terminus of the respective proteins. The epitope-tagged proteins were transfected into Cos-7 cells and the localization of the expressed proteins determined by indirect immunofluorescence using monoclonal antibodies specific for the epitope tag. The use of transfection favors the formation of homotetrameric complexes (i.e., α2β2, α′2β2) instead of heterotetrameric complexes (i.e., αα′β2) that are present in many cells. Epitope-tagged CK2α and CK2α′ displayed kinase activity and the ability to form complexes with CK2β. The results of these studies also indicate definitively that CK2α and CK2α′ are both localized predominantly within the nucleus. Mutation of conserved lysine residues within the ATP binding domains of CK2α and CK2α′ resulted in loss of kinase activity. However, examination of these mutants indicates that kinase activity is not essential for formation of complexes between subunits of CK2 and is not required for nuclear localization of CK2. J. Cell. Biochem. 64: 525-537. © 1997 Wiley-Liss, Inc.
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  • 115
    Electronic Resource
    Electronic Resource
    Nuclear transport of H1 histones meets the criteria of a nuclear localization signal - mediated process (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 573-578 
    Details
    ISSN: 0730-2312
    Keywords: histone H1 ; nuclear transport ; permeabilized cells ; nuclear localization signal ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have studied the nuclear transport of H1 histones using the digitonin permeabilization assay system in order to establish the transport requirements for H1 translocation to the nucleus. Using HeLa cells and fluorescence-labeled calf thymus H1, we show that the H1 nuclear transport in permeabilized cells requires the addition of cytoplasmic extract. Furthermore, it can be blocked by energy depletion and by chilling or by addition of wheat germ agglutinin or by nonhydrolyzable GTP analogs. Thus, the import of H1 histones follows the criteria established for nuclear import mediated by nuclear localization signals (NLS). The distribution of basic amino acids in average H1 sequences, however, does not allow the assignment of a specific element as a classical NLS. J. Cell. Biochem. 64:573-578. © 1997 Wiley-Liss, Inc.
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    Fas-induced changes in cdc2 and cdk2 kinase activity are not sufficient for triggering apoptosis in HUT-78 cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 579-585 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Recent evidence suggested a role for the cell cycle dependent kinases cdc2 and cdk2 in apoptosis. An important mechanism by which many cell types could undergo apoptosis is through the activation of the Fas molecule on the cell membrane. To investigate whether Fas-induced cell death activated cdc2 and cdk2 kinases inappropriately, the human T lymphoma cells HUT-78, which express a high copy number of Fas, and two other previously characterized subclones of the same cell line which express mutant, cell death-deficient dominant-negative forms of Fas, were Fas-challenged and the changes in cdc2 and cdk2 kinase activity monitored. In both wild-type and Fas-mutated HUT-78 cells, apoptosis was associated simultaneously with decreased cdc2 and increased cdk2 activity. This association suggested that changes in cdc2 and cdk2 kinase activity are secondary events in cell death mediated by Fas. J. Cell. Biochem. 64:579-585. © 1997 Wiley-Liss, Inc.
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    Cytokine regulation of adult human osteoblast-like cell prostaglandin biosynthesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 618-631 
    Details
    ISSN: 0730-2312
    Keywords: cyclooxygenase ; transforming growth factor-β1 ; tumor necrosis factor-α ; interleukin-1β ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Prostaglandin (PG) biosynthesis by cytokine stimulated normal adult human osteoblast-like (hOB) cells was evaluated by thin layer chromatography, high performance liquid chromatography, and specific immunoassays. PGE2 was the predominant PG formed under all incubation conditions tested. Control samples produced measurable amounts of PGE2, and the measured level of this metabolite increased by 22-fold (from 7 to 152 ng/ml) following a 20 h treatment with the combination of TGFβ and tumor necrosis factor-α(TNF). The production of 6-keto-PGF1α (the stable metabolite of prostacyclin) and of PGF2α were each increased by about five-fold (from about 0.5 to 2.5 ng/ml) in samples treated with the cytokines. Thus, TGFβ and TNF exerted a regulation of hOB cell PG biosynthesis that was principally directed towards an increased PGE2 biosynthesis, with lesser effects on the production of other PG metabolites. COX-2 mRNA levels were increased within 2 h of cytokine stimulation, reached a maximum at 6-12 h, and levels had appreciably diminished by 24 h after treatment. Both TGFβ and TNF could independently increase COX-2 mRNA levels and PG biosynthesis. However, the increased production of PGE2 resulting from TNF stimulation was blocked by the addition of an interleukin-1β (IL-1β) neutralizing antibody, suggesting that TNF regulation of hOB cell PG synthesis was secondary to its capacity to increase hOB cell IL-1β production. TGFβ regulation of PG production was not affected by the addition of the neutralizing antibody. These studies support the proposition that PGs can be important autocrine/paracrine mediators of bone biology, whose production by hOB cells is responsively regulated by osteotropic cytokines. J. Cell. Biochem. 64:618-631. © 1997 Wiley-Liss, Inc.
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    Retinoic acid stimulates growth hormone synthesis in human somatotrophic adenoma cells: Characterization of its nuclear receptors (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 25-31 
    Details
    ISSN: 0730-2312
    Keywords: growth hormone ; retinoic acid ; retinoic acid nuclear receptors ; pituitary adenomas ; human pituitary ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In order to gain a better understanding on the possible role of retinoic acid (RA) on human GH secretion, we have characterized the expression of its nuclear receptors in somatotropic adenoma cell extracts. By immunoblotting with rabbit polyclonal antibodies directed against RARα, β, and γ and RXRα and β, we could only detect the presence of RARα and RXRα proteins. The predominant expression of RXRα was confirmed at the mRNA level by Northern and slot-blot analysis. When then investigated the effect of RA on GH synthesis in cell culture of adenomatous somatotrophs. In cultured cells, RA (1 μM) stimulated GH secretion, increased intracellular GH content and GH mRNA levels within 72 h, suggesting a modulation of GH synthesis by RA. J. Cell. Biochem 65:25-31. © 1997 Wiley-Liss, Inc.
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    Major internal nuclear matrix proteins are common to different human cell types (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 42-52 
    Details
    ISSN: 0730-2312
    Keywords: nuclear matrix ; human cell types ; 2-D gel electrophoresis ; heterogeneous nuclear ribonucleoproteins ; B23 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The nuclear matrix may be involved in the structural and functional organization of the cell nucleus. However, we still do not understand the molecular basis of the intranuclear network that is part of the nuclear matrix. We recently described a method to identify internal nuclear matrix proteins [Mattern et al. (1996): J Cell Biochem 62:275-289], which was done by comparing two nuclear matrix preparations: one with and one without the internal structure by using quantitative two-dimensional gel electrophoresis. In the present study, we use the same approach to compare the nuclear matrix proteins of four different human cell types to investigate whether they have a similar internal nuclear matrix protein composition. Major nuclear matrix proteins present in all these cell types likely represent the base of the internal nuclear matrix. We demonstrate that the 25 most abundant internal nuclear matrix proteins are common to all four cell types. Together, these common proteins represent more than 75% of the total internal nuclear matrix protein mass in each cell type. This set of proteins includes B23 and most hnRNP proteins. The quantity of most of these proteins is very similar in the four cell types. The fact that the internal nuclear matrix consists mainly of hnRNP proteins, which may be involved in transcription, transport, and processing of hnRNA, supports the idea that the internal nuclear matrix is the result of these processes. J. Cell. Biochem. 65:42-52. © 1997 Wiley-Liss, Inc.
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    Breast cytology and biomarkers obtained by random fine needle aspiration: Use in risk assessment and early chemoprevention trials (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 101-110 
    Details
    ISSN: 0730-2312
    Keywords: biomarker ; breast ; breast cancer development ; chemoprevention ; clinical trials ; cytology ; ER ; EGFR ; fine needle aspiration ; FNA ; HER-2/neu ; high risk ; p53 ; ploidy ; risk assessment ; surrogate endpoint ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In a prospective pilot study, we performed breast fine needle aspirations (FNAs) on 224 high-risk and 30 low-risk women and analyzed these aspirates for cytologic changes and biomarker abnormalities of aneuploidy and overexpressed estrogen receptor (ER), epidermal growth factor receptor (EGFR), p53 and HER-2/neu. High-risk women had a first-degree relative with breast cancer (74%), prior biopsy indicating premalignant breast disease (25%), a history of breast cancer (13%), or some multiple of these risk factors (12%). Median ages of the high- and low-risk groups were 44 and 42, respectively. Seventy percent of high-risk and 17% of low-risk women had cytologic evidence of hyperplasia with or without atypia (P〈. 0001). Aneuploidy and overexpression of EGFR and p53 occurred in 27, 37, and 29% of high-risk subjects but only 0, 3, and 3% of low-risk subjects (P〈. 0023). Overexpression of ER and HER-2/neu occurred in 7 and 20% of high-risk women but in none of the low-risk subjects. Biomarker abnormalities were more frequent with increasing cytologic abnormality. Restricting the analysis to those 3 biomarkers most frequently overexpressed in the high-risk group (ploidy, EGFR, p53), 13% of high-risk women with normal cytology, 19% of high-risk women with epithelial hyperplasia, and 49% of high-risk women with hyperplasia with atypia had abnormalities of 2 or more of these 3 biomarkers (P =. 00004). At a median follow-up of 32 months, four women have been diagnosed with invasive cancer and two with ductal carcinomain situ (DCIS). Later detection of these neoplastic conditions was associated (P ≤. 016) by univariate analysis with prior FNA evidence of hyperplasia with atypia; overexpression of p53 and EGFR; the modified Gail risk of breast cancer development at 10 years; and multiple biomarker abnormalities. By multivariate analysis, later detection of cancer was primarily predicted by the number of biomarker abnormalities in the 3-test battery (P=. 0005) and secondarily by the Gail risk at 10 years (P =. 0049). In turn, hyperplasia with atypia was associated with multiple biomarker abnormalities, particularly p53 and EGFR overexpression. Thus, hyperplasia with atypia and cytologic markers in breast FNAs have promise as risk predictors and as surrogate endpoint biomarkers for breast cancer chemoprevention trials. J. Cell. Biochem. Suppls. 28/29:101-110. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
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    Polyamine measurements in the uterine cervix (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 125-132 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; cervical intraepithelial neoplasia (CIN) ; surrogate endpoint biomarker (SEB) ; α-difluoromethylornithine (DFMO) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cervical cancer remains a significant health problem. New strategies based on the molecular aspects of cervical carcinogenesis are needed. Chemoprevention represents a novel strategy for cervical cancer prevention. Our group plans phase I and II trials using α-difluoromethylornithine, a suicide inhibitor of ornithine decarboxylase and potent antiproliferative chemopreventive agent. We conducted a study to identify which polyamines in tissue could best serve as surrogate endpoint biomarkers for future trials. Thirty patients with biopsy-proven cervical intraepithelial neoplasia grade 3 underwent colposcopically directed biopsies of normal and abnormal areas of the uterine cervix for analysis of polyamine synthesis biomarkers. Statistically significant differences were found in the ornithine decarboxylase value and the spermidine:spermine ratio between normal and abnormal areas of the cervix. In general, the ranges in measurements varied widely. Differences in polyamine synthesis biomarkers between colposcopically normal and abnormal areas can be demonstrated. However, studies using polyamine synthesis biomarkers in the cervix would require large numbers of patients to achieve significance. J. Cell. Biochem. Suppls. 28/29:125-132. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
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    New rodent models for studies of chemopreventive agents (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 144-147 
    Details
    ISSN: 0730-2312
    Keywords: mice ; gastrointestinal neoplasms ; colonic lesions ; Western-style diet ; chemopreventive agents ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Some recent studies of the effects of chemopreventive agents have begun to use new rodent models to improve the analysis of stages of colonic preneoplasia, and how chemopreventive agents modify progressive abnormal cell development. In one of the models of inherited predisposition to colon cancer, mice carrying a truncated Apc allele with a nonsense mutation in exon 15 have been generated by gene targeting and embryonic stem cell technology (Apc1638 mice). These mice develop multiple gastrointestinal lesions, including adenomas and carcinomas, focal areas of high-grade dysplasia (FAD), and polypoid hyperplasias with FADS. The incidence of inherited colonic neoplasms has now been modulated by a chemopreventive regimen. Colonic lesions significantly increased in Apc1638 mice on a Western-style diet, which has higher fat content and lower calcium and vitamin D compared to the same mice on AIN-76A diet. In another rodent model, Min mice were treated with sulindac, which markedly reduced the incidence of intestinal tumors. A third new rodent model containing a targeted mutation in the gene Mcc (mutated in colorectal cancer) recently became available for chemoprevention studies. These mice develop multiple types of neoplasms including adenocarcinomas, focal areas of gastrointestinal dysplasia, papillomas of the forestomach, and tumors in other organs including lung, liver, and lymphoid tissue. Feeding a Western-style diet to the Mcc mutant mice also resulted in significantly increased gastrointestinal lesions. These nutrient modifications also have been given to normal mice, demonstrating without any chemical carcinogen that a Western-style diet induced colonic tumorigenesis. Western-style diets also have now induced modulation of cell proliferation in other organs including mammary gland, pancreas, and prostate. These findings help develop new preclinical rodent models to aid the analysis of genetic and environmental factors leading to neoplasia, as well as new methods for evaluating the chemopreventive efficacy of specific nutrients and pharmacological agents. J. Cell. Biochem. Suppls. 28/29:144-147. © 1998 Wiley-Liss, Inc.
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    Colon cancer chemoprevention: Clinical development of aspirin as a chemopreventive agent (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 148-158 
    Details
    ISSN: 0730-2312
    Keywords: aspirin ; colon cancer chemoprevention ; cyclooxygenase isoforms (COX-1 and COX-2) ; NSAIDs ; prostaglandins (PGE2 and PGF2α) ; surrogate end-point biomarkers (SEBs) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have studied aspirin as a potential chemopreventive for colorectal cancer, completing Phase I studies on aspirin pharmacology and potential biomarker assays (prostaglandins, PGE2 and PGF2α and cyclooxygenase modulation) in normal human subjects. These studies have determined the optimal dose of aspirin for future Phase IIa and IIb chemopreventive trials in high-risk cohorts of patients for colon cancer. Aspirin's effects on rectal prostaglandins are prolonged, detectable even after aspirin and its metabolite are removed from the plasma. Aspirin-mediated inhibition of prostaglandin production in the human rectal epithelium may be related to direct suppression of cyclooxygenase transcription and not to enzyme inactivation by acetylation. A systematic method to monitor adherence (self-report, telephone contact, pill count, and microelectronic monitoring) has been established for future trials. Strategies to improve recruitment of high-risk cohorts have been developed. Phase IIa non-randomized studies with aspirin at 81 mg in high-risk cohorts (resected Duke's A colon cancer, Duke's C colon cancer treated with adjuvant therapy and disease-free at 5 years, history of colon adenomas 〉 1 cm, two or more first-degree relatives with colon cancer, and familial adenomatous polyposis and hereditary non-polyposis colorectal cancer syndromes) are currently being conducted for surrogate end-point biomarker (prostaglandins, cyclooxygenase, cellular mucins, and proliferation) modulation. J. Cell. Biochem. Suppls. 28/29:148-158. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
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    Development of human prostate cancer models for chemoprevention and experimental therapeutics studies (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 174-181 
    Details
    ISSN: 0730-2312
    Keywords: prostate cancer progression ; stromal-epithelial interaction ; three-dimensional growth models ; prostate cancer bone metastasis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The progression of human prostate cancer from histomorphologic to clinical expression often requires several decades. This study emphasizes the importance of developing relevant human prostate cancer models to study the molecular events leading to prostate cancer progression. These models will provide a rational basis for chemopreventive and treatment strategies to retard the progression of human prostate cancer from its localized to its metastatic state. In our laboratory, we have established the LNCaP progression and ARCaP models and the in vitro three-dimensional growth models involving prostate cancer and bone stroma to study the progression of prostate cancer. We propose that prostate cancer may progress from an androgen-dependent to an androgen-independent state. While existing as androgen-independent tumors (defined as tumors capable of growing in castrated hosts and secreting PSA in serum), prostate cancer may assume three different phenotypes as it progresses: androgen-independent while remaining androgen-responsive; androgen-independent and unresponsive to androgen stimulation; and androgen-independent but suppressed by androgen. It is conceivable that any androgen-independent human prostate cancer may contain variable proportions of cells that exhibit these three phenotypes. This concept may have important implications in determining strategies for chemopreventive and therapeutic trials. We have established three-dimensional growth models of prostate cancer cells either in collagen gel or microgravity-simulated growth conditions to form viable and functional organoids which contain prostate cancer epithelial cells admixed with prostate or bone stromal cells. These in vitro models combined with the in vivo models described above will enhance our understanding of the regulatory mechanism of prostate cancer growth and progression, and hence could improve efficiency in screening chemopreventive and therapeutic agents which alter the biologic behaviors of human prostate cancer. J. Cell. Biochem. Suppls. 28/29:174-181. © 1998 Wiley-Liss, Inc.
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    Effects of TPA, bryostatin 1, and retinoic acid on PO-B, AP-1, and AP-2 DNA binding during HL-60 differentiation (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 308-324 
    Details
    ISSN: 0730-2312
    Keywords: PO-B ; HL-60 ; differentiation ; AP-1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: PO-B was originally characterized as a transcriptional regulatory factor of the pro-opiomelanocortin (POMC) gene; however, it has become increasingly clear that this protein may be active in tissues outside the pituitary, since it is present in diverse cell types, including differentiated HL-60 promyelocytic leukemia cells. We previously showed that PO-B DNA-binding is progressively induced during differentiation of promyelomonocytic leukemia HL-60 cells to the macrophage-like lineage (with phorbol esters). We now report that PO-B DNA-binding in HL-60 cells is similarly induced during differentiation to the granulocytic lineage (with either retinoic acid or dimethylsulfoxide). Either a genetic or pharmacologic blockade of HL-60 differentiation prohibited these inductive effects. These studies have prompted our interest in the dynamics of other transcription factor changes during HL-60 differentiation. Of these, we observed that another transcription factor (AP-1) is also robustly induced at the DNA-binding level during macrophagelike HL-60 differentiation, but not during granulocytic differentiation. Conversely, the DNA-binding of the transcription factor AP-2 was slightly reduced by TPA-induced HL-60 differentiation but unchanged during granulocyte differentiation. From these data, we conclude that the induction of PO-B DNA binding is a general marker of HL-60 myelomonocytic differentiation, but that qualitative aspects of the induction of additional distinct transcription factors, such as AP-L may contribute to lineage-specific determinants of cell fate. J. Cell. Biochem. 65:308-324. © 1997 Wiley-Liss, Inc.
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    In vitro and in vivo expression of inducible nitric oxide synthase during experimental endotoxemia: Involvement of other cytokines (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 349-358 
    Details
    ISSN: 0730-2312
    Keywords: inducible NOS ; TNF-α ; IL 1-β ; IL-6 ; endotoxemia ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In this study, we investigated the expression of genes for inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6) of Kupffer cells in the presence of lipopolysaccharide (LPS), and the tissue expression of iNOS in a rat liver after LPS injection at various time intervals. The effects of L-NG-nitroarginine-methyl-esther HCI (L-NAMF), a NO inhibitor, also were examined. The mRNA transcripts of TNF-α IL-1β and IL-6 were rapidly detected no more than at 1 h after LPS stimulation, whereas the iNOS transcript was detectable from 3 h after LPS stimulation and maximally increased at 12 h. This fact suggested that these early induced cytokines were related to expression of iNOS. Using an anti-iNOS antiserum raised against recombinant iNOS protein, immunohistochemical analysis was made to reveal kinetics of NO producing cells. The cells immunoreactive for iNOS appeared at 6 h post-LPS injection in the sinusoids of the liver. By structural and immunohistochemical studies, almost all iNOS positive cells were identified as Kupffer cells and endothelial cells. The number of cells immunoreactive for iNOS increased until 12 h post-LPS injection. At 24 h after LPS injection, iNOS positive cells were restricted to the foci of spotty necrosis. Hepatic injury measured by released enzymes was increased by pretreatment of L-NAME before LPS injection. J. Cell. Biochem. 65:349-358. © 1997 Wiley-Liss, Inc.
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    Characterization and localization of mitochondrial oligopeptidase (MOP) (EC 3.4.24.16) activity in the human cervical adenocarcinoma cell line HeLa (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 297-308 
    Details
    ISSN: 0730-2312
    Keywords: oligopeptidase M ; neurolysin ; thimet oligopeptidase ; peptide hydrolysis ; TGFα ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In this study we describe the partial purification and characterization of the HeLa cell oligopeptidase M or endopeptidase 3.4.24.16. The HeLa enzyme was isolated initially by its ability to hydrolyse a nonapeptide substrate (P9) which was cognate to the N-terminal cleavage site of preproTGFα. The enzyme was shown to be a metalloprotease as it was inhibited by Zn2+-chelating agents and DTT, and had an approximate molecular weight of 55-63 kD determined by gel filtration. Neurotensin, dynorphin A1-17 and GnRH1-9 were rapidly degraded by the enzyme while GnRH1-10 and somatostatin were not. Neurotensin was cleaved at the Pro10-Tyr11 bond, leading to the formation of neurotensin (1-10) and neurotensin (11-13). The Km for neurotensin cleavage was 7 μM and the Ki for the specific 24.16 dipeptide inhibitor (Pro-Ile) was 140 μM which were similar to those observed from the human brain enzyme [Vincent et al. (1996): Brain Res 709:51-58].Through the use of specific antibodies, the purified HeLa enzyme was shown to be oligopeptidase M. This enzyme and its closely related family member thimet oligopeptidase were shown to co-elute during the isolation procedure but were finally separated using a MonoQ column. Oligopeptidase M is located mainly in mitochondria though it was detected on the plasma membrane in an inactive form. The results obtained demonstrate the first recorded instance of this enzyme in human tissue cultured cells, and raise the issue of its function therein. J. Cell. Biochem. 66:297-308, 1997. © 1997 Wiley-Liss, Inc.
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    Differential effects of tamoxifen-like compounds on osteoclastic bone degradation, H+-ATPase activity, calmodulin-dependent cyclic nucleotide phosphodiesterase activity, and calmodulin binding (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 358-369 
    Details
    ISSN: 0730-2312
    Keywords: calmodulin antagonists ; calmodulin binding proteins ; osteoclast ; phosphodiesterase ; H+-ATPase ; trifluoperazine ; centchroman ; cischroman ; calcium ; bone resorption ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We studied effects of calmodulin antagonists on osteoclastic activity and calmodulin-dependent HCl transport. The results were compared to effects on the calmodulin-dependent phosphodiesterase and antagonist-calmodulin binding affinity. Avian osteoclast degradation of labeled bone was inhibited ∼40% by trifluoperazine or tamoxifen with half-maximal effects at 1-3 μM. Four benzopyrans structurally resembling tamoxifen were compared: d-centchroman inhibited resorption 30%, with half-maximal effect at ∼100 nM, cischroman and CDRI 85/287 gave 15-20% inhibition, and l-centchroman was ineffective. No benzopyran inhibited cell attachment or protein synthesis below 10 μM. However, ATP-dependent membrane vesicle acridine transport showed that H+-ATPase activity was abolished by all compounds with 50% effects at 0.25-1 μM. All compounds also inhibited calmodulin-dependent cyclic nucleotide phosphodiesterase at micromolar calcium. Relative potency varied with assay type, but d- and l-centchroman, surprisingly, inhibited both H+-ATPase and phosphodiesterase activity at similar concentrations. However, d- and l-centchroman effects in either assay diverged at nanomolar calcium. Of benzopyrans tested, only the d-centchroman effects were calcium-dependent. Interaction of compounds with calmodulin at similar concentrations were confirmed by displacement of labeled calmodulin from immobilized trifluoperazine. Thus, the compounds tested all interact with calmodulin directly to varying degrees, and the observed osteoclast inhibition is consistent with calmodulin-mediated effects. However, calmodulin antagonist activity varies between specific reactions, and free calcium regulates specificity of some interactions. Effects on whole cells probably also reflect other properties, including transport into cells. J. Cell. Biochem. 66:358-369, 1997. © 1997 Wiley-Liss, Inc.
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    Calpain II expression is increased by changes in mechanical loading of muscle in vivo (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 55-66 
    Details
    ISSN: 0730-2312
    Keywords: protease ; proteolysis ; calcium ; rat ; muscle injury ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In the present investigation, we have tested the hypothesis that calpain expression or activity in skeletal muscle is influenced by changes in mechanical loading in vivo. Muscle unloading for 10 days produced no change in the concentrations of calpain I, or II, and no change in calpain activation, as assessed by measurements of the proportion of calpain I or II isoforms that exhibited autoproteolytic modifications. However, muscle reloading for 2 days produced a 90% increase in calpain II concentration per unit wet weight of muscle relative to ambulatory controls. Although no change in the activation index for calpain I or II was identified for reloaded muscle, this index is an expression of the proportion of the total mass of each calpain isoform that is autoproteolyzed. Thus, there is also approximately a 90% increase in autolyzed calpain II in muscle experiencing increased loading than in controls. Northern analysis shows that the concentration of mRNA for calpain II is increased in reloaded muscle, but no change in calpain II mRNA concentration in unloaded muscle. In situ reverse transcription polymerase chain reaction was used to confirm that nearly all calpain II mRNA in reloaded muscle is located in muscle fibers, with very little detectable calpain II mRNA in non-muscle cells present in the tissue. Together, these findings show that increased muscle loading causes a selective increase in the expression of calpain II isoform, thereby indicating that its regulation is independent from other calpain isoforms. J. Cell. Biochem. 64:55-66. © 1997 Wiley-Liss, Inc.
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    Tissue-specific protein-DNA interactions of the mouse protamine 2 gene promoter (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 94-105 
    Details
    ISSN: 0730-2312
    Keywords: mouse protamine 2 ; gene promoter ; protein-DNA interactions ; spermatogenesis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: During spermiogenesis, the haploid phase of spermatogenesis, the genome is packaged into a highly compacted form and this process requires replacement of histones by protamines. In the mouse, protamines are encoded by two genes, which are transcriptionally regulated in testis. To understand the regulation of transcription of the mouse protamine 2 (mP2) gene, the tissue-distribution of sequence-specific interactions between nuclear proteins and promoter DNA sequences have been analyzed. Protein binding to the promoter region from -370 to +65 was studied using DNase 1 footprinting and gel shift assays. Five protein binding sites were identified, which are recognized by nuclear proteins from either testis or liver. Site 1 from -64 to -48, contains part of a cAMP responsive element (CRE), which in testis is recognized by CREMτ, an activator of post-meiotic transcription. Testicular protein(s) also binds to three other promoter domains: site 2, -87 to -67, a region containing a CAAT box, and sites 4 and 5, -239 to -210 and -328 to -311, sequences with similarity to consensus steroid hormone responsive elements (HRE). In contrast, interactions between the mP2 promoter and nuclear factors from liver, a tissue in which the mP2 gene is not transcribed, are observed at sites 1, 2, and 4, as well as at an additional region at site 3, -202 to -175. Because occupancy at site 3 appears to correlate with inactivation of the gene in non-testicular tissues, whereas testicular protein binding at site 5 appears to be associated with active transcription, we conclude that the mP2 promoter displays intricate tissue-specific patterns of protein/DNA interactions at key regulatory elements. J. Cell. Biochem. 64:94-105. © 1997 Wiley-Liss, Inc.
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    Proteases in Fas-mediated apoptosis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 43-49 
    Details
    ISSN: 0730-2312
    Keywords: apoptosis ; Fas ; proteases ; substrates ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Involvement of a unique family of cysteine proteases in the multistep apoptotic process has been documented. Cloning of several mammalian genes identifies some components of this cellular response. However, it is currently unclear which protease plays a role as a signal and/or effector of apoptosis. We summarize contributions to the data concerning proteases in Fas-mediated apoptosis. J. Cell. Biochem. 64:43-49. © 1997 Wiley-Liss, Inc.
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    Macromolecular substrates for the ICE-like proteases during apoptosis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 50-54 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The interleukin-1β-converting enzyme (ICE) family of proteases is an important component of the mechanism of the apoptotic process, but the physiologic roles of the different homologs during apoptosis remain unclear. Significant information about the roles of proteolysis in apoptosis will be gained through identification of the distal substrates through which these proteases achieve their pro-apoptotic effects. Identification of these substrates therefore remains an important challenge. A subset of autoantibodies from patients with systemic lupus erythematosus (SLE) recognize molecules that are specifically cleaved early during apoptosis. Several of the identified autoantigens are nuclear proteins (PARP, U1-70 kDa, and DNA-PKCS) that are substrates for CPP32 in vitro and in apoptotic cells. Of note, these substrates are catalytic proteins involved in homeostatic pathways, suggesting that abolition of homeostasis is one fundamental feature ensuring the rapid irreversibility of the apoptotic process. Identification of the other substrates for this protease family will provide the tools to assess the roles of the different proteases in apoptotic death. J. Cell. Biochem. 64:50-54. © 1997 Wiley-Liss, Inc.
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    Transient expression of M-CSF is important for osteoclast-like cell differentiation in a monocytic leukemia cell line (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 67-76 
    Details
    ISSN: 0730-2312
    Keywords: TRAP ; bone resorption ; M-CSF ; c-fms ; monocytic cell ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cells of U937, a human monocytic leukemia cell line, differentiate into macrophages by treatment with 12-o-tetradecanoylphorbol-13-acetate (TPA), whereas cells treated with 1α,25-dihydroxyvitamin D3 [1,25-(OH)2D3] continue to grow without undergoing differentiation. When U937 cells were successively treated with TPA and 1,25-(OH)2D3, tartrate-resistant acid phosphatase-positive multinucleated cells appeared at 5 days after the treatment. These osteoclast-like cells released a soluble form of 45Ca from 45Ca-labeled bone particles. These cells were not formed when the order of treatment with TPA and 1,25-(OH)2D3 was reversed. Use of either dexamethasone or interferon-γ (IFN-γ) was effective in inhibiting the formation of these osteoclast-like cells. The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Furthermore, both dexamethasone and IFN-γ impaired the attenuation of M-CSF expression, suggesting that the transient expression of M-CSF may be important for the formation of osteoclast-like cells. J. Cell. Biochem. 64:67-76. © 1997 Wiley-Liss, Inc.
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    Structural analysis and characterization of tissue and hormonal responsive expression of the avian bone sialoprotein (BSP) gene (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 77-93 
    Details
    ISSN: 0730-2312
    Keywords: skeletal ; gene ; promoter ; regulation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Bone sialoprotein (BSP) is an extracellular matrix protein that has a highly restricted expression to mineralized skeletal tissues. The chicken bone sialoprotein-encoding gene (bsp) was isolated and shown to contain two less exons than similar mammalian genes, with the absence of an untranslated 5′ exon and the fusion of the first two exons that encode the signal peptide and amino terminal end of the mature BSP peptide. Primer extension analysis showed one strong transcriptional start point (tsp) in mRNA prepared from embryonic bone. Comparison of the avian bsp promoter sequence to those of other genes expressed in vertebrate skeletal tissues, identified the presence of homeobox protein binding sequence motifs for engrailed (en-1) and Msx 2 (Hox 8.1), and two collagen type II gene silencer elements. Two TATA sequences one at -21 bp and the second at -172 bp to the tsp were identified. For the first TATA element no CCAAT sequence was observed at an appropriate cis position however two Sp1 sequences (GGGCGG) were identified at -66 and -85 bp. A CCAAT element was seen in an appropriate cis position in relationship to the second upstream TATA, but transient expression analysis in embryonic chicken calvaria osteoblasts using two separate promoter/reporter constructs (+24 to -1244 bp or -121 to -1244 bp), confirmed that only the proximal TATA and Sp1 elements were functional. The +24 to -1244 bp promoter sequence demonstrated 33.6, 13.2, and 3.2 fold activity above base line respectively, within cells prepared from embryonic chicken calvaria bone, cephalic sterna, a cartilage that undergoes mineralization and caudal sterna, a cartilage that does not mineralize during embryogenesis. Only base line activity was observed within cells prepared from embryonic dermal fibroblasts a non-skeletal tissue, which does not express BSP. These same cells demonstrated comparable steady state mRNA levels, corroborating that this segment of promoter DNA had tissue specific activity. A series of nested deletions from the 5′ end of the -1244 construct demonstrated that a portion of the tissue specific regulation was controlled by the presence of a silencer element(s) between -1244 and -620 bp since deletion of this segment of DNA resulted in a 6 fold increase in the promoter activity in dermal skin fibroblasts. The -1244-+24 nt promoter construct was shown to be stimulated by dexamethasome ∼ 1.5 fold over control, inhibited by 1,25(OH)2D3 ∼60% of control and was strongly stimulated ∼5.0 fold by parathyroid hormone (PTH) in embryonic calvaria osteoblasts. These data define the proximal promoter of the avian bsp gene and identify several potential regulatory elements that have been observed in the promoters of other genes expressed in skeletal tissues. These elements imparted both tissue and hormone specific promoter activity to bsp expression within skeletal cells. J. Cell. Biochem. 64:77-93. © 1997 Wiley-Liss, Inc.
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    Effect of tumor necrosis factor-α on the phosphorylation of tyrosine kinase receptors is associated with dynamic alterations in specific protein-tyrosine phosphatases (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 117-127 
    Details
    ISSN: 0730-2312
    Keywords: insulin receptor ; epidermal growth factor receptor ; insulin resistance ; tyrosine phosphorylation ; TNF-α ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Tumor necrosis factor-α (TNF-α) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-α has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. In order to determine whether the effects of TNF-α might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-α, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-α on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. TNF-α caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. Overall PTPase activity in the cytosol fraction did not change with TNF-α treatment, and PTPase activity in the particulate fraction was decreased by 55-66%, demonstrating that increases in total cellular PTPase activity did not account for the observed alterations in receptor signalling. However, immunoblot analysis showed that TNF-α treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. These data suggest that at least part of the TNF-α effect on pathways of reversible tyrosine phosphorylation may be exerted through the dynamic modulation of the expression of specific PTPases. Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase may mediate the TNF-α effect to inhibit signalling through these proteins. Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-α on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. J. Cell. Biochem. 64:117-127. © 1997 Wiley-Liss, Inc.
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    Binding site on human C-reactive Protein (CRP) recognized by the Leukocyte CRP-receptor (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 140-151 
    Details
    ISSN: 0730-2312
    Keywords: human ; C-reactive protein ; acute phase reactant ; monocytes ; leukocyte ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: C-reactive protein (CRP), the prototypical inflammatory acute phase reactant in humans, interacts with monocytes and neutrophils via a specific receptor. To map the site on CRP recognized by the CRP receptor (CRP-R), synthetic peptides corresponding to the surface region on each of the five identical subunits were tested as competitors vs. [125l]-CRP for cell binding. A peptide of residues 27-38 (TKPLKAFTVCLH) efficiently inhibited CRP binding when compared to other nonoverlapping peptides. This peptide was termed the cell-binding peptide (CB-Pep). The F(ab′)2 of an IgG Ab to the CB-Pep specifically inhibited CRP binding upon reacting with the ligand. Competitive binding studies with synthetic peptides truncated from either the NH2- or COOH-terminus of the CB-Pep revealed that the minimum length recognized by the CRP-R consisted of residues 31-36: KAFTVC. Conservative substitutions of residues within the CB-Pep indicated that the four residues AFTV were critical for CRP-R binding. The CB-Pep also inhibited induced superoxide generation by HL-60 granulocytes. The minimum length required for the inhibition was also KAFTVC; however, only Phe-33 and Leu-37 were critical residues in this assay. Anti-CB-Pep IgG Ab reacted more extensively with heat-modified CRP, suggesting that an altered conformation of CRP is preferentially recognized by the CRP-R. The results suggest that this contiguous sequence on a β-strand on one face of each of five subunits of the CRP pentamer serves as a unique recognition motif for inflammatory leukocytes. J. Cell. Biochem. 64:140-151. © 1997 Wiley-Liss, Inc.
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    Multiple G-protein involvement in parathyroid hormone regulation of acid production by osteoclasts (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 161-170 
    Details
    ISSN: 0730-2312
    Keywords: calcium-regulating hormone ; bone cells ; acridine orange ; signal transduction ; GTP-binding protein ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The involvement of multiple G-proteins in parathyroid hormone regulation of acid production was demonstrated in a highly enriched osteoclast population. Osteoclasts were isolated from the endosteum of 2.5 to 3-week-old chicken tibia using sequential enzymatic digestion. Single cell analysis of acid production was accomplished using microscope photometry and vital staining with acridine orange, a hydrogen ion concentration sensitive fluorescent dye. Lithium chloride, an uncoupler of G-proteins from their respective receptors, blocked parathyroid hormone stimulated production of acid. Cholera toxin, which permanently activates Gs-proteins, mimicked PTH stimulation. Pertussis toxin, which prevents receptor interaction with Gi- and Go-proteins, blocked both 10 8 M and 10 11 M PTH stimulated acid production, suggesting that the pertussis toxin-sensitive G-protein is utilized at both PTH concentrations. Immunoblots of osteoclast plasma membrane proteins, using a panel of antibodies generated against specific G-protein α subunits, revealed a 48 kDa Gsα, a 41 Goα, a 34 kDa Giα-3, and a unique 68 kDa Gα subunit, with the 41 kDa and 34 kDa bands being the most intense. Immunoblots of osteoblast plasma membrane proteins had a substantially different profile with the most intense bands being a Gsα (48 kDa) and a Goα (36 and 38 kDa). The studies suggest the utilization of at least two different G-proteins in the parathyroid hormone regulation of acid formation by osteoclasts, a Gs and a pertussis toxin-sensitive G-protein (Go and/or Giα-3). J. Cell. Biochem. 64:161-170. © 1997 Wiley-Liss, Inc.
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    Inhibition of MG-63 cell proliferation and PDGF-stimulated cellular processes by inhibitors of phosphatidylinositol 3-kinase (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 182-195 
    Details
    ISSN: 0730-2312
    Keywords: LY294002 ; wortmannin ; signal transduction ; tyrosine kinase ; mitogen ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Studies on a platelet-derived growth factor (PDGF) responsive osteosarcoma cell line, MG-63, were initiated to determine the effects of phosphatidylinositol (Ptdlns) 3-kinase inhibitors on serum-stimulated cell proliferation and PDGF-stimulated DNA replication, actin rearrangements, or Ptdlns 3-kinase activity. In a dose-dependent manner, the fungal metabolite wortmannin and a quercetin derivative, LY294002 (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one), inhibited serum-stimulated MG-63 cell proliferation. The mitogenic effects of PDGF on MG-63 cells, as determined by incorporation of [3H]-thymidine, were also substantially inhibited in the presence of 0.10 μM wortmannin or 10 μM LY294002. Furthermore, MG-63 cells stimulated by PDGF form distinct actin-rich, finger-like membrane projections which are completely inhibited by either 0.10 μM wortmannin or 10 μM LY294002. At these same concentrations, wortmannin and LY294002 were also effective at reducing levels of phosphatidylinositol 3-phosphate in PDGF-stimulated MG-63 cells. Treatment of these cells with increasing concentrations of wortmannin reduced the level of PDGF stimulated tyrosine phosphorylation of the PDGF receptor but did not significantly affect the amount of the Ptdlns 3-kinase regulatory subunit, p85, associated with the receptor. Additionally, pretreatment of cells with 0.250 μM wortmannin followed by stimulation with PDGF resulted in a slightly reduced level of receptor autokinase activity; however, similar treatment with 50 μM LY294002 did not affect the level of autokinase activity. These results demonstrate the effects of two different Ptdlns 3-kinase inhibitors on serum- and PDGF-stimulated MG-63 cell proliferation and PDGF-stimulated morphological changes and suggest a greater role for Ptdlns 3-kinase in these processes. J. Cell. Biochem. 64:182-195. © 1997 Wiley-Liss, Inc.
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    Cyclosporin A and its non-immunosuppressive derivative exhibit a differential effect on cell-mediated mineralization in culture (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 209-216 
    Details
    ISSN: 0730-2312
    Keywords: cyclosporin A ; cell-mediated ; mineralization ; marrow-stroma ; mitochondria ; membrane potential ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Chronic immunosuppressive treatment with cyclosporin A (CsA) is associated with decreased bone density. However, in culture, CsA inhibits osteoclast differentiation and bone resorption. This raises the question as to whether CsA also affects osteoblast function. Immunophilin, one of the CsA-binding cyclophilins that is implicated in the immunosuppressive action of CsA via calcineurin, is a peptidyl prolyl cis-trans isomerase (PPI). CsA also binds a mitochondrial membrane PPI which is implicated in controlling permeability transition pores. Therefore, in the present study we tested the effect of CsA on cell mediated mineralization in parallel with mitochondrial rhodamine retention as an indicator of mitochondrial membrane potential. Rat marrow stromal cells were grown in dexamethasone (DEX) medium to stimulate mineralization in culture, and CsA was added to various cultures using different treatment schedules. Low dose (0.1 μM) CsA inhibited mineralization, compared to controls, when present in the cultures during days 3-11 of DEX stimulation. Contrarily, high dose CsA (1.0 μM) resisted the inhibitory effect of the low dose. SDZ 220-384 (SDZ), a non-immunosuppressive derivative of CsA which is known, like CsA, to bind to mitochondrial cyclophilin but does not inhibit calcineurin, was also tested. Both high and low doses of SDZ decreased mineralization when present in the cultures from day 3 or from day 0. The similar effect of the low CsA dose and SDZ on mineralization is in accord with their ability to block permeability transition pores. The differential effect, on day 21 mineralization, between high CsA dose and SDZ took place in parallel to their opposing effects on mitochondrial membrane potential. On days 4-8, mitochondrial rhodamine retention was higher under CsA than under SDZ. Under these conditions there was no significant difference between the effects of these drugs on cell proliferation measured on day 11; there was a minor decrease in specific alkaline phosphatase activity by SDZ, too small to explain the extent of mineralization inhibition by SDZ. These results suggest that permeability transition pores might be involved in controlling mineralization. Unlike SDZ, CsA exhibits an additional effect on the mitochondrial membrane potential and on mineralization when applied at a high dose on day 3. Therefore identifying the additional activity of high dose CsA, which is missing in SDZ, may be beneficial. Such activity is expected to resist changes in rhodamine retention and decreased mineralization induced by SDZ, and yet enable preservation of immunosuppressive activity of CsA. J. Cell. Biochem. 64:209-216. © 1997 Wiley-Liss, Inc.
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    Chloroquine, quinine and quinidine inhibit calcium release from macrophage intracellular stores by blocking inositol 1,4,5-trisphosphate binding to its receptor (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 225-232 
    Details
    ISSN: 0730-2312
    Keywords: chemotherapy of malaria ; inositol trisphosphate receptors ; chloroquine ; cytosolic calcium ; endocytosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The binding of many ligands to cellular receptors induces a signaling cascade which generates inositol 1,4,5-trisphosphate (IP3). IP3 binding to its receptors in various internal compartments causes a rapid Ca2+ efflux into the cytosol. We now demonstrate that chloroquine blocks ligand-induced Ca2+ mobilization without affecting IP3 synthesis. The effect is independent of the ligand employed and occurred with five unrelated ligands; namely, α2-macroglobulin-methylamine, angiotensin II, bradykinin, carbachol, and epidermal growth factor. Chloroquine, quinidine, and quinine, however, block binding of [3H]IP3 to its receptors by 90%, 88%, and 71%, respectively. These observations suggest a previously undetected mechanism by which these agents may in part function as antimalarials. J. Cell. Biochem. 64:225-232. © 1997 Wiley-Liss, Inc.
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    Protective role of intraperitoneally administrated vitamin E and selenium on the levels of total lipid, total cholesterol, and fatty acid composition of muscle and liver tissues in rats (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 233-241 
    Details
    ISSN: 0730-2312
    Keywords: intraperitoneally administrated ; vitamin E ; Se ; liver ; muscle ; fatty acids ; rats ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The aim of this work was to determine the protective effects of intraperitoneally administrated vitamin E and Se on total lipid, total cholesterol, and fatty acid composition of rat liver and muscle tissues. Total lipid content of muscle tissue in Se and combination groups decreased as compared to the control group. However, the level of total lipid in the liver tissues was seen to decrease only in the combination group (P 〈 0.05). While the amount of total cholesterol in liver tissue was lower (P 〈 0.05) in the vitamin E and combination groups, the amount of total cholesterol in muscle tissue decreased (P 〈 0.05) in the combination group.The amount of linoleic acid in muscle tissue slightly decreased (P 〈 0.05), whereas the eicosenoic and eicosatrienoic acid amounts significantly increased (P 〈 0.01, P 〈 0.001) in the vitamin E group as compared to the control group. The amounts of most fatty acid decreased (P 〈 0.05) in the combination group. The proportions of eicosenoic, eicosatrienoic, and total polyunsaturated fatty acid (PUFA) within the total fatty acid were higher (P 〈 0.05) in vitamin E group, whereas these fatty acids proportions were lower (P 〈 0.05) in the Se group. Although the proportions of palmitic, linolenic, and total saturated fatty acids were low (P 〈 0.05), oleic and total unsaturated fatty acid proportions were higher (P 〈 0.05) in the combination group than in the control group.The amount of palmitic acid and total saturated fatty acid in liver tissue decreased (P 〈 0.01 and P 〈 0.05, respectively) in the vitamin E and combination groups. However, the amount of linoleic acid only decreased (P 〈 0.05) in the combination group. The amount of PUFA was slightly higher (P 〈 0.05) in vitamin E. The proportions of stearic acid and linoleic acid decreased (P 〈 0.05) both in the Se and combination groups. However, the proportions of eicosatrienoic, ω 6, and PUFA were slightly higher (P 〈 0.05) in the vitamin E group, but total saturated fatty acid proportion significantly decreased (P 〈 0.01) in both the vitamin E and combination groups. In conclusion, the level of total lipid and cholesterol in muscle and liver tissues were reduced by administrating vitamin E and Se together. Additionally, the fatty acid synthesis in the muscle and liver tissues was decreased by this process. However, it was observed that the protective effect of intraperitoneally administrated vitamin E was higher than Se on fatty acid composition in muscle and liver tissues. J. Cell. Biochem. 64:233-241. © 1997 Wiley-Liss, Inc.
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    Peripheral benzodiazepine receptors in isolated human pancreatic islets (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 273-277 
    Details
    ISSN: 0730-2312
    Keywords: peripheral benzodiazepine receptor ; [3H]PK-11195 ; human islets ; insulin release ; Ro 5-4864 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Peripheral benzodiazepine receptors have been shown in some endocrine tissues, namely the testis, the adrenal gland, and the pituitary gland. In this work we evaluated whether peripheral benzodiazepine receptors can be found in the purified human pancreatic islets and whether they may have a role in insulin release. Binding of the isoquinoline compound [3H]1-(2-chlorophenyl-N-methyl-1-methyl-propyl)-3-isoquinolinecarboxamide ([3H]PK-11195), a specific ligand of peripheral benzodiazepine receptors, to cellular membranes was saturable, and Scatchard's analysis of the saturation curve demonstrated the presence of a single population of binding sites, with an affinity constant value of 9.20 ± 0.80 nM and a maximum number of binding sites value of 8913 ± 750 fmol/mg of proteins. PK-11195 and 7-chloro-1,3-dihydro-1-methyl-5-(p-chlorophenyl)-2H-1,4-benzodiazepin-2-on (Ro 5-4864) significantly potentiated insulin secretion from freshly isolated human islets at 3.3 mM glucose. These results show the presence of peripheral benzodiazepine receptors in purified human pancreatic islets and suggest their role in the mechanisms of insulin release. J. Cell. Biochem. 64:273-277. © 1997 Wiley-Liss, Inc.
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    Nonchromatin nuclear proteins of mammalian lens epithelial cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 644-650 
    Details
    ISSN: 0730-2312
    Keywords: nuclear matrix proteins ; transgenic murine lens epithelial cells ; vimentin ; human transgenic lens epithelial cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The nuclear matrix (NM) proteins of six tissue cultured lens epithelial cell lines and one embryonic rabbit epidermal cell line were analyzed to determine possible tissue and species specificity of these proteins. The NM proteins were isolated by the modified Penman technique. The tissue cultured cells were pulsed with [35S] methionine and nuclear matrix proteins were fractionated by two-dimensional (2-D) gel electrophoresis. The 2-D gels were dried and autoradiographed. The relative abundance of spot patterns of nuclear matrix proteins of different cells were compared. The data from these experiments revealed that all the examined cell lines have distinct spot patterns, however, all of NM profile showed a spot pattern in the 45 kDa region with acidic pH. Some of these spots cross-reacted with anti-vimentin antibodies, whereas a prominent protein spot in this region did not cross react with either vimentin or actin antibodies. The observed variations in the NM protein patterns of lens epithelial cells may reflect tissue and species specificity and also a role in the regulatory properties of these nuclear proteins in the eye tissue development. J. Cell. Biochem. 64:644-650. © 1997 Wiley-Liss, Inc.
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    HLH transcription factor activity in osteogenic cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 1-10 
    Details
    ISSN: 0730-2312
    Keywords: bHLH functional activity ; osteoblast differentiation ; gene expression ; osteogenesis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: To examine possible mechanisms underlying osteoblast differentiation from mesenchymal stem cells, we investigated bHLH functional activity in cell lines representing different stages of osteoblast maturation. Interaction of nuclear proteins with oligonucleotides corresponding to various bHLH binding sequences (known as E-boxes) was determined in mobility shift assays. Both ADD-1 oligonucleotide, a binding site for transcription factor ADD-1, and OCE-1, an E-box from osteocalcin promoter, produced retarded bands after incubation with nuclear extracts from osteogenic cells. Cells at different stages of osteogenic maturation demonstrated similar patterns and intensity of binding, as did cells treated with different osteogenic inducers. Binding to ADD-1 and OCE-1 was not tissue-specific as it was also observed in fibroblastic 10T1/2 cells. MEF-1 oligonucleotide, the E-box sequence from the muscle creatine kinase enhancer, demonstrated no changes in binding with nuclear extracts from moderately differentiated (W-20) or relatively mature (ROS 17/2.8) cells under any conditions tested. However, in poorly differentiated R1-2J cells, which do not express osteogenic markers unless treated with dexamethasone, induction of differentiation was reflected in transient inhibition of binding to MEF-1. Inhibition of binding was not seen under differentiation-restrictive conditions. Promoter-reporter studies also demonstrated inhibition of MEF-1 driven CAT expression by dexamethasone under differentiation-permissive conditions in R1-2J cells. These data suggest that bHLH gene expression is not required for the early steps of osteogenesis; moreover, inhibition of bHLH protein binding to a MEF1-type E box might be an integral part of osteogenic commitment. J. Cell. Biochem. 65:1-10. © 1997 Wiley-Liss, Inc.
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    State of methylation of the human osteocalcin gene in bone-derived and other types of cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 404-412 
    Details
    ISSN: 0730-2312
    Keywords: osteocalcin ; osteosarcoma cells ; methylation ; bone-derived cells ; DNA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: DNA methylation is a general mechanism of controlling tissue-specific gene expression. Osteocalcin is a bone matrix protein whose expression is limited almost entirely to osteoblasts. We were interested in determining whether the state of methylation of the osteocalcin gene plays a role in its expression by studying human bone-derived (MG-63, U2-Os, SaOs-2) and other types (normal lymphocytes, A-498, Hep G2) of cells. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that osteocalcin mRNA production is stimulated by 1,25(OH)2D3 in MG-63 and induced in SaOs-2 but not in U2-Os osteoblast-like osteosarcoma cells. Genomic analysis of the human osteocalcin gene showed that the local surroundings of this single-copy gene are identical in all cell lines studied. Using an isoschizomeric pair of restriction enzymes and Southern analysis, we found that the osteocalcin gene is identically methylated in all three osteosarcoma cell lines. The same sites are also methylated in human normal lymphocytes and A-498 kidney cells, whereas the degree of methylation is higher in Hep G2 human hepatocellular carcinoma cells. Furthermore, the osteocalcin gene was identically protected against enzymatic digestion at the chromatin level in normal lymphocytes and in all cell lines studied. Induction of hypomethylation of DNA by 5-azacytidine treatment did not cause an induction of osteocalcin synthesis in these cell lines. On the contrary, it attenuated the induction by 1,25(OH)2D3 in MG-63 cells. In gel mobility shift assays, human vitamin D receptor and the AP-1 transcription factor bound to an unmethylated response element oligonucleotide of the osteocalcin gene with greater affinity than to an in vitro methylated response element. These results indicate that the in vivo methylation state of the osteocalcin gene at sites determined in this study does not correlate with the inducibility of this gene. Nevertheless, the in vitro results clearly indicated that hypomethylation of critical regions of the osteocalcin gene promoter is a potential mechanism influencing effective binding of specific nuclear factors and, consequently, gene expression. J. Cell. Biochem. 66:404-412, 1997. © 1997 Wiley-Liss, Inc.
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    Reciprocal modulation between Sp1 and Egr-1 (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 489-499 
    Details
    ISSN: 0730-2312
    Keywords: competition ; gel retardation ; synthetic DNA binding site ; reporter gene activation ; immunoblotting ; overexpression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Many ubiquitously expressed genes, including oncogenes, lack a proximal TATA or CAAT box but have a region of G + C-rich sequences that appears to replace the usual promoter initiation site. The zinc-finger protein Sp1 is one of the prevalent activators of these genes. The Egr-1 zinc-finger protein has a similar binding site and if the two sites occur in the same region, a variety of activation or inhibitory responses may be obtained. We show that competition between the two factors for overlapping sites on growth-promoting genes could explain why the overexpression of Egr-1 suppresses transformed growth in a number of cell types [Huang et al. (1995): Cancer Res 55:5054-5062; Huang et al. (1997): Int J Cancer]. We demonstrate here that Egr-1 and Sp1 can bind to the same G + C-rich sites and that Egr-1 can displace Sp1 and hence inhibit its activity. We measured the responses of synthetic consensus binding sites and natural promoter sequences linked to a reporter gene and showed that Egr-1 inhibited the activation of transcription by Sp1 on overlapping Sp1/Egr-1 sites. In contrast, Sp1 activity could be augmented by Egr-1 at nonoverlapping sites in the Egr-1 gene promoter, in transient reporter gene studies in Drosophila SL2 cells. In addition, over-expression of exogenous Sp1 in mammalian cells, also leads to increased Egr-1 protein expression, which further inhibits Sp1 transactivation of numerous genes. Therefore, we can account for some of the complex responses of G + C-rich enhancer/promoters by a form of “facilitated inhibition” of Sp1 by Egr-1 at overlapping sites. J. Cell. Biochem. 66:489-499, 1997. © 1997 Wiley-Liss, Inc.
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    Induction of intracellular ceramide by interleukin-1β in oligodendrocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 532-541 
    Details
    ISSN: 0730-2312
    Keywords: oligodendrocytes ; II-1β ; ceramide ; sphingomyelin cycle ; apoptosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The sphingomyelin pathway has been implicated in mediating the effect of several extracellular agents leading to important biochemical and cellular changes. The aim of this investigation is to study interleukin-1β (IL-1β) signaling in oligodendrocytes. For this purpose, the CG4 oligodendrocyte cells were differentiated and incubated with IL-1β. This treatment induced a time- and dose-dependent increase of the endocellular ceramide. To mimic the effect of the elevation of endogenous ceramide, the CG4 cells were treated with the ceramide analogue C2-ceramide. Cell survival, measured with the MTT assay, showed that, by increasing the concentration of ceramide, up to 40% of CG4 cells were dying within 6 h, similar data were obtained with the primary differentiated oligodendrocytes. Condensation of chromatin, nuclear fragmentation, and formation of apoptotic bodies indicated that apoptosis was the cause of death. Surprisingly, long-term exposure (72 h) to increasing concentrations of IL-1β, which increases intracellular ceramide, did not induce oligodendroglial cell death. These results show that an increase of intracellular ceramide is not sufficient to induce apoptosis in oligodendrocytes and that IL-1β signaling through the ceramide pathway in these cells can mediate functions other than programmed cell death. J. Cell Biochem. 66:532-541, 1997. © 1997 Wiley-Liss, Inc.
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    Downregulation of telomerase activity in HL60 cells by differentiating agents is accompanied by increased expression of telomerase-associated protein (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 13-23 
    Details
    ISSN: 0730-2312
    Keywords: telomerase ; TP1 ; HL60 cells ; leukemia ; differentiation therapy ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Telomerase activity provides a mechanism for the unlimited division potential of neoplastic cells. Induced differentiation of these cells was found to be associated with repression of telomerase activity irrespective of the inducing agent. We have employed a series of sublines of human promyelocytic leukemia line HL60 with differing degrees of resistance to differentiation to determine how tightly the expression of the differentiated phenotype is coupled to the downregulation of telomerase activity and to the expression of the recently identified telomerase-associated protein 1 (TP1). As expected, in the 1,25D3-dihydroxyvitamin D3 (1,25D3)-resistant subclones (20A-100A cells), telomerase activity was not significantly downregulated by 1,25D3 and, in most cases, by all-trans retinoic acid (atRA), to which these cells were cross-resistant, but telomerase activity was repressed by dimethylsulfoxide (DMSO) and phorbol-12-myristate-13-acetate (TPA), to which the sublines were in general sensitive. However, there were exceptions; in some instances telomerase activity was repressed in the absence of the expression of markers of differentiation. Also, there was an inverse relationship between telomerase activity and the cellular levels of TP1 transcripts. We conclude that in HL60 cells downregulation of telomerase is loosely associated with upregulation of differentiation markers and with other cellular changes which include an upregulation of TP1. J. Cell. Biochem. 67:13-23, 1997. © 1997 Wiley-Liss, Inc.
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    Suppression of extracellular signals and cell proliferation through EGF receptor binding by (-)-epigallocatechin gallate in human A431 epidermoid carcinoma cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 55-65 
    Details
    ISSN: 0730-2312
    Keywords: (-)-epigallocatechin gallate ; epidermal growth factor receptor ; platelet-derived growth factor ; fibroblast growth factor ; protein tyrosine kinases ; receptor tyrosine kinases ; protein kinase A ; protein kinase C ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Tea polyphenols are known to inhibit a wide variety of enzymatic activities associated with cell proliferation and tumor progression. The molecular mechanisms of antiproliferation are remained to be elucidated. In this study, we investigated the effects of the major tea polyphenol (-)-epigallocatechin gallate (EGCG) on the proliferation of human epidermoid carcinoma cell line, A431. Using a [3H]thymidine incorporation assay, EGCG could significantly inhibit the DNA synthesis of A431 cells. In vitro assay, EGCG strongly inhibited the protein tyrosine kinase (PTK) activities of EGF-R, PDGF-R, and FGF-R, and exhibited an IC50 value of 0.5-1 μg/ml. But EGCG scarcely inhibited the protein kinase activities of pp60v-src, PKC, and PKA (IC50 〉 10 μg/ml). In an in vivo assay, EGCG could reduce the autophosphorylation level of EGF-R by EGF. Phosphoamino acid analysis of the EGF-R revealed that EGCG inhibited the EGF-stimulated increase in phosphotyrosine level in A431 cells. In addition, we showed that EGCG blocked EGF binding to its receptor. The results of further studies suggested that the inhibition of proliferation and suppression of the EGF signaling by EGCG might mainly mediate dose-dependent blocking of ligand binding to its receptor, and subsequently through inhibition of EGF-R kinase activity. J. Cell. Biochem. 67:55-65, 1997. © 1997 Wiley-Liss, Inc.
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    Regulation of the rat interstitial collagenase promoter by IL-1β, c-Jun, and ras-dependent signaling in growth plate chondrocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 92-102 
    Details
    ISSN: 0730-2312
    Keywords: collagenase promoter ; TRE ; chondrocyte ; interleukin-1β ; DNA binding ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In an attempt to better define molecular influences on rat interstitial collagenase gene expression in cartilage, the promoter function was characterized using transient transfection assay, electrophoresis mobility shift assay, and genetic analysis in isolated growth plate chondrocytes. Data from 5′-flanking deletion and selected mutations suggest that multiple cis elements in both the proximal and distal regions of the promoter were important in the regulation of promoter activity. A proximal tumor response element (TRE) was shown to be necessary for basal and interleukin (IL)-1β-inducible reporter gene activity. Cells stimulated by IL-1β (1 ng/ml; 18 h) had elevated TRE binding activity, and one of the factors involved was identified as the nuclear protein, c-Jun. Indeed, c-Jun directed antisense oligonucleotides reduced rat interstitial collagenase mRNA. A sense oligonucleotide was ineffective. Regulation of promoter activity was susceptible to Ras-dependent signaling as expression of dominant negative mutant of Ras kinase (pZIP-RasN17) reduced reporter gene activity. In a comparison of proximal promoter reporter plasmid activity between proliferative and hypertrophic cells, inhibition of Ras-dependent signaling was less effective in the later cell type. This study suggests that the activation of nuclear binding proteins that bind TRE may be a common event with IL-1β regulation. Moreover, these data suggest that the regulation of rat interstitial collagenase gene expression is a combinatorial process and multiple cis-acting regulatory sites may interact to exert different effects dependent on the stage of chondrocyte differentiation. J. Cell. Biochem. 67:92-102, 1997. Published 1997 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
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    Expression of meltrin-α mRNA is not restricted to fusagenic cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 136-142 
    Details
    ISSN: 0730-2312
    Keywords: Meltrin-α ; ADAM ; osteoblast ; cell fusion ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Meltrin-α is a myoblast gene product reported to be required for cell fusion [Yagami-Hiromasa et al. (1995): Nature 377:652-656]. Because Northern blots revealed expression only in muscle and bone, the suggestion was made that meltrin-α is expressed exclusively by fusagenic cells in these tissues (myoblast and osteoclast). We studied expression of meltrin-α mRNA in a panel of tissues and cell lines using the polymerase chain reaction and found it widely expressed. Meltrin-α mRNA was readily detected in the osteoblast, the most abundant cell type in bone. In situ hybridization analysis on sections of neonatal mice revealed high levels of expression in the trabecular meshwork of long bones, the basal regions of the dermis and its underlying mesenchyme. We conclude that expression of meltrin-α mRNA is not restricted to fusagenic cells and that, in bone, the osteoblast is the major source. J. Cell. Biochem. 67:136-142, 1997. © 1997 Wiley-Liss, Inc.
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    Insulin-like growth factor I inhibits the transcription of collagenase 3 in osteoblast cultures (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 176-183 
    Details
    ISSN: 0730-2312
    Keywords: bone matrix ; collagen ; growth factors ; interstitial collagenase ; matrix metalloproteinases ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin-like growth factor (IGF) I is an autocrine regulator of bone remodeling which inhibits bone collagen degradation and interstitial collagenase 3 mRNA levels. The mechanism of this inhibitory effect on collagenase 3 expression is not known. We tested the effects of IGF I on collagenase 3 gene expression in cultures of osteoblast-enriched cells from 22 day fetal rat calvariae (Ob cells) to determine whether transcriptional or posttranscriptional mechanisms were involved in the regulation of the collagenase 3 gene. IGF I at 10-100 nM caused a dose-dependent decrease in collagenase mRNA and protein levels. IGF I did not modify the half-life of collagenase 3 mRNA in transcriptionally arrested Ob cells, whereas it decreased the levels of interstitial collagenase 3 heterogeneous nuclear RNA. In addition, IGF I decreased the rates of transcription of the collagenase gene and the activity of a 2.1 kilobase collagenase 3 promoter construct transiently transfected into Ob cells. In conclusion, IGF I decreases the expression of collagenase 3 mRNA by transcriptional mechanisms. J. Cell. Biochem. 67:176-183, 1997. © 1997 Wiley-Liss, Inc.
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    Role of cell cycle regulators in tumor formation in transgenic mice expressing the human neurotropic virus, JCV, early protein (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 223-230 
    Details
    ISSN: 0730-2312
    Keywords: human JC virus ; p53 ; T-antigen ; transgenic mice ; tumor cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Transgenic mice harboring the early genome from the human neurotropic JC virus, JCV, develop massive abdominal tumors of neural crest origin during 6-8 months after birth and succumb to death a few weeks later. The viral early protein, T-antigen, which possesses the ability to transform cells of neural origin, is highly expressed in the tumor cells. Immunoblot analysis of protein extract from tumor tissue shows high level expression of the tumor suppressor protein, p53, in complex with T-antigen. Expression of p21, a downstream target for p53, which controls cell cycle progression by regulating the activity of cyclins and their associated kinases during the G1 phase, is extremely low in the tumor cells. Whereas the level of expression and activity of cyclin D1 and its associated kinase, cdk6, was modest in tumor cells, both cyclin A and E, and their kinase partners, cdk2 and cdk4, were highly expressed and exhibited significant kinase activity. The retinoblastoma gene product, pRb, which upon phosphorylation by cyclins:cdk induces rapid cell proliferation, was found in the phosphorylated state in tumor cell extracts, and was detected in association with JCV T-antigen. The transcription factor, E2F-1, which dissociates from the pRb-E2F-1 complex and stimulates S phase-specific genes upon phosphorylation of pRb and/or complexation of pRb with the viral transforming protein, was highly expressed in tumor cells. Accordingly, high level expression of the E2F-1-responsive gene, proliferating cell nuclear antigen (PCNA), was detected in the tumor cells. These observations suggest a potential regulating pathway that, upon expression of JCV T-antigen, induces formation and progression of tumors of neural origin in a whole animal system. J Cell. Biochem. 67:223-230, 1997. © 1997 Wiley-Liss, Inc.
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    1α,25-Dihydroxyvitamin D3 receptor as a mediator of transrepression of retinoid signaling (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 287-296 
    Details
    ISSN: 0730-2312
    Keywords: vitamin D3 receptor ; regulation of transcription ; retinoid signaling transrepression ; tumor necrosis factor-α receptor type I ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The receptors for retinoic acid (RA) and for 1α,25-dihydroxyvitamin D3 (VD), RAR, RXR, and VDR are ligand-inducible members of the nuclear receptor superfamily. These receptors mediate their regulatory effects by binding as dimeric complexes to response elements located in regulatory regions of hormone target genes. Sequence scanning of the tumor necrosis factor-α type I receptor (TNFαRI) gene identified a 3′ enhancer region composed of two directly repeated hexameric core motifs spaced by 2 nucleotides (DR2). On this novel DR2-type sequence, but not on a DR5-type RA response element, VD was shown to act through its receptor, the vitamin D receptor (VDR), as a repressor of retinoid signalling. The repression appears to be mediated by competitive protein-protein interactions between VDR, RAR, RXR, and possibly their cofactors. This VDR-mediated transrepression of retinoid signaling suggests a novel mechanism for the complex regulatory interaction between retinoids and VD. J. Cell. Biochem. 67:287-296, 1997. © 1997 Wiley-Liss, Inc.
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    Cyclic strain stimulates isoform-specific PKC activation and translocation in cultured human keratinocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 327-337 
    Details
    ISSN: 0730-2312
    Keywords: protein kinase C (PKC) ; keratinocytes ; cyclic strain ; proliferation ; morphology ; PKC isoforms ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Previous studies have demonstrated that cyclic strain induces keratinocyte proliferative and morphological changes. Since protein kinase C (PKC) is known to play an important role in the regulation of keratinocyte growth and differentiation, the objective of this study was to determine the role of the PKC signaling pathway as a mediator of strain modulation of the keratinocyte phenotype. In particular, we tested the following specific hypotheses: (1) cyclic strain stimulates PKC activity and translocation, (2) cyclic strain activates PKC in an isoform-specific manner, and (3) PKC mediates the strain activated proliferative and morphological response in cultured human keratinocytes. To test these hypotheses, keratinocytes were subjected to vacuum-generated cyclic strain (10% average strain), followed by measurement of PKC activity, PKC isoform distribution by Western blot analysis and confocal microscopy, and examination of the effect of PKC inhibitors (calphostin C and staurosporine) on strain induced proliferative and morphological changes. We observed stimulation of PKC activity (62.3 ± 5.1% increase) coupled with translocation of PKC from the cytosolic to the membrane fraction in keratinocytes subjected to acute cyclic strain. Cyclic strain also caused translocation of PKC α and δ, but not ζ isoforms, from the cytosolic to the membrane fraction as demonstrated by both Western blot analysis and confocal microscopy. PKC β was not detected in these cells. PKC inhibitors, calphostin C (10 nM), and staurosporine (5 nM), inhibited strain-induced PKC activation and keratinocyte proliferation, but did not block the effects of strain on cellular morphology or alignment. We conclude that these data support our hypothesis that cyclic strain stimulates PKC activity and translocation in an isoform-specific manner in cultured human keratinocytes. Moreover, our studies with PKC inhibitors support the hypothesis that strain-induced changes in the keratinocyte phenotype may be selectively modulated by PKC. J. Cell. Biochem. 67:327-337, 1997. © 1997 Wiley-Liss, Inc.
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    Increased expression of c-jun, but not retinoic acid receptor β, is associated with F9 teratocarcinoma stem cell differentiation induced by polyamine depletion (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 378-385 
    Details
    ISSN: 0730-2312
    Keywords: α-difluoromethylornithine ; ornithine decarboxylase ; parietal endoderm ; retinoic acid receptor α ; retinoic acid receptor γ ; tissue plasminogen activator ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: α-Difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ornithine decarboxylase, and all-trans-retinoic acid (RA) are known to induce F9 teratocarcinoma stem cell differentiation. Both compounds induce the formation of the same cell type, i.e., parietal endoderm-like cells expressing tissue plasminogen activator and collagen type IV α-1. The present study shows that DFMO and RA induce terminal differentiation of F9 cells through different pathways. Thus, retinoic acid receptor (RAR) α mRNA is weakly expressed during DFMO treatment, but strongly induced during an early phase of RA treatment. RAR β mRNA is not detectable in DFMO-treated cells, but very strongly induced by RA and maintained at a high level throughout the differentiative process. RAR γ mRNA is relatively strongly expressed in untreated control cells and remains at approximately the same level during DFMO-induced differentiation. In RA-treated cells, however, RAR γ mRNA is rapidly down-regulated and becomes nondetectable during the final course of differentiation. These experiments show that the differentiation of F9 cells into parietal endoderm-like cells does not necessarily involve changes in any of the RAR mRNA subtypes. Even though the steady-state levels of the RAR α and RAR γ transcripts may be sufficient to support the differentiative process, our data clearly show that induction of RAR β mRNA transcription is neither a prerequisite for F9 cell differentiation, nor an absolute consequence of the elevated c-jun mRNA expression that is consistently observed during the course of parietal endoderm differentiation. J. Cell. Biochem. 67:378-385, 1997. © 1997 Wiley-Liss, Inc.
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    Synergistic role of E1A-Binding proteins and tissue-specific transcription factors in differentiation (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 423-431 
    Details
    ISSN: 0730-2312
    Keywords: differentiation ; E1A-binding proteins ; DNA tumor viruses ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In this review, the complex relationship between tissue-specific transcription factors and genes regulating cell cycle is taken into account. Both E1-A binding proteins belonging to the family of the retinoblastoma gene product and the CBP/p300 coactivator of transcription interact physically and functionally with tissue-specific transcription factor. The relationship between these two classes of molecules regulates cell fate in differentiating cells, deciding whether cells continue to replicate, undergo apoptosis or terminally differentiate. We provide here an update on the recent advances in this field and some models of interaction between E1A binding protein and tissue-specific transcription factors. J. Cell. Biochem. 67:423-431, 1997. © 1997 Wiley-Liss, Inc.
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    Identification of a cellular protein that binds to tat-responsive element of TGFβ-1 promoter in glial cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 466-477 
    Details
    ISSN: 0730-2312
    Keywords: Tat ; TAR ; HIV-1 ; TGFβ-1 promoter ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Tat is a transcriptional transactivator produced by the human immunodeficiency virus type 1 (HIV-1) and plays a pivotal role in enhancing expression of the viral genome in the infected cells. Although initial studies have suggested that interaction of Tat with the transactivation responsive element (TAR), located within the LTR, is essential for Tat function, subsequent studies indicated that Tat has the ability to augment transcription of viral and cellular genes by a TAR-independent mechanism. In early studies we demonstrated that HIV-1 Tat stimulates transcription of the transforming growth factor, TGFβ-1, gene in glial cells. In this study, we have identified a cellular protein that interacts with the Tat-responsive region located between nucleotides -323 to -453 of the regulatory sequence of the TGFβ-1 promoter. Results from footprinting analysis revealed association of cellular proteins with the 130 nucleotide sequence located in the Tat-responsive region. Analysis of the associated protein by UV-crosslinking suggested the involvement of a protein between 40-45 kDa in size which preferentially interacts with the GC/GA rich sequence of the TGFβ-1 Tat-responsive sequence in a single-stranded configuration. The ability of the previously identified 40 kDa protein, named Pur α to bind to the GC/GA sequence in the single-stranded configuration, similar to those from TGFβ-1 promoter prompted us to investigate its binding capacity to the TGFβ-1 sequence and its transcriptional activity on the TGFβ-1 promoter. Results from band shift studies indicated the association of the bacterially produced Pur α to the TGFβ-1 DNA sequences positioned within the Tat-responsive region. Overexpression of Pur α in glial cells constitutively producing Tat augmented transcription of the TGFβ-1 gene. These results are consistent with previous reports on the cooperative action of Pur α and Tat in modulating other eukaryotic promoters. The importance of these findings with regard to deregulation of other cellular genes by HIV-1 Tat is discussed. J. Cell. Biochem. 67:466-477, 1997. © 1997 Wiley-Liss, Inc.
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    Effect of osteogenic protein-1 on the development and mineralization of primary cultures of avian growth plate chondrocytes: Modulation by retinoic acid (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 498-513 
    Details
    ISSN: 0730-2312
    Keywords: chondrocytes ; osteogenic protein-1 ; retinoic acid ; mineralization ; ALP ; proteoglycans ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Osteogenic protein-1 (OP-1), a member of the TGF-β family of proteins, induces endochondral bone formation. Here we studied the effect of OP-1 on the development of primary cultures of avian growth plate (GP) chondrocytes in either serum-free or serum-containing medium, in the absence or presence of retinoic acid (RA). OP-1 was added on day 7 of culture and continued for 7 days, or until the cultures were harvested, typically on day 21. Alone, OP-1 caused ∼2-fold increase in proteoglycan synthesis into both the medium and the cell:matrix layer. Additionally, OP-1 caused a dosage-dependent increase in alkaline phosphatase (ALP) activity, and an increase in protein, when given from days 7-14 and examined on day 14. This stimulation was greater in cells grown in serum-free than in serum-containing media (3-5-fold vs. 2-3-fold increase in ALP; ∼40% vs. ∼20% increase in protein). Such stimulation of ALP activity and proteoglycan (PG) synthesis in cultured GP cells indicates that OP-1 elicits differentiation of chondrocytes. OP-1 minimally affected cell division (DNA content); however, a slight increase was seen when examined early in the culture. Alone, OP-1 increased mineral (Ca and Pi) content of the cultures by ∼2-fold in both types of media. As early as day 14, clusters of mineral encircled many of the OP-1 treated cells. Thus, as in vivo, OP-1 strongly promoted mineral formation by the cultured GP chondrocytes. When present together, OP-1 and RA generally blocked the action of the other. Separately OP-1 and RA each stimulated protein synthesis, ALP activity, and Ca2+ deposition; together they were inhibitory to each. Also, RA blocked the stimulation of PG synthesis induced by OP-1; whereas OP-1 decreased cell division engendered by RA. Thus, this GP chondrocyte culture system is a good model for studying factors that influence differentiation and mineral deposition during bone growth in vivo. J. Cell. Biochem. 67:498-513, 1997. © 1997 Wiley-Liss, Inc.
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    Progress in cancer chemoprevention: Agents (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. vi 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: No abstract.
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    Protocol design considerations that relate to demonstrating the safety and effectiveness of chemopreventive agents (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 1-6 
    Details
    ISSN: 0730-2312
    Keywords: cancer ; chemoprevention ; clinical trial ; surrogate endpoint biomarker ; protocol design ; safety ; efficacy ; FDA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: As with other drugs, applications for marketing approval of new chemopreventive agents in the United States must include data from adequate and well-controlled clinical trials that demonstrate effectiveness and safety for the intended use. Knowledge of a drug's pharmacologic actions and metabolism may benefit protocol design, by identifying the patient populations and dosing schedules associated with a favorable risk/benefit profile. With availability of appropriate preclinical data, including standard assessments of an agent's toxicology, effects on reproductive performance, and genotoxicity, initial Phase I studies of 1-3 months may be performed in normal volunteers or an appropriate higher-risk population. For chronic dosing studies of longer duration, preclinical toxicology studies of longer duration are relevant. Enrollment in chemoprevention studies should be directed toward individuals at sufficient risk of developing cancer so that potential benefit may counterbalance the unpredictable and possibly serious adverse effects that may be observed with prolonged administration of a study drug. Phase I and II studies with clinical dosing lasting up to 12 months often afford opportunities to assess drug effect on surrogate endpoint biomarkers that may correlate with endpoints of clinical effectiveness. Phase III and late phase II chemopreventive investigations should routinely utilize a prospective, randomized study design (double-masked and placebo-controlled, when possible). To support marketing approval, there must be evidence that a chemopreventive agent significantly delays or prevents the occurrence of malignancy, with acceptable safety. In some circumstances, modulation of a surrogate marker may provide a basis for marketing approval, before more definitive endpoint data become available. However, the acceptability of a surrogate depends on the nature and quality of the data supporting its predictive value. Given the considerations of large study size, long duration, and high cost that may hamper development of potential agents, studies designed to examine the predictive value of surrogate endpoint biomarkers are of great importance to the future development of chemoprevention research. J. Cell. Biochem. Suppl. 27:1-6. Published 1998 Wiley-Liss, Inc.
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    Research and development of cancer chemopreventive agents in China (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 7-11 
    Details
    ISSN: 0730-2312
    Keywords: cancer chemoprevention ; N-4-(carboxyphenyl)retinamide ; chalcone retinoid ; red ginseng ; glycyrrhetinic acid ; Chinese gallotannin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Since the late 1970s, a comprehensive search for cancer chemopreventive agents has been established in our Institute. A series of new retinoids have been synthesized and screened on the basis of established methodologies of experimental chemoprevention in vitro as well as in vivo. Pharmacological studies demonstrated that N-4-(carboxyphenyl)retinamide (RII) induces cell differentiation of HL-60 cells and inhibits dimethylnitrosamine-induced carcinogenesis of the forestomach in mice, 7,12-dimethylbenz[a]anthracene (DMBA)-induced papilloma in mouse skin, and DMBA-induced carcinogenesis of the buccal pouch in Syrian golden hamsters. It significantly promoted lymphoblastic transformation and activated macrophages. In further studies, RII significantly inhibited ornithine decarboxylase activity. After 6 months of chronic toxicological studies in rats and dogs, RII was recommended for clinical trial. Phase II studies found that RII is effective in treating oral and vulvar leukoplakia. It is also effective in treating myelodysplastic syndrome and dysplasia of uterine cervix. The chalcone retinoidal compounds were discovered when the search for new retinoids with less toxicity and higher potency led to third-generation retinoids, which were synthesized and screened. Structure-activity relationship studies found that 3,5-di-tert-butyl-4-methoxy-4-carboxyl chalcone (R9158) is the most active inhibitor of a variety of cancer cells. It has no effect on the Colony Forming Unit-Granulocyte/Macrophage (CFU-GM) of bone marrow in mice. In in vivo studies, R9158 showed a remarkable inhibition of chondrosarcoma in rats. It had no cross-resistance to vincristine, but was cross-resistant to all-trans retinoic acid. Red ginseng, a processed Panax ginseng, is considered a typical tonic in traditional Chinese medicine. Our studies demonstrated that red ginseng extract inhibited DMBA-induced skin papilloma significantly. Experiments showed that glycyrrhetinic acid inhibited croton oil-induced ear edema in mice. It also inhibited epidermal ornithine decarboxylase as well as the rapid DNA damage induced by the carcinogen benzo[a]pyrene (B[a]P). Our pharmacological studies demonstrated that Chinese gallotannin inhibited the malignant transformation of B[a]P-induced V79 cells in vitro and B[a]P-induced pulmonary adenoma in A/J mice in vivo significantly. J. Cell. Biochem. Suppl. 27:7-11 © 1998 Wiley-Liss, Inc.
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    Chemopreventive properties of Indole-3-Carbinol (I3C): Inhibition of DNA adduct formation of the dietary carcinogen, 2-Amino-1-Methyl-6-Phenylimidazo [4,5-b]Pyridine (PhIP), in female F344 rats (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 42-51 
    Details
    ISSN: 0730-2312
    Keywords: food mutagens ; indole-3-carbinol ; chemoprevention ; DNA adducts ; PhIP ; heterocyclic amines ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Indole-3-carbinol (I3C), a naturally occurring inhibitor of experimental carcinogenesis, was evaluated for its possible inhibitory effect on DNA-adduct formation of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a dietary mutagen, in female F344 rats. PhIP is a mammary carcinogen in female F344 rats and a colon carcinogen in male F344 rats. Four-week-old animals (4/group) were maintained on powdered AIN-76A diet with or without I3C (0.02% or 0.1%, w/w) for 58 days. PhIP (0.04%, w/w) was added to the diet from days 15 through 42. Animals were killed on days 43 and 58. DNA isolated from mammary epithelial cells (MECs), colon, liver, and white blood cells (WBCs) was analyzed for PhIP-DNA adducts by 32P-postlabeling assays. On day 43, adduct levels of the group receiving 0.1% dietary I3C decreased in MECs (91.9%), colon (67.2%), liver (69.2%), and WBCs (82.3%). On day 58, DNA adduct formation was inhibited in the colon (81.3-82.2%) at both dietary I3C concentrations, and in liver (46.8%) only in the animals fed 0.1% I3C. When incorporated in the diet after exposure to dietary PhIP (0.04% for 2 weeks), I3C (0.1%) had no effect on the rate of removal of PhIP-DNA adducts over the next 28 days. It is concluded that dietary I3C inhibits PhIP-DNA adduct formation in the female F344 rat but does not affect adduct removal. I3C may be a promising chemopreventive agent in PhIP-induced carcinogenesis in rats. J. Cell. Biochem. Suppl. 27:42-51. © 1998 Wiley-Liss, Inc.
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    Binding of SPAAT, the 44-residue C-terminal peptide of α1-antitrypsin, to proteins of the extracellular matrix (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 346-357 
    Details
    ISSN: 0730-2312
    Keywords: α1-antitrypsin ; collagen binding protein ; laminin-1 binding protein ; extracellular matrix binding protein ; Matrigel ; Amgel ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: SPAAT (short piece of α1-antitrypsin [AAT]), the 44-residue C-terminal peptide of AAT, was originally isolated from human placenta [Niemann et al. (1992): Matrix 12:233-241]. It was shown to be a competitive inhibitor of serine proteases [Niemann et al. (in press): Biochem Biophys Acta]. The binding of SPAAT to one or more proteins of the extracellular matrix (ECM) was initially suggested on the basis of its recovery from tissue residues following a series of extractions designed to remove easily solubilized proteins [Niemann et al. (1992): Matrix 12:233-241]. Our binding studies with the model ECMs, Matrigel and Amgel, suggested that SPAAT might be bound by a specific collagen type as well as one or more non-collagenous ECM proteins. Individual ECM components were screened for their ability to bind SPAAT. When the four commonly occurring fiber-forming collagens (types I, II, III, and V) were evaluated, type III was found to be preferred. In addition, although SPAAT bound to preformed type III collagen fibers in a concentration dependent fashion, it did not bind to type III collagen molecules undergoing fibril formation. This is consistent with a physiological mode of interaction between SPAAT and type III collagen in vivo. Of the non-collagenous ECM macromolecules (laminin-1, fibronectin, entactin, and heparan sulfate) tested, laminin-1 was preferred. The binding of radiolabelled SPAAT to type III collagen and laminin-1 was competitively inhibited by unlabelled SPAAT as well as an unrelated protein, human serum albumin (HSA), to establish binding specificity. The kinetics of the release of the bound radiolabelled SPAAT were also examined to substantiate the non-covalent and reversible nature of this association. These results support the view that susceptible proteins of the ECM may actually be coated with SPAAT in vivo, possibly affording protection against inappropriate protease digestion. J. Cell. Biochem. 66:346-357, 1997. © 1997 Wiley-Liss, Inc.
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    Transcriptional and posttranscriptional mechanisms of glucocorticoid-mediated repression of phosphoenolpyruvate carboxykinase gene expression in adipocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 386-393 
    Details
    ISSN: 0730-2312
    Keywords: glucocorticoids ; PEPCK ; gene expression ; adipocytes ; dexamethasone ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Glucocorticoids exert pleiotropic effects, among which negative regulation of transcription has been recognized as of crucial importance. While glucocorticoids induce phosphoenolpyruvate carboxykinase (PEPCK) gene expression in liver cells, it represses gene activity in adipose cells. We used the 3T3-F442A adipocytes to analyze the underlying mechanisms. In these cells, the synthetic glucocorticoid dexamethasone exerts a dominant repression either on basal or on β-agonist stimulation of PEPCK gene expression. To determine whether glucocorticoid action required protein synthesis, we employed cycloheximide, anisomycin, and puromycin, three different translation inhibitors. None of these affected induction by isoprenaline or repression by dexamethasone of isoprenaline stimulation. In contrast, dexamethasone inhibitory action on basal PEPCK mRNA was totally prevented by the three translation inhibitors. Time courses of glucocorticoid action on basal and on induction by β-agonist were similar. Half-maximal effect of dexamethasone on isoprenaline-induced PEPCK mRNA was obtained at about 10 nM, a tenfold higher concentration than that observed for the reduction of basal mRNA. Using the transcription inhibitor DRB, we showed that dexamethasone did not alter mRNA half-life, while isoprenaline strongly stabilized mRNA. In a 3T3-F442A stable transfectant bearing -2,100 base pairs of the PEPCK promoter fused to the chloramphenicol acetyltransferase (CAT) gene, isoprenaline stimulated CAT activity, whereas dexamethasone reduced basal and isoprenaline-induced CAT expression. Hence, β-agonists exert both transcriptional and posttranscriptional regulation, while glucocorticoid action is purely transcriptional. However, mechanisms of glucocorticoid repression of basal and of β-agonist stimulation appear different. J. Cell. Biochem. 66:386-393, 1997. © 1997 Wiley-Liss, Inc.
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    Presence of an unusually high concentration of an ubiquitinated histone-like protein in Trypanosoma cruzi (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 433-440 
    Details
    ISSN: 0730-2312
    Keywords: ubiquitin ; Trypanosoma cruzi ; histone proteins ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The conjugation of ubiquitin to histones H2A and H2B has been established in higher eukaryotes and has been related to changes in chromatin organization. In Trypanosoma cruzi, no condensation of chromatin occurs during mitosis. In order to determine the presence of histone ubiquitination in T. cruzi epimastigotes, histones were extracted from chromatin and analyzed by three electrophoretic systems: acid-urea, triton-acid-urea and sodium-dodecyl-sulphate polyacrylamide gel. The immunochemical detection of ubiquitin-histone conjugates by Western blotting showed a strong reaction with a slow migrating band of Mr 19 kDa. The high percentage of ubiquitin-histone conjugates present in T. cruzi chromatin may be related to the inability of this parasite to condense chromatin into a 30 nm fiber. J. Cell. Biochem. 66:433-440, 1997. © 1997 Wiley-Liss, Inc.
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    Hybrid structural analogues of 1,25-(OH)2D3 regulate chondrocyte proliferation and proteoglycan production as well as protein kinase C through a nongenomic pathway (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 457-470 
    Details
    ISSN: 0730-2312
    Keywords: vitamin D ; analogue ; chondrocytes ; nongenomic ; differentiation ; 1,25-(OH)2D3 ; 24,25-(OH)2D3 ; proteoglycan ; protein kinase C ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: 1,25-(OH)2D3 and 24,25-(OH)2D3 mediate their effects on chondrocytes through the classic vitamin D receptor (VDR) as well as through rapid membrane-mediated mechanisms which result in both nongenomic and genomic effects. In intact cells, it is difficult to distinguish between genomic responses via the VDR and genomic and nongenomic responses via membrane-mediated pathways. In this study, we used two hybrid analogues of 1,25-(OH)2D3 which have been modified on the A-ring and C,D-ring side chain (1α-(hydroxymethyl)-3β-hydroxy-20-epi-22-oxa-26,27-dihomo vitamin D3 (analogue MCW-YA = 3a) and 1β-(hydroxymethyl)-3α-hydroxy-20-epi-22-oxa-26,27-dihomo vitamin D3 (analogue MCW-YB = 3b) to examine the role of the VDR in response of rat costochondral resting zone (RC) and growth zone (GC) chondrocytes to 1,25-(OH)2D3 and 24,25-(OH)2D3. These hybrid analogues are only 0.1% as effective in binding to the VDR from calf thymus as 1,25-(OH)2D3. Chondrocyte proliferation ([3H]-thymidine incorporation), proteoglycan production ([35S]-sulfate incorporation), and activity of protein kinase C (PKC) were measured after treatment with 1,25-(OH)2D3, 24,25-(OH)2D3, or the analogues. Both analogues inhibited proliferation of both cell types, as did 1,25-(OH)2D3 and 24,25-(OH)2D3. Analogue 3a had no effect on proteoglycan production by GCs but increased that by RCs. Analogue 3b increased proteoglycan production in both GC and RC cultures. Both analogues stimulated PKC in GC cells; however, neither 3a nor 3b had an effect on PKC activity in RC cells. 1,25-(OH)2D3 and 3a decreased PKC in matrix vesicles from GC cultures, whereas plasma membrane PKC activity was increased, with 1,25-(OH)2D3 having a greater effect. 24,25-(OH)2D3 caused a significant decrease in PKC activity in matrix vesicles from RC cultures; 24,25-(OH)2D3, 3a, and 3b increased PKC activity in the plasma membrane fraction, however. Thus, with little or no binding to calf thymus VDR, 3a and 3b can affect cell proliferation, proteoglycan production, and PKC activity. The direct membrane effect is analogue-specific and cell maturation-dependent. By studying analogues with greatly reduced affinity for the VDR, we have provided further evidence for the existence of a membrane receptor(s) involved in mediating nongenomic effects of vitamin D metabolites. J. Cell. Biochem. 66:457-470, 1997. © 1997 Wiley-Liss, Inc.
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    Electromagnetic field exposure induces rapid, transitory heat shock factor activation in human cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 482-488 
    Details
    ISSN: 0730-2312
    Keywords: cellular stress ; heat shock element (HSE) ; heat shock factor (HSF) ; electrophoretic mobility shift assay (EMSA) ; electromagnetic (EM) field ; heat shock protein (hsp) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Stimulation of human promyelocytic HL60 cells by a 60Hz magnetic field at normal growth temperatures results in heat shock factor 1 activation and heat shock element binding, a sequence of events that mediates the stress-induced transcription of the stress gene HSP70 and increased synthesis of the stress response protein hsp70kD. Thus, the events mediating the electromagnetic field-stimulated stress response appear to be similar to those reported for other physiological stresses (e.g., hyperthermia, heavy metals, oxidative stress) and could well be the general mechanism of interaction of electromagnetic fields with cells. J. Cell. Biochem. 66:482-488, 1997. © 1997 Wiley-Liss, Inc.
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    Epitope conservation and immunohistochemical localization of the guanylin/stable toxin peptide receptor, guanylyl cyclase C (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 500-511 
    Details
    ISSN: 0730-2312
    Keywords: heat-stable enterotoxin ; guanylyl cyclase C ; monoclonal antibody ; immunohistochemical localization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The heat-stable enterotoxins (ST) are a family of cysteine-rich low-molecular weight peptides produced by pathogenic bacteria, and are one of the major causes of watery diarrhea all over the world. These toxins mediate their action by binding to an intestinal cell surface receptor that is a membrane-associated guanylyl cyclase (GCC). This receptor also serves as the receptor for the recently characterised endogenous ligand, guanylin. We have expressed various domains of the receptor in Escherichia coli and used purified proteins for the generation of both polyclonal and monoclonal antibodies. While polyclonal antibodies were able to partially inhibit ST binding to the native receptor present in the T84 human colonic cell line, GCC:B10 monoclonal antibody did not interfere with ligand binding. Western blot analysis, using membranes prepared from human colonic T84 cells, detected two bands of size 160 and 140 kDa, representing alternately glycosylated forms of the receptor. Using the recombinant proteins, we could map the epitope of GCC:B10 monoclonal antibody to the intracellular domain of the receptor. We used the antibody to localize the receptor throughout the rat intestine, and in the porcine and bonnet monkey colon. We could detect receptor expression in the villus and the crypts of the duodenum, jejunum, ileum, and caecum, and in the crypts of the colon. Receptor expression was observed in cells that had earlier been shown to express cGMP-dependent kinase, but not the cystic fibrosis transmembrane regulator, a known downstream target of cGMP/G-kinase, which suggests that GCC/cGMP could regulate additional cellular signal transduction machinery. J. Cell. Biochem. 66:500-511, 1997. © 1997 Wiley-Liss, Inc.
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    Development and characterization of a conditionally immortalized human osteoblastic cell line stably transfected with the human androgen receptor gene (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 542-551 
    Details
    ISSN: 0730-2312
    Keywords: androgens ; androgen receptor ; bone cells ; dehydroepiandrosterone ; dihydrotestosterone ; hydroxyflutamide ; osteoblasts ; stable transfection ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Androgens have significant beneficial effects on the skeleton. However, studies on the effects of androgens on osteoblasts are limited due to the absence of appropriate model systems that combine completness of the osteoblastic phenotype, rapid proliferation rate, and stable expression of the androgen receptor (AR). Thus, we stably transfected the conditionally immortalized human fetal osteoblastic cell line (hFOB) with the human wild-type AR (hAR) cDNA. Compared to nontransfected hFOB cells, constitutive hAR mRNA expression in three independent hAR-transfected hFOB clones (hFOB/AR) was 15-fold higher in hFOB/AR-16, 62-fold higher in hFOB/AR-2, and 72-fold higher in hFOB/AR-6 cells, respectively, as assessed by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Detectable constitutive levels of hAR mRNA by Northern blot analysis were present in hFOB/AR-2 and hFOB/AR-6 cells, but not in hFOB/AR-16 or hFOB cells, respectively. Treatment with 5α-dihydrotestosterone (5α-DHT) (10-8 M) for 24 h did not alter hAR mRNA steady state levels in the hFOB/AR cell lines. Nuclear binding studies demonstrated 152 ± 73 (mean ± SEM) functional hARs/nucleus in non-transfected hFOB cells, 3,940 ± 395 functional hARs/nucleus in hFOB/AR-2 cells, and 3,987 ± 823 hARs/nucleus in hFOB/AR-6 cells, respectively. Treatment with 5α-DHT increased the expression of a transiently transfected androgen response element-chloramphenicol acetyltransferase (ARE-CAT) reporter construct in hFOB/AR-6 cells in a dose- and time-dependent manner; no such effect was observed in transiently transfected hFOB cells lacking exogenously transfected hARs. Moreover, 5α-DHT-induced ARE-CAT expression was inhibited by the selective androgen receptor antagonist, hydroxyflutamide. In summary, we have developed and characterized androgen-responsive osteoblastic cell lines derived from normal human fetal bone that express physiological levels of functional hARs. These cell lines should provide a suitable model for further studies on the effects of androgens on osteoblast function, including the identification of potential androgen-regulated growth factors and cytokines. J. Cell. Biochem. 66: 542-551, 1997. © 1997 Wiley-Liss, Inc.
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    Distinct roles for Sp1 and E2F sites in the growth/cell cycle regulation of the DHFR promoter (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 24-31 
    Details
    ISSN: 0730-2312
    Keywords: growth control ; transcription ; repression ; dihydrofolate reductase ; retinoblastoma ; Balb/c 3T3 cells ; TATAA-less promoter ; gene expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Dihydrofolate reductase activity is required for many biosynthetic pathways including nucleotide synthesis. Its expression is therefore central to cellular growth, and it has become a key target for cancer chemotherapy. Transcription of the dihydrofolate reductase gene is regulated with growth, being expressed maximally in late G1/early S phase following serum stimulation of quiescent cells. This regulation is directed by a promoter which contains binding sites for only the transcription factors Sp1 and E2F. In this study, the role of these promoter elements in growth/cell cycle regulation of dihydrofolate transcription was addressed directly by transient transfection of Balb/c 3T3 cells with mutant promoter-reporter gene constructs. The E2F sites were found to repress transcription in G0 and early G1 but did not contribute to the level of transcription in late G1/S phase. In contrast, Sp1 sites were able to mediate induction of transcription from the dihydrofolate reductase promoter, as well as a heterologous promoter, following serum stimulation of quiescent cells. These findings add dihydrofolate reductase to a growing list of genes at which E2F sites are primarily repressive elements and delineate a role for Sp1 sites in the growth/cell cycle regulation of transcription. J. Cell. Biochem. 67: 24-31, 1997. © 1997 Wiley-Liss, Inc.
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    Scleraxis messenger ribonucleic acid is expressed in C2C12 myoblasts and its level is down-regulated by bone morphogenetic protein-2 (BMP2) (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 66-74 
    Details
    ISSN: 0730-2312
    Keywords: scleraxis ; C2C12 myoblasts ; mRNA ; BMP2 ; HLH-type transcription factor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We examined the mRNA expression of scleraxis, a non-myogenic helix-loop-helix type transcription factor in C2C12 myogenic cells. Scleraxis mRNA has been shown to be expressed in sclerotome and perichondrium of the embryos. We found that C2C12 cells express 1.2 kb scleraxis mRNA constitutively. Since BMP was reported to induce ectopic bone formation when implanted in muscle, we examined the effects of BMP on scleraxis expression. Scleraxis mRNA expression in C2C12 cells was suppressed by the treatment with BMP2. This suppression was observed at 200 ng/ml but not at the lower concentrations. BMP2 treatment suppressed scleraxis mRNA level within 24 h and lasted at least up to 48 h. Electrophoresis mobility shift assay showed that the proteins in the crude nuclear extracts prepared from C2C12 cells bound to an Scx-E-box sequence, CATGTG, which is preferentially recognized by scleraxis. This binding was competed out by 100-fold molar excess of cold Scx-E-box sequence but not by the one with mutations in the E-box. This band was supershifted by the addition of antiserum raised against scleraxis. BMP2 treatment suppressed the Scx-E binding activity in C2C12 cells. This suppression of the Scx-E-box binding activity was in parallel to the BMP2 suppression of the transcriptional activity of the Scx-E-CAT reporter gene transfected into C2C12 cells. These data indicated that although the default pathway for C2C12 cells is to differentiate into muscle cells, these cells do express non-myogenic transcription factor, scleraxis, whose expression is suppressed by BMP2. J. Cell. Biochem. 67:66-74, 1997. © 1997 Wiley-Liss, Inc.
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    Quantitative immunofluorescence and immunoelectron microscopy of the topoisomerase IIα associated with nuclear matrices from wild-type and drug-resistant Chinese hamster ovary cell lines (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 112-130 
    Details
    ISSN: 0730-2312
    Keywords: DNase II ; decatenation ; in situ nuclear matrix ; mitotic chromosomes ; VP-16 ; RNP ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Topo IIα is considered an important constituent of the nuclear matrix, serving as a fastener of DNA loops to the underlying filamentous scaffolding network. To further define a mechanism of drug resistance to topo II poisons, we studied the quantity of topo IIα associated with the nuclear matrix in drug-resistant SMR16 and parental cells in the presence and absence of VP-16. Nuclear matrices were prepared from nuclei isolated in EDTA buffer, followed by nuclease digestion with DNase II in the absence of RNase treatment and extraction with 2 M NaCl. Whole-mount spreading of residual structures permits, by means of isoform-specific antibody and colloidal-gold secondary antibodies, an estimate of the amount of topo IIα in individual nuclear matrices. There are significant variations in topo IIα amounts between individual nuclear matrices due to the cell cycle distribution. The parental cell line contained eight to ten times more nuclear matrix-associated topo IIα than the resistant cell line matrices. Nuclear matrix-associated topo IIα from wild-type and resistant cell lines correlated well with the immunofluorescent staining of the enzyme in nuclei of intact cells. The amount of DNA associated with residual nuclear structures was five times greater in the resistant cell line. This quantity of DNA was not proportional to the quantity of topo IIα in the same matrix; in fact they were inversely related. In situ whole-mount nuclear matrix preparations were obtained from cells grown on grids and confirmed the results from labeling of isolated residual structures. J. Cell. Biochem. 67:112-130, 1997. © 1997 Wiley-Liss, Inc.
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    Reduced utilization of Man5GlcNAc2-P-P-lipid in a Lec9 mutant of Chinese hamster ovary cells: Analysis of the steps in oligosaccharide-lipid assembly (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 201-215 
    Details
    ISSN: 0730-2312
    Keywords: dolichol ; polyprenol ; translocation ; glycosylation sites ; eukaryotic cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Recently we reported that CHB11-1-3, a Chinese hamster ovary cell mutant defective in glycosylation of asparagine-linked proteins, is defective in the synthesis of dolichol [Quellhorst et al., 343:19-26, 1997: Arch Biochem Biophys]. CHB11-1-3 was found to be in the Lec9 complementation group, which synthesizes polyprenol rather than dolichol. In this paper, levels of various polyprenyl derivatives in CHB11-1-3 are compared to levels of the corresponding dolichyl derivatives in parental cells. CHB11-1-3 was found to maintain near normal levels of Man5GlcNAc2-P-P-polyprenol and mannosylphosphorylpolyprenol, despite reduced rates of synthesis, by utilizing those intermediates at a reduced rate. The Man5GlcNAc2 oligosaccharide attached to prenol in CHB11-1-3 cells and to dolichol in parental cells is the same structure, as determined by acetolysis. Man5GlcNAc2-P-P-polyprenol and Man5GlcNAc5-P-P-dolichol both appeared to be translocated efficiently in an in vitro reaction. Glycosylation of G protein was compared in vesicular stomatitus virus (VSV)-infected parent and mutant; although a portion of G protein was normally glycosylated in CHB11-1-3 cells, a large portion of G was underglycosylated, resulting in the addition of either one or no oligosaccharide to G. Addition of a single oligosaccharide occurred randomly rather than preferentially at one of the two sites. J. Cell. Biochem. 67:201-215, 1997. © 1997 Wiley-Liss, Inc.
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    Apoptosis in C3H-10T1/2 cells: Roles of intracellular pH, protein kinase C, and the Na+/H+ antiporter (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 231-240 
    Details
    ISSN: 0730-2312
    Keywords: 5-(N, N-hexamethylene)-amiloride (HMA) ; 12-O-tetradecanoylphorbol-13-acetate (TPA) ; chelerythrine ; protein kinase C (PKC) ; serum withdrawal ; internucleosomal DNA cleavage ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Changes in intracellular ion concentrations have been correlated with the activation of an endogenous endonuclease and thus internucleosomal DNA cleavage during apoptosis in many cell types. We investigated whether intracellular pH could play a significant role in apoptotic initiation and progression in C3H-10T1/2 cells, a cell strain that does not exhibit double-stranded DNA cleavage during apoptosis. Protein kinase C and the Na+/H+ antiporter, known regulators of intracellular pH, also were assessed for their involvement in apoptosis of C3H-10T1/2 cells. When a H+ ionophore was used to clamp intracellular pH to 6.0 or below, a significant level of apoptosis was induced in these cells within 6 h, whereas clamping at pH 6.75 did not induce significant amounts of apoptosis until 36 h after acidification. The acidified cells exhibited classic apoptotic morphology and chromatin condensation, similar to serum withdrawn cells, but failed to show internucleosomal DNA cleavage with electrophoresis of genomic DNA. Our results also suggest that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-mediated inhibition of apoptosis in serum withdrawn C3H-10T1/2 cells functions through a sequential activation of protein kinase C and the Na+/H+ antiporter; thus, an alkalinization or an inhibition of acidification is involved in this apoptotic block. Serum withdrawal itself does not appear to act through a negative effect on either protein kinase C or the Na+/H+ antiporter. TPA was also capable of inhibiting the apoptosis induced by specific inhibitors of protein kinase C and the Na+/H+ antiporter, but the inhibition was successful only if the TPA was administered at least 20 min prior to the addition of the enzyme inhibitor. These results indicate that apoptosis in C3H-10T1/2 cells follows a pathway that involves intracellular acidification, but is independent of detectable endonuclease activity. J. Cell. Biochem. 67:231-240, 1997. © 1997 Wiley-Liss, Inc.
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    Novel nuclear matrix protein HET binds to and influences activity of the HSP27 promoter in human breast cancer cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 275-286 
    Details
    ISSN: 0730-2312
    Keywords: hsp27 expression ; breast cancer ; nuclear matrix protein ; DNA-binding ; promoter ; repressor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Since the small heat shock protein hsp27 enhances both growth and drug resistance in breast cancer cells, and is a bad prognostic factor in certain subsets of breast cancer patients, we have characterized the transcriptional regulation of hsp27, with the long-term goal of targeting its expression clinically. The majority of the promoter activity resides in the most proximal 200 bp. This region contains an imperfect estrogen response element (ERE) that is separated by a 13-bp spacer that contains a TATA box. Gel-shift analysis revealed the binding of a protein (termed HET for Hsp27-ERE-TATA-binding protein) to this region that was neither the estrogen receptor nor TATA-binding protein. We cloned a complete cDNA (2.9 kb) for HET from an MCF-7 cDNA library. To confirm the identity of the HET clone, we expressed a partial HET clone as a glutathione S-transferase fusion protein, and showed binding to the hsp27 promoter fragment in gel-retardation assays. The HET clone is almost identical to a recently published scaffold attachment factor (SAF-B) cloned from a HeLa cell cDNA library. Scaffold attachment factors are a subset of nuclear matrix proteins (NMP) that interact with matrix attachment regions. Analyzing how HET could act as a regulator of hsp27 transcription and as a SAF/NMP, we studied its subnuclear localization and its effect on hsp27 transcription in human breast cancer cells. We were able to show that HET is localized in the nuclear matrix in various breast cancer cell lines. Furthermore, in transient transfection assays using hsp27 promoter-luciferase reporter constructs, HET overexpression resulted in a dose-dependent decrease of hsp27 promoter activity in several cell lines. J. Cell. Biochem. 67:275-286, 1997. © 1997 Wiley-Liss, Inc.
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    Binding-induced activation of overexpressed p185HER2 is essential in triggering neuronal differentiation of PC12 cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 316-326 
    Details
    ISSN: 0730-2312
    Keywords: erbB-2/neu ; p185HER2 overexpression ; PC12 ; cell differentiation ; monoclonal antibodies ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: To determine whether p185HER2 overexpression per se triggers p185HER2 cellular signaling or whether an extracellular signal is required, we transfected PC12 cells with the human erbB-2 proto-oncogene, and established a cell line that overexpresses p185HER2. PC12-HER2 cells, maintained in suspension culture or plated on a collagen layer, showed the same morphology and growth rate as PC12 and PC12 mock-transfected control cells. When treated with monoclonal antibody (MAb) MGr6 or other anti-p185HER2 MAbs, PC12-HER2 cells specifically underwent neuronal differentiation comparable to that induced by nerve growth factor (NGF), and the differentiation-inducing effect of the MAb was dramatically enhanced by the addition of a second anti-mouse IgG. MAb-induced cell differentiation correlated with p185HER2 phosphorylation, recruitment of Shc and Grb-2 transducer molecules into complexes, and MAPK phosphorylation. These data indicate the requirement for a specific binding-induced activation of the overexpressed p185HER2 receptor in inducing PC12 cell differentiation. PC12-HER2 cells represent a suitable system for selection of p185HER2-activating ligands (peptides, phage-displayed peptides or proteins) or specific inhibitors of its tyrosine kinase activity. J. Cell. Biochem. 67:316-326, 1997. © 1997 Wiley-Liss, Inc.
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    cAMP-dependent protein kinase inhibits the mitogenic action of vascular endothelial growth factor and fibroblast growth factor in capillary endothelial cells by blocking Raf activation (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 353-366 
    Details
    ISSN: 0730-2312
    Keywords: PKA ; Raf-1 ; MAPK ; endothelial cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Proliferation of endothelial cells is regulated by angiogenic and antiangiogenic factors whose actions are mediated by complex interactions of multiple signaling pathways. Both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) stimulate cell proliferation and activate the mitogen-activated protein kinase (MAPK) cascade in bovine brain capillary endothelial (BBE) cells. We have extended these findings to show that both mitogens activate MAPK via stimulation of Raf-1. Activation of Raf/MAPK is inhibited by increasing intracellular cAMP levels pharmacologically or via stimulation of endogenously expressed β-adrenergic receptors. Both VEGF- and bFGF-induced Raf-1 activity are blocked in the presence of forskolin or 8-bromo-cAMP by 80%. The actions of increased cAMP appear to be mediated by cAMP-dependent protein kinase (PKA), since treatment with H-89, a the specific inhibitor of PKA, reversed the inhibitory effect of elevated cAMP levels on mitogen-induced cell proliferation and Raf/MAPK activation. Moreover, elevations in cAMP/PKA activity inhibit mitogen-induced cell proliferation. These findings demonstrate, in cultured endothelial cells, that the cAMP/PKA signaling pathway is potentially an important physiological inhibitor of mitogen activation of the MAPK cascade and cell proliferation. J. Cell. Biochem. 67:353-366, 1997. © 1997 Wiley-Liss, Inc.
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    Inhibition of cytoskeletal reorganization stimulates actin and tubulin syntheses during injury-induced cell migration in the corneal endothelium (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 409-421 
    Details
    ISSN: 0730-2312
    Keywords: corneal endothelium ; actin ; tubulin ; upregulation ; autoregulation ; migration ; wound repair ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A single layer of squamous epithelial cells termed the “endothelium” resides upon its natural basement membrane (Descemet's membrane) along the posterior surface of the vertebrate cornea. A well-defined circular freeze injury to the center of the tissue exposes the underlying basement membrane and results in the directed migration of surrounding cells into the wound center. This cellular translocation is characterized by the reorganization of the actin and tubulin cytoskeletons. During migration, circumferential microfilament bundles are replaced by prominent stress fibers while microtubules, observed as delicate lattices in non-injured cells, become organized into distinct web-like patterns. To determine whether this cytoskeletal reorganization requires actin or tubulin synthesis, injured rabbit endothelia were organ cultured for various times and metabolically labeled with 35S-methionine/cystine (250 μCi/ml) for the final 6 h of each experiment. Analysis of actin and tubulin immunoprecipitates indicated no significant increases in 35S incorporation occurred during the course of wound repair when compared to isotope incorporation in noninjured tissues. However, when cytoskeletal reorganization was hampered, either by pre-treating tissues with 7 μM phalloidin to stabilize their circumferential microfilament bundles, or culturing in the presence of 10-8M colchicine to dissociate microtubules, 35S incorporation increased significantly into both actin and tubulin immunoprecipitates at 48 h post-injury. Furthermore, in both cases, exposure to actinomycin D substantially suppressed isotope incorporation. These results indicate that cytoskeletal rearrangement of microfilaments and microtubules during wound repair, in corneal endothelial cells migrating along their natural basement membrane, utilizes existing actin and tubulin subunits for filament reorganization. Disrupting this disassembly/reassembly process prevents cytoskeletal restructuring and leads to the subsequent initiation of actin and tubulin syntheses, as a result of increased transcriptional activity. J. Cell. Biochem. 67:409-421, 1997. © 1997 Wiley-Liss, Inc.
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    Topoisomerase II expression in osseous tissue (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 451-465 
    Details
    ISSN: 0730-2312
    Keywords: bone ; differentiation ; nuclear matrix ; osteoblast ; topoisomerase II ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The molecular mechanisms that mediate the transition from an osteoprogenitor cell to a differentiated osteoblast are unknown. We propose that topoisomerase II (topo II) enzymes, nuclear proteins that mediate DNA topology, contribute to coordinating the loss of osteoprogenitor proliferative capacity with the onset of differentiation. The isoforms topo II-α and -β, are differentially expressed in nonosseous tissues. Topo II-α expression is cell cycle-dependent and upregulated during mitogenesis. Topo II-β is expressed throughout the cell cycle and upregulated when cells have plateaued in growth. To determine whether topo II-α and -β are expressed in normal bone, we analyzed rat lumbar vertebrae using immunohistochemical staining. In the tissue sections, topo II-α was expressed in the marrow cavity of the primary spongiosa. Mature osteoblasts along the trabecular surfaces did not express topo II-α, but were immunopositive for topo II-β, as were cells of the marrow cavity. Confocal laser scanning microscopy was used to determine the nuclear distribution of topo II in rat osteoblasts isolated from the metaphyseal distal femur and the rat osteosarcoma cells, ROS 17/2.8. Topo II-α exhibited a punctate nuclear distribution in the bone cells. Topo II-β was dispersed throughout the interior of the nucleus but concentrated at the nuclear envelope. Serum starvation of the cells attenuated topo II-α expression but did not modulate expression of the β-isoform. These results indicate that the loss of osteogenic proliferation correlates with the downregulation of topo II-α expression. J. Cell. Biochem. 67:451-465, 1997. © 1997 Wiley-Liss, Inc.
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    Chemoprevention of cancer of uterine cervix: A study on chemoprevention of Retinamide II from cervical precancerous lesions (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 140-143 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; precancerous lesions ; uterine cervix Retinamide II (RII) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Dysplasia of the uterine cervix is a recognized precancerous condition. Because of the observed ability of retinoids to suppress various cell lines in vitro, a number of clinical studies have examined the effect these agents have on cervical dysplasia, with the object of developing a means of chemoprevention of cervical malignancies in women at risk. Three cervical cancer chemoprevention trials with Retinamide II (RII) have been conducted at the Cancer Institute, Chinese Academy of Medical Sciences, Beijing, China.A pilot study used RII to intervene in cases of precancerous cervical dysplasia. Twenty-seven women with mild, moderate, or servere cervical dysplasia, pathologically confirmed, were treated by RII suppositories, 10 mg QD, given intravaginally for 6 months (each course lasting 3 months). The results indicated that after the second course, the overall response rate was 96.29% and the complete response rate was 88.89%. In general, side effects were mild. A little cervical and vaginal irritation was well tolerated. In the second double-blind study, patients with precancerous cervical lesions were randomized into two groups, one treated with RII suppository intravaginally and the other with a placebo, once daily for 50 days in two courses. Precancerous lesions in 68.76% of patients in the treatment arm disappeared, with an overall effective rate of 74.29% after two courses of treatment with RII. Its curative effect was approximately that of laser beam radiation and electrocautery (P 〉 0.05), and differed significantly (P 〈0.01) from that of traditional antiinflammatories. RII can be a major measure in prevention and treatment of cervical cancer in high-incidence areas in China. In the third trial, we are conducting a randomized double-blind study placebo controlled, in a high-incidence area of cervical cancer (Xiang-Yuan county, Shang Xi Province, China). At present, the patients are being followed up and the study will be completed after 2 years. J. Cell. Biochem. Suppls. 28/29:140-143. © 1998 Wiley-Liss, Inc.
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    Esophageal and gastric cardia epithelial cell proliferation in northern Chinese subjects living in a high-incidence area (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 159-165 
    Details
    ISSN: 0730-2312
    Keywords: esophagus ; gastric cardia ; precancerous lesions ; cell proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Linxian and the nearby county Huixian, in the Henan province in Northern China, have a very high incidence of esophageal squamous cell carcinoma (SCC). Previous studies from these counties have suggested that increased proliferation of esophageal epithelial cells, morphologically manifested as basal cell hyperplasia (BCH) and dysplasia (DYS), is an early indicator of abnormality in persons predisposed to SCC. A high incidence of gastric cardia adenocarcinoma (AC) was also found in these areas. To determine proliferation patterns of esophageal and gastric cardia epithelia with normal and different severities of precancerous lesions, we measured proliferating cell nuclear antigen (PCNA), Ki-67, and bromodeoxyuridine (BrdU) incorporation and compared the results. Esophageal biopsies (175) and gastric cardia biopsies (41) were collected from symptom-free subjects in Huixian. Of these, 23 esophageal biopsies were incubated with BrdU. The avidin-biotin-peroxidase complex (ABC) method was used to detect PCNA, Ki-67, and BrdU. The number of immunostain-positive cells was counted manually. Intense immunostaining for PCNA, Ki-67, and BrdU was observed in the cell nuclei of tissues with normal and different severities of precancerous lesions. With esophageal biopsies, both PCNA and Ki-67 increased significantly as the epithelia progressed from normal to BCH and to DYS. The number of PCNA- and Ki-67-positive cells was three times higher than that of BrdU incorporation in the same category of BCH. With cardia biopsies, the number of Ki-67 positive cells was lower in normal tissue and increased significantly from chronic superficial gastritis to chronic atrophic gastritis to DYS. Staining patterns for PCNA and Ki-67 were correlated with the histopathology of the esophagus. The correlation was not as clear with gastric cardia. BrdU studies appear to be more complicated. The PCNA and Ki-67 methods may be useful for screening high-risk esophageal and gastric cardia cancer subjects, and for monitoring chemoprevention effects. J. Cell. Biochem. Suppls. 28/29:159-165. © 1998 Wiley-Liss, Inc.
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    Interracial comparative study of prostate cancer in the United States, China, and Japan (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 182-186 
    Details
    ISSN: 0730-2312
    Keywords: prostate cancer in Chinese men ; angiogenesis ; neuroendocrine factors ; p53 protein ; ras oncogene ; androgen receptor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The interracial differences of prostate cancer progression have long been documented; however, underlying molecular and cellular mechanisms remain obscure. This study focuses on the histopathologic, immunohistochemical, biochemical, and molecular characterization of prostate cancer tissues unselectively obtained from US, Chinese, and Japanese men. Histopathologic analyses indicate that 74.5% of the prostate cancers in Chinese patients were poorly differentiated, compared with 28.6 and 32.8% of the prostate cancers in US and Japanese men, respectively. These differences cannot be attributed to patient age, clinical stage of disease, or methods of tissue sampling. Furthermore, the high proportion of poorly differentiated prostate cancer tissues in the Chinese group was not related to the patients' access to medical service or their geographic origins within China. We found significantly higher levels of tumor angiogenesis (2- to 4-fold), serotonin (2- to 20-fold), and bombesin (7- to 16-fold), but not chromogranin A, in tissue specimens obtained from Chinese prostate cancer patients compared with those from US and Japanese patients. We also found marked differences in p53 protein accumulation among various ethnic groups. The p53 protein was frequently detected in prostate cancer tissue specimens from Chinese (90.2%), but less frequently in US black (3.7%), US white (17.4%), and Japanese (7.1%) men. Further analysis of 31 prostate cancer tissues from Chinese men indicated that mutational changes in the p53 gene occurred between exons 5 and 8. J. Cell. Biochem. Suppls. 28/29:182-186. © 1998 Wiley-Liss, Inc.
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    Inhibitory effects of curcumin on tumorigenesis in mice (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 26-34 
    Details
    ISSN: 0730-2312
    Keywords: anti-inflammatory agent ; antioxidant ; chemoprevention ; Curcuminoid ; cyclooxygenase inhibitor ; food coloring agent ; lipoxygenase inhibitor ; plant phenol ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Curcumin (diferuloylmethane), the naturally occurring yellow pigment in turmeric and curry, is isolated from the rhizomes of the plant Curcuma longa Linn. Curcumin inhibits tumorigenesis during both initiation and promotion (post-initiation) periods in several experimental animal models. Topical application of curcumin inhibits benzo[a]pyrene (B[a]P)-mediated formation of DNA-B[a]P adducts in the epidermis. It also reduces 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increases in skin inflammation, epidermal DNA synthesis, ornithine decarboxylase (ODC) mRNA level, ODC activity, hyperplasia, formation of c-Fos, and c-Jun proteins, hydrogen peroxide, and the oxidized DNA base 5-hydroxymethyl-2′-deoxyuridine (HmdU). Topical application of curcumin inhibits TPA-induced increases in the percent of epidermal cells in synthetic (S) phase of the cell cycle. Curcumin is a strong inhibitor of arachidonic acid-induced edema of mouse ears in vivo and epidermal cyclooxygenase and lipoxygenase activities in vitro. Commercial curcumin isolated from the rhizome of the plant Curcuma longa Linn contains 3 major curcuminoids (approximately 77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin). Commercial curcumin, pure curcumin, and demethoxycurcumin are about equipotent as inhibitors of TPA-induced tumor promotion in mouse skin, whereas bisdemethoxycurcumin is somewhat less active. Topical application of curcumin inhibits tumor initiation by B[a]P and tumor promotion by TPA in mouse skin. Dietary curcumin (commercial grade) inhibits B[a]P-induced forestomach carcinogenesis, N-ethyl-N′-nitro-N-nitrosoguanidine (ENNG)-induced duodenal carcinogenesis, and azoxymethane (AOM)-induced colon carcinogenesis. Dietary curcumin had little or no effect on 4-(methylnitosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis and 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast carcinogenesis in mice. Poor circulating bioavailability of curcumin may account for the lack of lung and breast carcinogenesis inhibition. J. Cell. Biochem. Suppl. 27:26-34. © 1998 Wiley-Liss, Inc.
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    Chemoprevention by naturally occurring and synthetic agents in oral, liver, and large bowel carcinogenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 35-41 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; tongue ; liver ; large bowel ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A number of naturally occurring compounds and several related synthetic agents were confirmed to exert chemopreventive properties against carcinogenesis in the digestive organs. Phenolic compounds, widely distributed as plant constituents, possess chemopreventive activities in tongue, liver, and large bowel of rodents. Of them, a simple phenolic protocatechuic acid seems to be a promising compound. Organosulfur compounds contained in the cruciferous vegetables and known to activate detoxifying enzymes are regarded as a candidate group for cancer preventive agents. We proved a strong protective effect of S-methylmethanethiosulfonate, a constituent in these vegetables, on azoxymethane (AOM)-induced large bowel carcinogenesis. Some oxygenated carotenoids (xanthophylls) are reported to have antitumor effects. Naturally occurring xanthophylls astaxanthin and canthaxanthin have considerable preventive activities on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and AOM-induced large bowel carcinogenesis. A novel synthesized retinoidal butenolide, KYN-54, which suppresses large bowel as well as tongue carcinogenesis, could be a useful agent for prevention of digestive organ cancers. Some trace elements are known to have anticarcinogenic effects. Magnesium hydroxide, a protective agent in colorectal carcinogenesis, inhibits c-myc expression and ornithine decarboxylase activity in the mucosal epithelium of the intestine. Our results show that many agents with preventive effects in tongue, liver, and large bowel control carcinogen-induced hyperproliferation of cells in these organs. Carcinogens used to induce large bowel cancers also induce apoptosis in the target sites. Telomerase activity is increased in the tissues of preneoplastic as well as neoplastic lesions in experimental models such as dimethylbenz[a]anthracene-induced oral carcinogenesis in hamsters. These could be useful biomarkers in studies for cancer chemoprevention. J. Cell. Biochem. Suppl. 27:35-41. Published 1998 Wiley-Liss, Inc.
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    Cancer prevention by natural carotenoids (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 86-91 
    Details
    ISSN: 0730-2312
    Keywords: cancer prevention ; natural carotenoids ; lycopene ; lutein ; phytoene ; crtB gene ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Epidemiological investigations have shown that cancer risk is inversely related to the consumption of green and yellow vegetables and fruits. Since β-carotene is present in abundance in these vegetables and fruits, it has been investigated extensively as a possible cancer preventive agent. However, various carotenoids that coexist with β-carotene in vegetables and fruits also have anticarcinogenic activity. Some of them, such as α-carotene, showed higher potency than β-carotene in suppressing experimental carcinogenesis. Thus, we have carried out more extensive studies on cancer-preventive activities of natural carotenoids, which found that lycopene and lutein had potent anticarcinogenic activity. In the present study, the cancer-preventive activity of phytoene was also comfirmed biotechonologically when mammalian cells producing phytoene were resistant to H-ras-induced cell transformation. Further studies on various natural carotenoids besides β-carotene should be continued to obtain more information about the potential of natural carotenoids in the field of cancer prevention. J. Cell. Biochem. Suppl. 27:86-91. © 1998 Wiley-Liss, Inc.
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    Effect of early vs. late administration of 4-Hydroxyphenylretinamide (4-HPR) on N-Methyl-N-Nitrosourea (MNU)-induced mammary tumorigenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 92-99 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; H-ras ; PCNA ; rat ; retinoid ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Mammary tumors were induced in 48-52-day-old female Sprague-Dawley rats in metestrus or diestrus with a single jugular injection of MNU (50 mg/kg). Control rats received the saline vehicle (Group 4 n = 9). Rats were fed 4% Teklad diet containing either 0 (Group 3, n = 20) or 782 mg 4-HPR/kg diet. 4-HPR supplementation was initiated either 1 week prior to (Group 1, n = 14) or 4 weeks following MNU administration (Group 2, n = 19). Neither body weight nor food intake differed significantly between treatment groups. Feeding of 4-HPR 1 week prior to tumor induction reduced the number of tumors (0.8±.2) when compared to MNU control rats (2.1±.4). Immunohistochemical staining of mammary tumor sections for PCNA was quantitated by microdensitometry and expressed as an HSCORE. No differences in HSCORE were observed between tumor groups although the percentage of nuclear area occupied by intermediate and darkly stained nuclei was reduced in the late 4-HPR group. GC→AT transitions in codon 12 of the H-ras gene were detected in 50% (12/24) of MNU control tumors, 60% (6/10) of early 4-HPR tumors, and 38% (6/16) of late 4-HPR tumors. Mutation rates did not differ significantly between groups. 4-HPR appears to be a more effective chemopreventive when fed during the initiation period. J. Cell. Biochem. Suppl. 27:92-99. © 1998 Wiley-Liss, Inc.
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  • 188
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    Initial study on naturally occurring products from traditional Chinese herbs and vegetables for chemoprevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 106-112 
    Details
    ISSN: 0730-2312
    Keywords: garlic ; elemene ; allicin ; antitumor activity ; carcinogenesis ; leukemia ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A number of naturally occurring products from vegetables and herbs exert chemopreventive properties against carcinogenesis. In this paper, two such compounds, isolated from garlic and from a traditional Chinese medicinal herb, are described for review. Elemene, isolated from the Chinese medicinal herb Rhizoma zedoariae, was shown to exhibit antitumor activity in human and murine tumor cells in vitro and in vivo. This novel antineoplastic agent has substantial clinical activity against various tumors. Thein vitro effect of elemene on the growth of leukemia cells was evaluated by MTT assay. The IC50values of elemene for promyelocytic leukemia HL-60 cells and erythroleukemia K562 cells were 27.5 μg/mL and 81 μg/mL, respectively, while IC50 for peripheral blood leukocytes (PBL) was 254.3 μg/mL. The inhibitory effect of elemene on proliferation of HL-60 cells was associated with cell cycle arrest from S to G2M phase transition and with induction of apoptosis. The apoptosis of tumor cells was confirmed by DNA ladder formation on gel electrophoresis and characteristic ultrastructural alterations. The results also demonstrated that inhibitory effects of allicin, a natural organosulfide from garlic, on proliferation of tumor cells were associated with the cell cycle blockage of S/G2M boundary phase and induction of apoptosis. These findings suggest that induction of apoptosis may contribute to the mechanisms of antitumor activity of elemene and allicin, which merit investigation as potential chemoprevention agents in humans. J. Cell. Biochem. Suppl. 27:106-112. © 1998 Wiley-Liss, Inc.
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    Genetic alterations in mouse lung tumors: Implications for cancer chemoprevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 49-63 
    Details
    ISSN: 0730-2312
    Keywords: mouse lung ; genetic alteration ; aberrant gene expression ; surrogate endpoint biomarkers ; cancer chemoprevention ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Specific genetic alterations affecting known tumor suppressor genes and proto-oncogenes occur during mouse lung tumorigenesis. These include mutational activation of the K-ras gene, commonly seen at a frequency of about 80% in both spontaneously occurring and chemically induced adenomas and adenocarcinomas of the lung, suggesting that it is an early event that persists into malignancy. Allelic loss of the p16 tumor suppressor gene also is a frequent event, occurring in about 50% of mouse lung adenocarcinomas, but rarely in lung adenomas, suggesting that it may play a role in malignant conversion or progression of lung tumors. Other genetic alterations detected in mouse lung tumors include reduced expression of Rb and p16, and increased c-myc expression. Alterations of these genes are also common in the genesis of human lung cancer. Genetic linkage analysis to identify human lung cancer susceptibility genes is difficult due to the genetic heterogeneity and exposure to environmental risk factors. The mouse lung tumor model has become a valuable alternative for identifying such genes. Recently, loci responsible for mouse lung tumor susceptibility have been mapped to chromosomes 6, 9, 17, and 19, while those linked to lung tumor resistance have been mapped to chromosomes 4, 11, 12, and 18. Known candidate susceptibility or resistance genes include the K-ras proto-oncogene on chromosome 6, and the p16 tumor supressor gene on chromosome 4. With evidence of considerable overlap between the genetic alterations that underlie human and mouse lung tumorigenesis, the mouse lung tumor model has been expanded to include pre-clinical screening of chemopreventive agents against human lung cancer. Studies on the modulation of genetic defects in mouse lung tumors by known and potential chemopreventive agents should further the goal of developing an effective prevention and treatment of lung cancer. J. Cell. Biochem. Suppls. 28/29:49-63. © 1998 Wiley-Liss, Inc.
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    Quantitation of preinvasive neoplastic progression in animal models of chemical carcinogenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 21-38 
    Details
    ISSN: 0730-2312
    Keywords: preinvasive neoplasia ; image analysis ; chemical carcinogenesis ; rat ; mouse ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: An assay method that precisely quantitates the cellular and tissue changes associated with early, preinvasive neoplasia is much needed as a surrogate endpoint biomarker (SEB) in clinical trials to predict the potential efficacy of chemopreventive agents in bringing about cancer incidence reduction. Quantification of histological changes at the tissue level are potentially powerful SEB's since these visually apparent changes are common in all neoplastic development, regardless of tissue type or neoplastic cause. Currently, subjective inspection of the histological appearance of sectioned and stained material, or “grading,” by experienced pathologists is used to evaluate neoplastic progression. This has well-known limitations of reproducibility, accuracy, and resolution of grading scale. Since neoplastic changes are visually apparent and morphologic in nature, quantification by image analysis is a measurement modality of choice.Image analysis was implemented through the use of high-resolution “tiled” images of complete tissue sections. A histological grading system, or “scale,” was developed that could be expressed in terms of normal deviate units of multiple and different morphometric descriptors. Neoplastic growth was characterized quantitatively with multiple measurements on each tissue image tile, which were combined into a single number for each tile, i.e., a histologic grade per tile, and parameters from the distributions of these measurements were used to represent the histologic grade for the entire region considered. This concept provided a uniform final scale in similar units of measurement, regardless of which tissues were graded. Also, the grading scale automatically adjusted measurement variance for different tissues by using normal tissue for each different type to obtain the normalization to standard deviation (z) units. This further defined a uniform final scale and maintained standard references.Using this method, results from two well-known animal models of carcinogenesis, squamous cell carcinoma of SENCAR mouse skin induced by benzo(a)pyrene (B[a]P), and squamous cell carcinoma of the rat esophagus induced by N-nitrosomethylbenzylamine (NMBA), were compared to each other. Image analysis was performed on skin tissue sections from a total of 64 SENCAR mice, and esophagus tissue sections from 96 Fischer-344 rats. In both cases, a quantitative expression of the preinvasive neoplastic response to the carcinogen as a function of time of exposure was expressed along a continuous grading scale in standard deviation units (z). In the SENCAR mouse skin animal model, similar cohorts of 4 mice at 20 weeks showed significant modulation of B[a]P-induced neoplasia by treatment with the antiproliferative agent difluoromethylornithine, P 〈. 05. In the rat esophagus animal model, similar cohorts of 6 rats at 10 and 15 weeks showed significant modulation of NMBA-induced neoplasia by treatment with the antimutagen phenethyl isothiocyanate, P 〈. 05. J. Cell. Biochem. Suppls. 28/29:21-38. © 1998 Wiley-Liss, Inc.
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    Dose-ranging study of Indole-3-Carbinol for breast cancer prevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 111-116 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; estrogen metabolites ; surrogate endpoint biomarker ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Sixty women at increased risk for breast cancer were enrolled in a placebo-controlled, double-blind dose-ranging chemoprevention study of indole-3-carbinol (I3C). Fifty-seven of these women with a mean age of 47 years (range 22-74) completed the study. Each woman took a placebo capsule or an I3C capsule daily for a total of 4 weeks; none of the women experienced any significant toxicity effects. The urinary estrogen metabolite ratio of 2-hydroxyestrone to 16α-hydroxyestrone, as determined by an ELISA assay, served as the surrogate endpoint biomarker (SEB). Perturbation in the levels of SEB from baseline was comparable among women in the control (C) group and the 50, 100, and 200 mg low-dose (LD) group. Similarly, it was comparable among women in the 300 and 400 mg high-dose (HD) group. Regression analysis showed that peak relative change of SEB for women in the HD group was significantly greater than that for women in the C and LD groups by an amount that was inversely related to baseline ratio; the difference at the median baseline ratio was 0.48 with 95 % confidence interval (0.30, 0.67). No other factors, such as age and menopausal status, were found to be significant in the regression analysis. The results in this study suggest that I3C at a minimum effective dose schedule of 300 mg per day is a promising chemopreventive agent for breast cancer prevention. A larger study to validate these results and to identify an optimal effective dose schedule of I3C for long-term breast cancer chemoprevention will be necessary. J. Cell. Biochem. Suppls. 28/29:111-116. © 1998 Wiley-Liss, Inc.
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    Embryonic morphogenesis signaling pathway mediated by JNK targets the transcription factor JUN and the TGF-β homologue decapentaplegic (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 1-12 
    Details
    ISSN: 0730-2312
    Keywords: DPP ; Drosophila ; mutations ; dorsal closure signaling pathway ; JNK pathway ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The dorsal surface of the Drosophila embryo is formed by the migration of the lateral epithelial cells to cover the amnioserosa. The Drosophila cJun-N-terminal kinase (DJNK) is essential for this process. Mutations in DJNK or the DJNK activator hemipterous (HEP) lead to incomplete dorsal closure, resulting in a hole in the dorsal cuticle. The molecules downstream of DJNK in this signaling pathway have not been established. Here we demonstrate that the basket1 (bsk1) mutation of DJNK causes decreased interaction with DJUN. Expression of decapentaplegic (DPP), a TGF-β homologue, in the leading edge of the dorsal epithelium, is identified as a genetic target of the JNK pathway. A constitutive allele of JUN is able to rescue the dorsal closure defect of bsk1 and restores DPP expression. Furthermore, ectopic DPP rescues the defects in dorsal closure caused by bsk1. These data indicate that the interaction of DJNK with DJUN contributes to the dorsal closure signaling pathway and targets DPP expression. J. Cell. Biochem. 67:1-12, 1997. © 1997 Wiley-Liss, Inc.
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    Activation-induced bi-dentate interaction of SHIP and Shc in B lymphocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 32-42 
    Details
    ISSN: 0730-2312
    Keywords: SHIP ; Ras signaling ; Shc ; bi-dentate interaction ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: SHIP is a SH2 domain-containing inositol polyphosphatase that is selectively tyrosine phosphorylated and associated with the adapter protein Shc in B lymphocytes upon co-crosslinking surface immunoglobulin and FcγRIIB1. We previously observed that this stimulation condition is associated with a reduction in the interaction of Grb2 with phosphorylated Shc, an enhanced interaction of Shc with SHIP, and a block in the Ras signaling pathway. We proposed that the SH2 domain of SHIP competes with Grb2 in binding to phospho-Shc, resulting in a block in Ras signaling. To test this model, we examined the mode of SHIP-Shc interaction. Using recombinant Shc and SHIP interaction domains and purified Shc and SHIP phosphopeptides, we show that the interaction is bi-dentate such that the SH2 domain of SHIP recognizes phosphorylated Y317 and doubly-phosphorylated Y239/Y240 of Shc and the Shc PTB domain recognizes phosphorylated NPxpY motifs within SHIP. We observed no role for the Shc SH2 domain in the interaction. These findings are consistent with our earlier model that SHIP and Grb2 compete for binding to phospho-Shc and support the notion that, in addition to the hydrolysis of inositol phosphates and phospholipids, SHIP contributes to anti-proliferative biochemistry by blocking protein-protein interactions. J. Cell. Biochem. 67:32-42, 1997. © 1997 Wiley-Liss, Inc.
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    Reorganization of a novel vimentin-associated protein in 3T3-L1 cells during adipose conversion (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 84-91 
    Details
    ISSN: 0730-2312
    Keywords: vimentin-associated protein ; capsule of lipid droplet ; vimentin cage ; adipocyte ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have found that the antibody A2, a marker for the capsule of steroidogenic lipid droplets, reacts with an intermediate filament-associated protein, P200, in 3T3-L1 preadipocytes. Supporting evidence came from the colocalization pattern of P200 with vimentin in double label experiments. The association of P200 with vimentin was further confirmed by its copurification with vimentin after high salt extraction and colocalization of these two proteins in high salt-extracted and vinblastine-treated cells. In preadipocytes this protein was distributed on the vimentin filament network. At the early stage of adipose conversion, this protein was found to encircle nascent lipid droplets ranging from 0.1 to 0.2 μm, accompanied with a decreased distribution on the vimentin filament system. This infers a possible translocation of P200 from the vimentin filaments to the droplet surface. Meanwhile, the vimentin filaments remained in a normal distribution in the cytoplasm and were apparently not associated with the nascent droplet. The association of vimentin filaments to droplet surfaces became prominent in lipid droplets larger than 0.2 μm, forming a typical vimentin cage. Immunogold staining also confirmed the translocation of P200 immunoreactivity from the droplet surface to the vimentin cage. The relocation of P200 from the cytoplasmic vimentin filaments to the droplet surface prior to the formation of the vimentin cage, as well as the reorganization of this protein in the vimentin cage, suggests a stabilizing role in the lipid droplet formation and an inducing function of this protein in the formation of the vimentin cage. J. Cell. Biochem. 67:84-91, 1997. © 1997 Wiley-Liss, Inc.
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    Protein kinase C activation by interleukin (IL)-1 limits IL-1-induced IL-6 synthesis in osteoblast-like cells: Involvement of phosphatidylcholine-specific phospholipase C (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 103-111 
    Details
    ISSN: 0730-2312
    Keywords: interleukin-1 ; interleukin-6 ; protein kinase C ; phosphatidylcholine ; phospholipase C ; osteoblast ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We investigated the regulatory mechanism of interleukin-6 (IL-6) synthesis induced by interleukin-1 (IL-1) in osteoblast-like MC3T3-E1 cells. IL-1 stimulated the secretion of IL-6 in a dose-dependent manner in the range between 0.1 and 100 ng/ml. Staurosporine and calphostin C, inhibitors of protein kinase C (PKC), significantly enhanced the IL-1-induced secretion of IL-6. The stimulative effect of IL-1 was markedly amplified in PKC down-regulated MC3T3-E1 cells. IL-1 produced diacylglycerol in MC3T3-E1 cells. IL-1 had little effect on the formation of inositol phosphates and choline. On the contrary, IL-1 significantly stimulated the formation of phosphocholine dose-dependently. D-609, an inhibitor of phosphatidylcholine-specific phospholipase C, suppressed the IL-1-induced diacylglycerol production. The IL-1-induced IL-6 secretion was significantly enhanced by D-609. These results indicate that IL-1 activates PKC via phosphatidylcholine-specific phospholipase C in osteoblast-like cells, and the PKC activation then limits IL-6 synthesis induced by IL-1 itself. J. Cell. Biochem. 67:103-111, 1997. © 1997 Wiley-Liss, Inc.
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    New insights into the metastasis-associated 67 kD laminin receptor (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 155-165 
    Details
    ISSN: 0730-2312
    Keywords: adhesion receptors ; tumor progression ; ribosomal proteins ; laminin ; cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The interactions between tumor cells and laminin or other components of the extracellular matrix have been shown to play an important role in tumor invasion and metastasis. These interactions are mediated by different cell surface molecules, including the monomeric 67 kD laminin receptor. This molecule appears to be very peculiar since so far only a full-length gene encoding a 37 kD precursor protein has been isolated and the mechanism by which the precursor reaches the mature form is not understood. Based on clinical data, which clearly demonstrate the importance of the receptor in tumor progression, studies were conducted to define the structure, expression, and function of this laminin receptor as a step toward developing therapeutic strategies that target this molecule. The data suggest that acylation of the precursor is the key mechanism in maturation of the 67 kD form. The function of the membrane receptor is to stabilize the binding of laminin to cell surface integrins, acting as an integrin-accessory molecule, although homology of the gene encoding the receptor precursor with other genes suggests additional functions. Downregulation of the receptor expression on tumor cells might open new therapeutic approaches to decrease tumor aggressiveness. J. Cell. Biochem. 67:155-165, 1997. © 1997 Wiley-Liss, Inc.
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    Transgene-coded chimeric proteins as reporters of intracellular proteolysis: Starvation-induced catabolism of a lacZ fusion protein in muscle cells of Caenorhabditis elegans (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 143-153 
    Details
    ISSN: 0730-2312
    Keywords: C. elegans ; E. coli ; immunoreactive degradation intermediates ; affinity-purified protein ; ubiquitin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The product of an integrated transgene provides a convenient and cell-specific reporter of intracellular protein catabolism in 103 muscle cells of the nematode Caenorhabditis elegans. The transgene is an in-frame fusion of a 5′-region of the C. elegans unc-54 (muscle myosin heavy-chain) gene to the lacZ gene of Escherichia coli [Fire and Waterston (1989): EMBO J 8:3419-3428], encoding a 146-kDa fusion polypeptide that forms active β-galactosidase tetramers. The protein is stable in vivo in well-fed animals, but upon removal of the food source it is inactivated exponentially (t1/2 = 17 h) following an initial lag of 8 h. The same rate constant (but no lag) is observed in animals starved in the presence of cycloheximide, implying that inactivation is catalyzed by pre-existing proteases. Both the 146-kDa fusion polypeptide (t1/2 = 13 h) and a major 116-kDa intermediate (t1/2 = 7 h) undergo exponential physical degradation after a lag of 8 h. Degradation is thus paradoxically faster than inactivation, and a number of characteristic immunoreactive degradation intermediates, some less than one-third the size of the parent polypeptide, are found in affinity-purified (active) protein. Some of these intermediates are conjugated to ubiquitin. We infer that the initial proteolytic cleavages occur in the cytosol, possibly by a ubiquitin-mediated proteolytic pathway and do not necessarily inactivate the fusion protein tetramer. J. Cell. Biochem. 67:143-153, 1997. © 1997 Wiley-Liss, Inc.
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    v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 184-200 
    Details
    ISSN: 0730-2312
    Keywords: maturation-promoting factor ; meiosis ; nuclear pore complex ; nucleocytoplasmic transport ; thyroid hormone receptor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The growth-promoting properties of the retroviral v-erbA oncogene, a highly mutated version of the chicken thyroid hormone receptor (TR) α, have so far exclusively been linked to dominant repression of the antimitogenic roles of TR and retinoic acid receptors. Here we show that when expressed in Xenopus oocytes v-ErbA induced ultrastructural changes characteristic of early and intermediate events of meiotic maturation by activating gene transcription. v-ErbA-induced maturation events occurred without activation of the cAMP/maturation-promoting factor signal pathway and were arrested prior to meiotic spindle formation. The effects of v-ErbA were not mimicked by a dominant negative in vitro-generated mutant of human TR, suggesting that v-ErbA can contribute to cell cycle reentry by interference with regulatory pathways distinct from those involving TR. Interestingly, a portion of v-ErbA expressed in oocytes was present at the cytoplasmic fibrils of the nuclear pore complexes, suggesting that in addition to its intranuclear function v-ErbA may modulate nucleocytoplasmic transport. J. Cell. Biochem. 67:184-200, 1997. © 1997 Wiley-Liss, Inc.
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    In vitro motility assay of atrial and ventricular myosin from pig (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 241-247 
    Details
    ISSN: 0730-2312
    Keywords: motility assay ; myosin ; atrium ; ventricle ; pig ; cardiac ; isoforms ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The role of myosin isoforms in determining contractile filament velocity in the atrium and ventricle of the pig heart was studied by measuring the motion of fluorescently labeled actin over myosin (in vitro motility assay). A rapid and relatively simple method for purification of myosin from small tissue samples was used. The relative extent of light chain-2 phosphorylation was about 30% in both atrial and ventricular myosin extracts. Although the extracted myosin was not free from contaminating proteins, mainly actin, the mean velocity at optimal pH and 32°C of both atrial (3.3 μm/s) and ventricular (2.3 μm/s) myosin were similar to those obtained using extensively purified myosin. The filament sliding velocities using isolated myosin and actin are lower than those estimated from previously published experiments on skinned fiber preparations, which might reflect an influence on sliding velocity by the filament organization or regulatory proteins in the muscle fiber. However, the ratio between velocities of atrial and ventricular myosin was similar in the motility assay (1.5) and muscle fiber experiments (1.6), which might suggest that these two methods reflect the same fundamental processes in cardiac contraction and that the difference in filament sliding velocity between the atrium and ventricle of the pig heart is determined my their myosin isoforms. J. Cell. Biochem. 67:241-247, 1997. © 1997 Wiley-Liss, Inc.
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    Parathyroid hormone (1-34)-mediated interleukin-6 induction (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 265-274 
    Details
    ISSN: 0730-2312
    Keywords: hPTH 1-34 ; IL-6 promoter ; CAT expression ; transfection ; osteoblast ; in vitro ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Parathyroid hormone (PTH) functions in part by regulating osteoblast cytokine expression. We recently demonstrated that PTH induced a rapid and transient increase in interleukin-6 (IL-6) mRNA expression in rat bones in vivo. To determine the molecular basis of this effect, we analyzed the human IL-6 promoter fused (-1,179 to +9) with the chloramphenicol acetyltransferase (CAT) reporter gene in stable transfections into human osteoblast-like osteosarcoma SaOS-2 cells. We compared the effects of PTH on IL-6 expression with adenylate cyclase activator forskolin, PKC activator phorbol 12-myristate 13-acetate (PMA), calcium ionophore A23187, interleukin-1α (IL-1α), prostaglandin E-2 (PGE-2), RS-66271 (a parathyroid hormone-related peptide analog), and platelet-derived growth factor-BB (PDGF-BB). Analyses of cell clones showed that IL-6 promoter expression was extremely low in the unstimulated state. Exposure to PTH (0.001-100 nM) for 12 h stimulated CAT expression in a dose-dependent manner (200-500% of control). Treatment with IL-1α was more potent than PTH in inducing transcription of the IL-6 promoter (900-1,000%). Activation of the cAMP-PKA pathway by treatment with forskolin induced a comparable level of induction with PTH. Together, the effects of PTH and forskolin were additive. RS-66271, previously shown to have PTH-like effects, induced a comparable level of IL-6 promoter expression. When examined together, PTH + RS-66271 effects were comparable to PTH effects alone. Exposure to PGE-2, PMA, PDGF-BB, or A23187 for 12 h did not significantly alter IL-6 promoter expression. These results demonstrate PTH, forskolin, the PTHrP analog RS-66271, and IL-1α stimulate IL-6 expression by stimulating gene transcription. The response to forskolin suggests that the messenger system mediated by PKA is sufficient to induce IL-6 expression. J. Cell. Biochem. 67:265-274, 1997. © 1997 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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