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  • 1995-1999  (2,833)
  • 1925-1929  (808)
  • 1890-1899  (195)
  • Cell & Developmental Biology  (3,836)
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  • 101
    Electronic Resource
    Electronic Resource
    Proteasome-mediated degradation of the vitamin D receptor (VDR) and a putative role for SUG1 interaction with the AF-2 domain of VDR (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 429-440 
    Details
    ISSN: 0730-2312
    Keywords: proteasome ; VDR ; SUG1 ; AF-2 domain ; 1,25-(OH)2D3 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The AF-2 helix of nuclear receptors is essential for ligand-activated transcription, and it may function to couple the receptor to transcriptional coactivator proteins. This domain also contacts components of the proteasome machinery, suggesting that nuclear receptors may be targets for proteasome-mediated proteolysis. In the present study, we demonstrate that mSUG1 (P45), a component of the 26S proteasome, interacts in a 1,25-(OH)2D3-dependent manner with the AF-2 domain of the vitamin D receptor (VDR). Furthermore, treatment of ROS 17/ 2.8 osteosarcoma cells with the proteasome inhibitors MG132 or β-lactone increased steady-state levels of the VDR protein. In the presence cycloheximide (10 μg/ ml), the liganded VDR protein was degraded with a half-life of approximately 8 h, and this rate of degradation was completely blocked by 0.05 mM MG132. The role of SUG1-VDR interaction in this process was investigated in transient expression studies. Overexpression of wild-type mSUG1 in ROS17/ 2.8 cells generated a novel proteolytic VDR fragment of approximately 50 kDa, and its production was blocked by proteasome inhibitors or by a nonhydrolyzable ATP analog. Parallel studies with SUG1(K196H), a mutant that does not interact with the VDR, did not produce the 50 kDa VDR fragment. Functionally, expression of SUG1 in a VDR-responsive reporter gene assay resulted in a profound inhibition of 1,25-(OH)2D3-activated transcription, while expression of SUG1(K196H) had no significant effect in this system. These data show that the AF-2 domain of VDR interacts with SUG1 in a 1,25-(OH)2D3-dependent fashion and that this interaction may target VDR to proteasome-mediated degradation as a means to downregulate the 1,25-(OH)2D3-activated transcriptional response. J. Cell. Biochem. 71:429-440, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
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  • 102
    Electronic Resource
    Electronic Resource
    Differentiation of HL-60 promyelocytic leukemia cells is accompanied by a modification of magnesium homeostasis (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 441-448 
    Details
    ISSN: 0730-2312
    Keywords: proliferation ; maturation ; intracellular magnesium pools ; receptor-mediated stimuli ; cyclic-AMP ; IFN-α ; cell permeabilization ; ionophore A23187 ; Na-Mg antiporter ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Magnesium homeostasis in HL-60 promyelocytic leukemia cells was compared to that in neutrophyl-like HL-60 cells obtained by 1.3% DMSO treatment. Magnesium homeostasis was studied by the characterization of magnesium efflux, the identification of intracellular magnesium pools, and the regulation of intracellular ionized Mg2+. In both undifferentiated and neutrophyl-like HL-60 cells, magnesium efflux occurred via the Na-Mg antiporter which was inhibited by imipramine and stimulated by db cAMP and forskolin. Receptor-mediated signals such as ATP, IFN-α, or PGE1, which can trigger cAMP-dependent magnesium efflux, were ineffective in undifferentiated HL-60 cells but induced 60-70% increase of magnesium efflux in neutrophyl-like HL-60 cells. Selective membrane permeabilization by the cation ionophore A23187 induced a large magnesium release when cells were treated with rotenone. In both cell populations, the addition of glucose to rotenone-treated cells restored magnesium release to the control level. Permeabilization by 0.005% digitonin provoked the release of 90% cell total magnesium in both cell types. Intracellular [Mg2+]i was 0.15 and 0.26 mM in undifferentiated and neutrophyl-like HL-60 cells, respectively. Stimuli that triggered magnesium efflux, such as db cAMP in undifferentiated and IFN-α in neutrophyl-like HL-60 cells, induced a slow but consistent increase of [Mg2+]i which was independent from Ca2+movements. Overall, these data indicate that magnesium homeostasis is regulated by receptor-mediated magnesium efflux which was modified during differentiation of HL-60 cells. Stimulation of magnesium efflux is paralleled by an increase of [Mg2+]i which reflects a release of magnesium from the bound cation pool. J. Cell. Biochem. 71:441-448, 1998. © 1998 Wiley-Liss, Inc.
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  • 103
    Electronic Resource
    Electronic Resource
    Regulation of insulin-like growth factors I and II and their binding proteins in human bone marrow stromal cells by dexamethasone (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 449-458 
    Details
    ISSN: 0730-2312
    Keywords: dexamethasone ; stromal cells ; IGF I ; IGF II ; IGFBPs ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Glucocorticoids inhibit the proliferation, but induce the differentiation, of bone marrow stromal cells into osteoblast-like cells. The mechanisms, however, are still conjectural. Since insulin-like growth factors (IGFs) have profound effects on osteoblast growth and differentiation, it is possible that glucocorticoids exert their effects on bone marrow stromal cells in part via regulation of IGFs. Therefore, we analyzed the effects of dexamethasone (Dex) on the expression of IGF I and IGF II in cultured preosteoblastic normal human bone marrow stromal cells (HBMSC). Whereas Dex decreased the concentration of IGF I in the conditioned medium since early in the treatment, the concentration of IGF II was increased progressively as culture period lengthened. As the activities of IGF I and IGF II are regulated by the IGF binding proteins (IGFBPs), we analyzed the effects of Dex on the expression of IGFBPs. Dex increased IGFBP-2 in a time-dependent manner. The increase in IGFBP-2, however, was only to the same extent as that of IGF II at most, depending on the length of treatment. Therefore, the increase in IGFBP-2 would dampen, but not eliminate, the increased IGF II activities. By contrast, Dex decreased IGFBP-3 levels, the latter increasing the bioavailability of IGF II. Although IGFBP-4 mRNA levels were stimulated by Dex, IGFBP-4 concentration in the conditioned medium was unchanged as measured by RIA. IGFBP-5 and IGFBP-6 mRNA levels were decreased by Dex in a time-dependent fashion. IGFBP-5 protein level was also decreased 1-4 days after Dex treatment. IGFBP-1 mRNA was not detectable in HBMSC. These accumulated data indicate that Dex regulates IGF I and IGF II and their binding proteins differentially in normal human bone marrow stromal cells. The progressive increase in IGF II may contribute to Dex-induced cell differentiation. J. Cell. Biochem. 71:449-458, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
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  • 104
    Electronic Resource
    Electronic Resource
    Erratum: Multivalent cations depress ligand affinity of insulin-like growth factor-binding proteins-3 and -5 on human GM-10 fibroblast cell surfaces. J Cell Biochem 69:364-375. (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 459-459 
    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: Sackett RL, McCusker RH (1998): Multivalent cations depress ligand affinity of insulin-like growth factor-binding proteins-3 and -5 on human GM-10 fibroblast cell surfaces. J Cell Biochem 69:364-375.
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  • 105
    Electronic Resource
    Electronic Resource
    TRAF2 expression in differentiated muscle (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 461-466 
    Details
    ISSN: 0730-2312
    Keywords: TRAF2 ; tumor necrosis factor ; NF-κB ; apoptosis ; myotube ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Recent data involving traf2 knockout mice have suggested a necessity of the protein in viability of skeletal muscle tissue. traf2-/- mice are born with decreased muscle mass that is hypothesized to be due to the increased circulating tumor necrosis factor in these mice. We show that TRAF2 protein is present at high levels in terminally differentiated skeletal muscle in the developing mouse. In vitro differentiation of mouse myoblasts displays a dramatic increase in TRAF2 protein levels. Although basal NF-κB activity decreases during myogenesis, TNF-induced NF-κB activity is 10 times greater in myotubes compared with myoblasts, presumably because of the stockpiling of TRAF2 protein in these cells. This may represent a strong anti-apoptotic TRAF2-mediated response specifically tailored to myotubes. These data help explain why muscle integrity is at risk in traf2-/- mice. J. Cell. Biochem. 71:461-466, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
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  • 106
    Electronic Resource
    Electronic Resource
    Binding of CDK9 to TRAF2 (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 467-478 
    Details
    ISSN: 0730-2312
    Keywords: cell cycle ; kinase ; signal transduction ; differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: CDK9 has been recently shown to have increased kinase activity in differentiated cells in culture and a differentiated tissue-specific expression in the developing mouse. In order to identify factors that contribute to CDK9's differentiation-specific function, we screened a mouse embryonic library in the yeast two-hybrid system and found a tumor necrosis factor signal transducer, TRAF2, to be an interacting protein. CDK9 interacts with a conserved domain in the TRAF-C region of TRAF2, a motif that is known to bind other kinases involved in TRAF-mediated signaling. Endogenous interaction between the two proteins appears to be specific to differentiated tissue. TRAF2-mediated signaling may incorporate additional kinases to signal cell survival in myotubes, a cell type that is severely affected in TRAF2 knockout mice. J. Cell. Biochem. 71:467-478, 1998. © 1998 Wiley-Liss, Inc.
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  • 107
    Electronic Resource
    Electronic Resource
    Macrophages and antioxidant status in the NOD mouse pancreas (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 479-490 
    Details
    ISSN: 0730-2312
    Keywords: macrophages ; antioxidant status ; NOD mice ; immunocytochemistry ; type 1 diabetes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This study showed that citiolone (CIT), a free radical scavenger, significantly increased superoxide dismutase (P 〈 0.001 vs. untreated NOD, NMMA-treated, and silica-treated animals), catalase (P 〈 0.01 vs. untreated NOD), and glutathione peroxidase (P 〈 0.001 vs. untreated NOD and C57BL6/J) values. Silica treatment was capable of counteracting the plasma antioxidant capacity (TRAP) decrease observed in untreated NOD mice, although it did not block the blood glucose rise and insulitis progression in type 1 diabetes significantly. Conversely, early silica administration was able to deplete macrophages (as demonstrated by immunocytochemistry) and to block the rise in blood glucose levels and insulitis progression significantly. Silica-treated animals in this study showed the highest TRAP levels, demonstrating that depletion of macrophages also was able to improve the antioxidant status. This study suggested that macrophages are essential for type 1 diabetes development and showed that they also are involved when the antioxidant status is affected. The reported findings are significant in view of previous studies indicating that oxygen and/or nitrogen free radicals contribute to the islet β-cell destruction in type 1 diabetes animal models. J. Cell. Biochem. 71:479-490, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
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  • 108
    Electronic Resource
    Electronic Resource
    Antiproliferative effect of elevated glucose in human microvascular endothelial cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 491-501 
    Details
    ISSN: 0730-2312
    Keywords: diabetic microangiopathy ; endothelium ; HMEC-1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Diabetic microangiopathy has been implicated as a fundamental feature of the pathological complications of diabetes including retinopathy, neuropathy, and diabetic foot ulceration. However, previous studies devoted to examining the deleterious effects of elevated glucose on the endothelium have been performed largely in primary cultured cells of macrovessel origin. Difficulty in the harvesting and maintenance of microvascular endothelial cells in culture have hindered the study of this relevant population. Therefore, the objective of this study was to characterize the effect of elevated glucose on the proliferation and involved signaling pathways of an immortalized human dermal microvascular endothelial cell line (HMEC-1) that possess similar characteristics to their in vivo counterparts. Human dermal microvascular endothelial cells (HMEC-1) were grown in the presence of normal (5 mM) or high D-glucose (20 mM) for 14 days. The proliferative response of HMEC-1 was compared under these conditions as well as the cAMP and PKC pathways by in vitro assays. Elevated glucose significantly inhibited (P 〈 0.05) HMEC-1 proliferation after 7, 10, and 14 days. This effect was not mimicked by 20 mM mannitol. The antiproliferative effect was more pronounced with longer exposure (1-14 days) to elevated glucose and was irreversible 4 days after a 10-day exposure. The antiproliferative effect was partially reversed in the presence of a PKA inhibitor, Rp-cAMP (10-50 μM), and/or a PKC inhibitor, Calphostin C (10 nM). HMEC-1 exposed to elevated glucose (20 mM) for 14 days caused an increase in cyclic AMP accumulation, PKA, and PKC activity but was not associated with the activation of downstream events such as CRE and AP-1 binding activity. These data support the hypothesis that HMEC-1 is a suitable model to study the deleterious effects of elevated glucose on microvascular endothelial cells. Continued studies with HMEC-1 may prove advantageous in delineation of the molecular pathophysiology associated with diabetic microangiopathy. J. Cell. Biochem. 71:491-501, 1998. © 1998 Wiley-Liss, Inc.
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  • 109
    Electronic Resource
    Electronic Resource
    Dolichol-like lipids with stimulatory effect on DNA synthesis: Substrates for protein dolichylation? (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 502-514 
    Details
    ISSN: 0730-2312
    Keywords: HMG-CoA ; MVA ; HPLC ; dolichol-like lipids ; DNA synthesis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Substantial evidence has suggested that a nonsterol product of mevalonic acid (MVA) is essential for the initiation of DNA synthesis in mammalian cells. Several possible isoprenoid candidates have been suggested, but the identity of this compound still remains unknown. In this study we have isolated and purified MVA products from SV40-transformed human fibroblasts and identified fractions with a growth-stimulatory effect. The cells were labelled with [14C]MVA in the presence of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. After lipid extraction, the [14C]MVA-labelled lipids were subjected to high performance liquid chromatography and size-exclusion chromatography, and the effect of the fractionated eluate on the DNA synthesis of arrested MVA-depleted target cells was tested. Thereby we found a fraction of [14C]MVA-labelled lipids with a substantial stimulatory effect on DNA synthesis. The chromatographic behavior suggested that the growth-stimulating fractions contained dolichol-20. This was confirmed by mass spectrometric analysis. Similar results were obtained when lipids from hepatocellular carcinoma cells and a sample from breast tumor were isolated and analyzed by the same procedure. The mechanisms by which these compounds induce DNA synthesis are unknown. Recent data obtained in our laboratory have provided evidence that dolichyl groups are covalently linked to tumor cell proteins, which implicates a new biological function for long-chain polyisoprenoid alcohols (Hjertman et al. [1997] FEBS Lett 416:235-238). In this study we demonstrate that tumor cells containing dolichol-like growth-stimulatory lipids also contained dolichylated proteins. This raises the question whether the growth-stimulatory dolichol-like lipids serve as substrates for the dolichylation reaction. J. Cell. Biochem. 71:502-514, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
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  • 110
    Electronic Resource
    Electronic Resource
    Additional protein factors play a role in the formation of VDR/RXR complexes on vitamin D response elements (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 515-523 
    Details
    ISSN: 0730-2312
    Keywords: binding ; complex formation ; retinoic X receptor ; TFIIB ; vitamin D receptor ; VDRE ; steroid receptor ; nuclear extract ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The vitamin D receptor (VDR) elicits a transcriptional response to 1,25-dihydroxyvitamin D3 by binding to specific response elements (VDRE) in the promoter of target genes. Retinoic X receptor (RXR) is required for formation of the VDR-VDRE complex when VDR is supplied at physiologic concentrations. When porcine intestinal nuclear extract is used as a source of VDR, two distinct complexes are always observed with native gel electrophoresis. Both complexes contain VDR and RXR. We now show that the faster-migrating complex requires another heretofore unknown nuclear factor for its formation. In addition, we provide evidence that the formation of the slower-migrating complex is enhanced by transcription factor IIB (TFIIB). Using ligand binding assays, we determined that both complexes contain the same ratio of VDR to VDRE. Using RXR subtype-specific antibodies in gel shift assays, we show that the complexes contain more than one RXR subtype. Therefore, the present results demonstrate VDR-RXR-VDRE complexes formed with pig intestinal nuclear extracts contain other proteins and that the complexes formed between VDR and VDRE are not simply heterodimers of VDR and RXR. J. Cell. Biochem. 71:515-523, 1998. © 1998 Wiley-Liss, Inc.
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  • 111
    Electronic Resource
    Electronic Resource
    Early effects of PP60v-src kinase activation on caveolae (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 524-535 
    Details
    ISSN: 0730-2312
    Keywords: caveolae ; caveolin-1 ; tyrosine kinase ; cell transformation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Members of the nonreceptor tyrosine kinase family appear to be targeted to caveolae membrane. We have used a Rat-1 cell expressing a temperature sensitive pp60v-src kinase to assess the initial changes that take place in caveolae after kinase activation. Within 24-48 h after cells were shifted to the permissive temperature, a set of caveolae-specific proteins became phosphorylated on tyrosine. During this period there was a decline in the caveolae marker protein, caveolin-1, a loss of invaginated caveolae, and a 70% decline in the sphingomyelin content of the cell. One of the phosphorylated proteins was caveolin-1 but it was associated in coimmunoprecipitation assays with both a 30 kDa and a 27 kDa tyrosine-phosphorylated protein. Finally, the cells changed from having a typical fibroblast morphology to a rounded shape lacking polarity. In light of the recent evidence that diverse signaling events originate from caveolae, pp60v-src kinase appears to cause global changes to this membrane domain that might directly contribute to the transformed phenotype. J. Cell. Biochem. 71:524-535, 1998. © 1998 Wiley-Liss, Inc.
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  • 112
    Electronic Resource
    Electronic Resource
    Molecular cloning of a mutated HOXB7 cDNA encoding a truncated transactivating homeodomain-containing protein (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 46-54 
    Details
    ISSN: 0730-2312
    Keywords: homeobox ; breast ; ligase chain reaction ; transcription ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Homeodomain-containing proteins regulate, as transcription factors, the coordinated expression of genes involved in development, differentiation, and malignant transformation. We report here the molecular cloning of a mutated HOXB7 transcript encoding a truncated homeodomain-containing protein in MCF7 cells. This is a new example of mutation affecting the coding region of a HOX gene. In addition, we detected two HOXB7 transcripts in several breast cell lines and demonstrated that both normal and mutated alleles were expressed at the RNA level in MCF7 cells as well as in a variety of breast tissues and lymphocytes, suggesting that a truncated HOXB7 protein might be expressed in vivo. Using transient co-transfection experiments, we demonstrated that both HOXB7 proteins can activate transcription from a consensus HOX binding sequence in breast cancer cells. Our results provide evidence that HOXB7 protein has transcription factor activity in vivo and that the two last amino acids do not contribute to this property. J. Cell. Biochem. 71:46-54. © 1998 Wiley-Liss, Inc.
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  • 113
    Electronic Resource
    Electronic Resource
    Osteoblastic phenotype of rat marrow stromal cells cultured in the presence of dexamethasone, β-glycerolphosphate, and L-ascorbic acid (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 55-62 
    Details
    ISSN: 0730-2312
    Keywords: osteoblast ; marrow stromal cell ; osteoblastic differentiation ; dexamethasone ; bone tissue engineering ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We investigated the effects of the time course of addition of osteogenic supplements dexamethasone, β-glycerolphosphate, and L-ascorbic acid to rat marrow stromal cells, and the exposure time on the proliferation and differentiation of the cells. It was the goal of these experiments to determine the time point for supplement addition to optimize marrow stromal cell proliferation and osteoblastic differentiation. To determine this, two studies were performed; one study was based on the age of the cells from harvest, and the other study was based on the duration of exposure to supplemented medium. Cells were seen to proliferate rapidly at early time points in the presence and absence of osteogenic supplements as determined by 3H-thymidine incorporation into the DNA of replicating cells. These results were supported by cell counts ascertained through total DNA analysis. Alkaline phosphatase (ALP) activity and osteocalcin production at 21 days were highest for both experimental designs when the cells were exposed to supplemented medium immediately upon harvest. The ALP levels at 21 days were six times greater for cells maintained in supplements throughout than for control cells cultured in the absence of supplements for both studies, reaching an absolute value of 75 × 10-7 μmole/min/cell. Osteocalcin production reached 20 × 10-6 ng/cell at 21 days in both studies for cells maintained in supplemented medium throughout the study, whereas the control cells produced an insignificant amount of osteocalcin. These results suggest that the addition of osteogenic supplements to marrow-derived cells early in the culture period did not inhibit proliferation and greatly enhanced the osteoblastic phenotype of cells in a rat model. J. Cell. Biochem. 71:55-62, 1998. © 1998 Wiley-Liss, Inc.
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  • 114
    Electronic Resource
    Electronic Resource
    Arachidonic acid metabolism by adult human osteoblast-like cells exhibits sexually dimorphic characteristics (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 74-81 
    Details
    ISSN: 0730-2312
    Keywords: prostaglandin ; phospholipase A2 ; age ; tumor necrosis factor-α ; transforming growth factor-β1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The eicosanoids, including prostaglandin E2 (PGE2) and other bioactive arachidonic acid metabolites, are important local mediators of bone remodeling. Presumably, the limited or excessive synthesis of the eicosanoids could compromise bone homeostasis. We have noted that the stimulated release of arachidonic acid by adult male donor derived human osteoblast-like (hOB) cells exceeded the stimulated release measured for female-derived hOB cells by 1.5-fold. Assays of PGE2 biosynthesis by cytokine-stimulated hOB cells also demonstrated a sex-linked difference, such that male hOB cell PGE2 production exceeded female cell production by 1.6-2.2-fold. The calcium-dependent cytoplasmic phospholipase A2 activity in subcellular fractions prepared from hOB cell homogenates was higher in both the cytosolic (1.6-fold) and particulate (1.5-fold) fractions from the male cells than in those prepared from female hOB cells, suggesting a molecular basis for the observed sexually dimorphic characteristics related to arachidonic acid metabolism by hOB cells. The relatively limited capacity of the female cells may limit needed intracellular and intercellular signaling during bone remodeling, thereby contributing to the development of bone pathology. J. Cell. Biochem. 71:74-81, 1998. © 1998 Wiley-Liss, Inc.
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  • 115
    Electronic Resource
    Electronic Resource
    β1 integrin cytoplasmic domain regulates the constitutive conformation detected by MAb 15/7, but not the ligand-induced conformation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 63-73 
    Details
    ISSN: 0730-2312
    Keywords: integrin ; activation epitopes ; ligand binding ; focal adhesions ; cytoplasmic domains ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The anti-integrin β1 MAb 15/7 sometimes may be a reporter of integrin activation or ligand occupancy. However, certain β1 tail deletions eliminate ligand binding despite inducing maximal constitutive 15/7 expression [Puzon-Mclaughlin et al. (1996): J Biol Chem 271:16580-16585]. Here we describe β1 tail mutations (e.g., double point mutations [D759L/F763L, F766L/E769L], or replacement of the β1 tail by the β5 tail) that prevent rather than induce constitutive appearance of the 15/7 epitope. Despite variable losses of constitutive 15/7 epitope, these mutants all retained a similar inducible 15/7 epitope component as seen upon incubation with GRGDSP peptide ligand. In addition, constitutive 15/7 expression did not correlate with integrin localization into focal adhesions. In conclusion, we show for the first time for a fully functional integrin that specific mutations within the β1 tail can down-regulate the constitutive appearance of an extracellular conformation defined by MAb 15/7. Because this regulation occurs away from the ligand binding site and does not correlate with responsiveness to integrin ligand, cell adhesion, or localization into focal adhesions, a novel type of conformational regulation is suggested. J. Cell. Biochem. 71:63-73, 1998. © 1998 Wiley-Liss, Inc.
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  • 116
    Electronic Resource
    Electronic Resource
    Shear stress down-regulates gene transcription and production of adrenomedullin in human aortic endothelial cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 109-115 
    Details
    ISSN: 0730-2312
    Keywords: fluid shear stress ; adrenomedullin ; endothelial cell ; SSRE ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Vascular endothelial cells are potent modulators of vascular tone in response to shear stress. Levels of vasoactive peptides such as adrenomedullin (AM), endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO) are affected by fluid shear stress. AM, a potent vasodilator and suppressor of smooth muscle cell proliferation, contains the shear stress responsive element (SSRE) “GAGACC” in its promoter region. To examine the role of AM in the shear stress response, cultured human aortic endothelial cells (HAoECs) were exposed to fluid shear stresses of 12 and 24 dynes/cm2 in a cone-plate shear stress loading apparatus for various time periods, and the levels of AM gene expression and peptide secretion from HAoECs were measured by Northern blotting analysis and radioimmunoassay (RIA), respectively. Both AM gene transcription and AM peptide levels were down-regulated by fluid shear stress in a time- and magnitude-dependent manner. Our results demonstrate that the normal level of arterial shear stress down-regulates AM expression in HAoECs, suggesting that AM participates in the modulation of vascular tone by fluid shear stress. J. Cell. Biochem. 71:109-115, 1998. © 1998 Wiley-Liss, Inc.
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    Effects of gonadal and adrenal androgens in a novel androgen-responsive human osteoblastic cell line (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 96-108 
    Details
    ISSN: 0730-2312
    Keywords: androgens ; androgen receptor ; antiandrogens ; differentiation ; osteoblasts ; proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: While androgens have important skeletal effects, the mechanism(s) of androgen action on bone remain unclear. Current osteoblast models to study androgen effects have several limitations, including the presence of heterogeneous cell populations. In this study, we examined the effects of androgens on the proliferation and differentiation of a novel human fetal osteoblastic cell line (hFOB/AR-6) that expresses a mature osteoblast phenotype and a physiological number (∼4,000/nucleus) of androgen receptors (AR). Treatment with 5α-dihydrotestosterone (5α-DHT) inhibited the proliferation of hFOB/AR-6 cells in a dose-dependent fashion, while it had no effect on the proliferation of hFOB cells, which express low levels of AR (〈200/nucleus). In hFOB/AR-6 cells, co-treatment with the specific AR antagonist, hydroxyflutamide abolished 5α-DHT-induced growth inhibition. Steady-state levels of transforming growth factor-β1 (TGF-β1) and TGF-β-induced early gene (TIEG) mRNA decreased after treatment of hFOB/AR-6 cells with 5α-DHT, suggesting a role for the TGF-β1-TIEG pathway in mediating 5α-DHT-induced growth inhibition of hFOB/AR-6 cells. In support of this, co-treatment of hFOB/AR-6 cells with TGF-β1 (40 pg/ml) reversed the 5α-DHT-induced growth inhibition, whereas TGF-β1 alone at this dose had no effect on hFOB/AR-6 cell proliferation. Furthermore, treatment of hFOB/AR-6 cells with 5α-DHT and testosterone (10-8 M) inhibited basal and 1,25-(OH)2D3-induced alkaline phosphatase (ALP) activity and type I collagen synthesis without affecting osteocalcin production. Thus, in this fetal osteoblast cell line expressing a physiological number of AR, androgens decrease proliferation and the expression of markers associated with osteoblast differentiation. These studies suggest that the potential anabolic effect of androgens on bone may not be mediated at the level of the mature osteoblast. J. Cell. Biochem. 71:96-108, 1998. © 1998 Wiley-Liss, Inc.
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    Role of M-line proteins in sarcomeric titin assembly during cardiac myofibrillogenesis (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 82-95 
    Details
    ISSN: 0730-2312
    Keywords: M-line proteins ; titin ; expression ; antibody perturbation ; immunocytochemistry ; cardiomyocyte ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A rat polyclonal anti-M-line protein antiserum and three mouse monoclonal anti-titin antibodies (E2, F3, and A12) were used to study the spatiotemporal relationship between M-line proteins and titin during myofibril assembly in cultured chicken cardiomyocytes by immunofluorescence microscopy. In day 2 cultures, M-line proteins and titin were detected as punctate staining in most cardiomyocytes, which possessed many nonstriated fibrils. At a late stage (day 3 cultures), M-line proteins were incorporated into dot-like structures along nonstriated fibrils, while titin staining was continuous on these structures. As development progressed, M-line proteins were registered in periodic pattern in the mid-A band. In cardiomyocytes from day 5 cultures, the titin bands were separated by an unstained region, and achieved their adult doublet pattern. Thus, the organization of titin in the sarcomere appears to occur later than that of M-line proteins in the M-line. Our morphological data indicate that the early registration of M-line proteins in primitive myofibrils may guide titin filament alignment via interaction between M-line proteins and titin. In order to investigate the role of M-line proteins in the assembly of titin filaments, anti-M-line protein or anti-titin antibodies were introduced into cultured cardiomyocytes by electroporation to functionally bind the respective proteins, and the profile of myofibril assembly was examined. Cardiomyocytes from day 2-3 cultures with incorporated anti-M-line protein antibodies became shrunk, and exhibited defective myofibrillar assembly, as shown by the failure of titin to assemble into a typical sarcomeric pattern. Incorporation of anti-titin antibody E2, which recognizes the M-line end domain of titin, resulted in the failure of M-line proteins organized into the M-line structure, as shown by random, sporadic staining with anti-M-line protein antibody. These studies confirm the essential role of M-line proteins in the organization of titin filaments in the sarcomere and that the interaction between titin and M-line proteins is crucial to the formation of the M-line structure. J. Cell. Biochem. 71:82-95, 1998. © 1998 Wiley-Liss, Inc.
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    Several novel transcripts of glyceraldehyde-3-phosphate dehydrogenase expressed in adult chicken testis (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 127-139 
    Details
    ISSN: 0730-2312
    Keywords: GAPDH gene expression ; spermatogenesis ; meiotic and postmeiotic cells ; heat shock ; polyadenylation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), in addition to being a classic glycolytic enzyme, is a multifunctional protein involved in relevant cell functions such as DNA replication, DNA repair, translational control of gene expression, and apoptosis. Although the multifunctional nature of GAPDH suggests versatility in the mechanisms regulating its expression, no major qualitative changes and few quantitative changes in the GAPDH transcripts have been reported. While studying the expression of GAPDH during spermatogenesis, we detected alternative initiations to TATA box and alternative splicings in the 5′ region of the pre-mRNA, resulting in at least six different types of mRNAs. The amount and the polyadenylation of the GAPDH transcripts increased in mature testis in relation to immature testis and further increased when cell suspensions from mature testis were exposed to heat shock. These results suggest that alternative initiation, alternative splicing, and polyadenylation could provide the necessary versatility to the regulation of the expression of this multifunctional protein during spermatogenesis. J. Cell. Biochem. 71:127-139, 1998. © 1998 Wiley-Liss, Inc.
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    Checking on the cell cycle (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 50-54 
    Details
    ISSN: 0730-2312
    Keywords: p53 ; cell cycle regulation ; p21 ; wip21 ; cancer ; 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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    Regulators and mediators of the p53 tumor suppressor (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 43-49 
    Details
    ISSN: 0730-2312
    Keywords: tumor suppression ; p53 ; angiogenesis ; signal transduction ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Tumor suppressors act along diverse biochemical pathways to function as safeguards against cancer. This review summarizes how these pathways can be regulated, primarily by focusing on the well-characterized wild-type p53 tumor suppressor as a paradigm. Specifically, we discuss recent data linking p53 to the processes of signal transduction and angiogenesis. J. Cell. Biochem. Suppls. 30/31:43-49, 1998 © 1998 Wiley-Liss, Inc.
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    Control of bone formation and resorption: Biological and clinical perspective (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 55-61 
    Details
    ISSN: 0730-2312
    Keywords: osteoblasts ; osteoclasts ; osteoporosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Bone is subject to continuous breakdown (resorption) by osteoclasts and rebuilding (formation) by osteoblasts in order to fulfill its functions. Most bone diseases including osteoporosis are due to excessive bone resorption relative to formation. Recent research has generated new insights into the regulation of osteoclast and osteoblast differentiation and function and the interaction between the two cell types. There is increased awareness of the role of mechanical stimuli in bone homeostasis and by inference the function of bone cells. This information can lead to new therapeutic modalities for maintaining a healthy skeleton into old age. J. Cell. Biochem. Suppls. 30/31:55-61, 1998. © 1998 Wiley-Liss, Inc.
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    Osteocalcin gene promoter: Unlocking the secrets for regulation of osteoblast growth and differentiation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 62-72 
    Details
    ISSN: 0730-2312
    Keywords: osteocalcin gene ; osteoblast growth ; osteoblast differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The bone tissue-specific osteocalcin gene remains one of a few genes that exhibits osteoblast-restricted expression. Over the last decade, characterization of the promoter regulatory elements and complexes of factors that control suppression of the osteocalcin gene in osteoprogenitor cells and transactivation in mature osteoblasts has revealed transcriptional regulatory mechanisms that mediate development of the osteoblast phenotype. In this review, we have focused on emerging concepts related to molecular mechanisms supporting osteoblast growth and differentiation based on the discoveries that the osteocalcin gene is regulated by homeodomain factors, AP-1 related proteins, and the bone restricted Cbfa1/AML3 transcription factor. J. Cell. Biochem. Suppls. 30/31:62-72, 1998. © 1998 Wiley-Liss, Inc.
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    Biomineralization: Conflicts, challenges, and opportunities (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 83-91 
    Details
    ISSN: 0730-2312
    Keywords: biomineralization ; calcification ; bone ; dentin ; matrix proteins ; matrix vesicles ; collagen ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Biomineralization is the process by which mineral crystals are deposited in an organized fashion in the matrix (either cellular or extracellular) of living organisms. Over the past 25 years, new insights into the mechanisms that control these processes have been obtained, yet questions asked then still persist, especially in terms of vertebrate mineralization. Specifically, there are still debates concerning the chemical nature of the first mineral crystals formed in bone, dentin, and cementum; the factors leading to the initial deposition of these crystals; and the functions of macromolecules found associated with these crystals. In this review, emphasis is placed on the currently accepted answers to these questions, drawing insight from nonvertebrate systems. It is suggested that there are redundant calcification mechanisms and that, by taking advantage of our current knowledge of these mechanisms, opportunities will be provided for therapeutic manipulation of diseases in which biomineralization is impaired. J. Cell. Biochem. Suppls. 30/31:83-91, 1998. © 1998 Wiley-Liss, Inc.
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    Expression of α2-macroglobulin receptor-associated protein in normal human epidermal melanocytes and human melanoma cell lines (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 149-157 
    Details
    ISSN: 0730-2312
    Keywords: RAP ; α2MR/LRP ; melanocytes ; melanoma ; cell culture density ; flow cytometry ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: α2-Macroglobulin receptor/low-density lipoprotein receptor-related protein is a multifunctional cell surface receptor known to bind and internalize a large number of ligands. α2-Macroglobulin receptor-associated protein acts as an intracellular “chaperone” for this receptor, and it has been shown to inhibit binding of all its known ligands. In this paper, we characterize the expression of the receptor-associated protein in both normal human epidermal melanocytes and in six different human melanoma cell lines, by the use of flow cytometry and Western blotting analysis. We show that all the melanoma cell lines and the normal melanocytes express the receptor-associated protein at similar levels, with most located intracellularly. No receptor-associated protein was detected at the cell surface in the melanocytes or in three of the cell lines. However, in two of the melanoma cell lines, large amounts of receptor-associated protein were found on the cell surface, these having the largest amounts of it reported to date; in a further melanoma cell line, there was a small amount at the cell surface. We have also shown that the melanocytes and all the melanoma cell lines express the receptor itself at a wide range of levels, the highest levels of both the cell surface receptor and the cell surface receptor-associated protein being found in one particular melanoma cell line. By growing the cell lines under controlled conditions, we have demonstrated that, although the total cellular content of the receptor is markedly increased at high cell culture density, this treatment has no effect on the level of expression of the receptor-associated protein. J. Cell. Biochem. 71:149-157, 1998. © 1998 Wiley-Liss, Inc.
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    Promiscuous subunit interactions: A possible mechanism for the regulation of protein kinase CK2 (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 129-136 
    Details
    ISSN: 0730-2312
    Keywords: protein kinase CK2 ; holoenzyme ; α- and β-subunits ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Protein kinase CK2 is a ubiquitous eukaryotic ser/thr protein kinase. The active holoenzyme is a heterotetrameric protein composed of catalytic (α and α′) and regulatory (β) subunits that phosphorylates many different protein substrates and appears to be involved in the regulation of cell division. Despite important structural studies, the intimate details of the interactions of the α catalytic subunits with the β regulatory subunits are unknown. Recent evidence that indicates that both CK2 subunits can interact promiscuously with other proteins in a manner that excludes the binding of their complementary CK2 partners has opened the possibility that the phosphorylating activity of this enzyme may be regulated in a novel way. These alternative interactions could limit the in vivo availability of CK2 subunits to generate fully active holoenzyme CK2 tetramers. Likewise, variations in the ratio of α- and β-subunits could determine the activity of several phosphorylating and dephosphorylating activities. The promiscuity of the CK2 subunits can be extrapolated to a more widespread phenomenon in which “wild-card” proteins could act as general switches by interacting and regulating several catalytic activities. J. Cell. Biochem. Suppls. 30/31:129-136, 1998. © 1998 Wiley-Liss, Inc.
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    Signaling mechanisms and molecular characteristics of G protein-coupled receptors for lysophosphatidic acid and sphingosine 1-phosphate (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 147-157 
    Details
    ISSN: 0730-2312
    Keywords: LPA ; S1P ; G protein ; intracellular signaling pathways ; Edg receptors ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are potent phospholipid mediators with diverse biological activities. Their appearance and functional properties suggest possible roles in development, wound healing, and tissue regeneration. The growth-stimulating and other complex biological activities of LPA and S1P are attributable in part to the activation of multiple G protein-mediated intracellular signaling pathways. Several heterotrimeric G proteins, as well as Ras- and Rho-dependent pathways play central roles in the cellular responses to LPA and S1P. Recently, several G protein-coupled receptors encoded by a family of endothelial differentiation genes (edg) have been shown to bind LPA or S1P and transduce responses of cAMP, Ca2+, MAP kinases, Rho, and gene transcription. This review summarizes our current understanding of signaling pathways critical for cellular responses to LPA and S1P and of recent progress in the molecular biological analyses of the Edg receptors. J. Cell. Biochem. Suppls. 30/31:147-157, 1998. © 1998 Wiley-Liss, Inc.
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    A role for cadherins in cellular signaling and differentiation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 168-176 
    Details
    ISSN: 0730-2312
    Keywords: cadherin ; catenin ; differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cadherins form a family of cell-cell adhesion proteins that are critical to normal embryonic development. Expression of the various family members is regulated in a complex pattern during embryogenesis. Both reduced and inappropriate expression of cadherins have been associated with abnormal tissue formation in embryos and tumorigenesis in mature organisms. Evidence is accumulating that signals unique to individual members of the cadherin family, as well as signals common to multiple cadherins, contribute to the differentiated phenotype of various cell types. While a complete understanding of the regulation of cadherin expression of the molecular nature of intracellular signaling downstream of cadherin adhesion is essential to an understanding of embryogenesis and tumorigenesis, our knowledge in both areas is inadequate. Clearly, elucidating the factors and conditions that regulate cadherin expression and defining the signaling pathways activated by cadherins are frontiers for future research. J. Cell. Biochem. Suppls. 30/31:168-176, 1998. © 1998 Wiley-Liss, Inc.
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    Steroid receptors at the nexus of transcriptional regulation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 185-193 
    Details
    ISSN: 0730-2312
    Keywords: steroid receptor action ; co-repressors ; co-activators ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: During the past few years, our understanding of nuclear receptor action has dramatically improved as a result of the identification and functional analysis of co-regulators such as factors involved in chromatin remodeling, transcription intermediary factors (co-repressors and co-activators), and direct interactions with the basal transcriptional machinery. Furthermore, the elucidation of the crystal structures of the empty ligand-binding domains of the nuclear receptor and of complexes formed by the nuclear receptor's ligand-binding domain bound to agonists and antagonists has contributed significantly to our understanding of the early events of nuclear receptor action. However, the picture of hormone- and hormone receptor-mediated mechanisms of gene regulation remain incomplete and extremely complicated when one also considers the “nontraditional” interactions of hormone-activated nuclear receptors, for example, interactions between the activated steroid receptors and components of the chromatin/nuclear matrix; and finally the nongenomic effects that steroid hormones can exhibit with other signaling pathways. In this prospectus on steroid receptors, we discuss the implications of various steroid hormone and nuclear receptor interactions and potential future directions of investigation. J. Cell. Biochem. Suppls. 30/31:185-193, 1998. © 1999 Wiley-Liss, Inc.
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    Role of histone deacetylases in acute leukemia (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 194-202 
    Details
    ISSN: 0730-2312
    Keywords: acute leukemias ; hematopoietic cells ; histone deacetylase complexes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Accumulating evidence points to a connection between cancer and transcriptional control by histone acetylation and deacetylation. This is particularly true with regard to the acute leukemias, many of which are caused by fusion proteins that have been created by chromosomal translocations. Genetic rearrangements that disrupt the retinoic acid receptor-α and acute myeloid leukemia-1 genes create fusion proteins that block terminal differentiation of hematopoietic cells by repressing transcription. These fusion proteins interact with nuclear hormone co-repressors, which recruit histone deacetylases to promoters to repress transcription. This finding suggests that proteins within the histone deacetylase complexes may be potential targets for pharmaceutical intervention in many leukemia patients. J. Cell. Biochem. Suppls. 30/31:194-202, 1998. © 1998 Wiley-Liss, Inc.
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    Macromolecular exchanges between the nucleus and cytoplasm (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 214-219 
    Details
    ISSN: 0730-2312
    Keywords: nucleus ; nuclear envelope ; nuclear export ; nuclear import ; regulation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The control of transcription and translation is of fundamental importance in cell biology. In this regard, the nuclear envelope is in a unique position to contribute to the regulation of these events, by directing macromolecular exchanges between the nucleus and cytoplasm. Such exchanges occur through the nuclear pore complexes, mainly by signal-mediated processes. Different signals are required for import and export. Specific cytoplasmic or nuclear receptors initially bind the signal-containing substrate, and the complex subsequently interacts with the pores. Additional factors then assist in translocation across the envelope. Current research is focused mainly on further characterization of transport receptors, translocation factors, as well as components of the nuclear pore complex, i.e., the nucleoporins. The ultimate goal is to understand the molecular interactions that occur among the different components of the transport apparatus, the energy sources for transport, and how variations in transport capacity are generated. J. Cell. Biochem. Suppls. 30/31:214-219, 1998. © 1998 Wiley-Liss, Inc.
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    In search of cellular control: Signal transduction in context (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 232-237 
    Details
    ISSN: 0730-2312
    Keywords: cytoskeleton, mechanotransduction, integrins, cell architecture, tensegrity ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The field of molecular cell biology has experienced enormous advances over the last century by reducing the complexity of living cells into simpler molecular components and binding interactions that are amenable to rigorous biochemical analysis. However, as our tools become more powerful, there is a tendency to define mechanisms by what we can measure. The field is currently dominated by efforts to identify the key molecules and sequences that mediate the function of critical receptors, signal transducers, and molecular switches. Unfortunately, these conventional experimental approaches ignore the importance of supramolecular control mechanisms that play a critical role in cellular regulation. Thus, the significance of individual molecular constituents cannot be fully understood when studied in isolation because their function may vary depending on their context within the structural complexity of the living cell. These higher-order regulatory mechanisms are based on the cell's use of a form of solid-state biochemistry in which molecular components that mediate biochemical processing and signal transduction are immobilized on insoluble cytoskeletal scaffolds in the cytoplasm and nucleus. Key to the understanding of this form of cellular regulation is the realization that chemistry is structure and hence, recognition of the importance of architecture and mechanics for signal integration and biochemical control. Recent work that has unified chemical and mechanical signaling pathways provides a glimpse of how this form of higher-order cellular control may function and where paths may lie in the future. J. Cell. Biochem. Suppls. 30/31:232-237, 1998. © 1998 Wiley-Liss, Inc.
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    The new paradigm: Integrating genomic function and nuclear architecture (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 238-242 
    Details
    ISSN: 0730-2312
    Keywords: nuclear matrix ; DNA replication sites ; transcription sites ; confocal microscopy ; nuclear domains ; higher-level nuclear organization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A new view of the cell nucleus is emerging based on the functional dynamics of nuclear architecture. The striking structural preservation of a variety of genomic processes on the nuclear matrix provides an important approach for correlating nuclear form and function. In situ labeling coupled with three-dimensional microscopy and computer imaging techniques shows that DNA replication and transcription sites are organized into higher-order units, or “zones,” in the cell nucleus. The dynamic interplay and “re-zoning” of replication and transcription regions during the cell cycle may form the structural basis for the elaborate global coordination of replicational and transcriptional programs in the mammalian cell. J. Cell. Biochem. Suppls. 30/31:238-242, 1998. © 1998 Wiley-Liss, Inc.
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    Hexose transporter expression and function in mammalian spermatozoa: Cellular localization and transport of hexoses and vitamin C (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 189-203 
    Details
    ISSN: 0730-2312
    Keywords: glucose transporters ; sperm ; dehydroascorbic acid ; fructose ; 2-deoxy-D-glucose ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We analyzed the expression of hexose transporters in human testis and in human, rat, and bull spermatozoa and studied the uptake of hexoses and vitamin C in bull spermatozoa. Immunocytochemical and reverse transcription-polymerase chain reaction analyses demonstrated that adult human testis expressed the hexose transporters GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5. Immunoblotting experiments demonstrated the presence of proteins of about 50-70 kD reactive with anti-GLUT1, GLUT2, GLUT3, and GLUT5 in membranes prepared from human spermatozoa, but no proteins reactive with GLUT4 antibodies were detected. Immunolocalization experiments confirmed the presence of GLUT1, GLUT2, GLUT3, GLUT5, and low levels of GLUT4 in human, rat, and bull spermatozoa. Each transporter isoform showed a typical subcellular localization in the head and the sperm tail. In the tail, GLUT3 and GLUT5 were present at the level of the middle piece in the three species examined, GLUT1 was present in the principal piece, and the localization of GLUT2 differed according of the species examined. Bull spermatozoa transported deoxyglucose, fructose, and the oxidized form of vitamin C, dehydroascorbic acid. Transport of deoxyglucose and dehydroascorbic acid was inhibited by cytochalasin B, indicating the direct participation of facilitative hexose transporters in the transport of both substrates by bull spermatozoa. Transport of fructose was not affected by cytochalasin B, which is consistent for an important role for GLUT5 in the transport of fructose in these cells. The data show that human, rat, and bull spermatozoa express several hexose transporter isoforms that allow for the efficient uptake of glucose, fructose, and dehydroascorbic acid by these cells. J. Cell. Biochem. 71:189-203, 1998. © 1998 Wiley-Liss, Inc.
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    Level of HgCl2-mediated phosphorylation of intracellular proteins determines death of thymic T-lymphocytes with or without DNA fragmentation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 243-253 
    Details
    ISSN: 0730-2312
    Keywords: T-lymphocyte ; apoptosis ; signal transduction ; HgCl2 ; tyrosine phosphorylation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Exposure to Hg2+ at a wide range of concentrations (approximately 1-100 μM) more or less caused the death of murine thymic T-lymphocytes, and exposure to 1 μM but not 10 μM (or more) of Hg2+ induced DNA fragmentation. Exposure of cells to Hg2+ caused phosphorylation of multiple cellular proteins at the tyrosine residue in a concentration-dependent manner. We found that not only the DNA fragmentation induced by 1 μM Hg2+ but also the cell death bypassing DNA fragmentation caused by 10 μM or more Hg2+ was partly inhibited by protein kinase inhibitors such as staurosporine and herbimycin A. This result suggested the involvement of a protein phosphorylation-linked signal in the mechanism of the Hg2+-mediated cell death with or without DNA fragmentation. Analysis of proteins by both one- and two-dimensional electrophoresis and immunoblot showed that a 52-kDa Shc protein was heavily phosphorylated by an early signal delivered by a high concentration of Hg2+, which also phosphorylated extracellular signal-regulated kinase 1 (ERK1; p44) and ERK2 (p42) of the mitogen-activated protein kinase (MAPK) family in a concentration- and time-dependent manner. The c-Jun amino terminal kinase (p54), which is a distant relative of the MAPK family, was also phosphorylated by the treatment with Hg2+. This eventually formed the signaling cascade that ended with a nuclear target by phosphorylating c-jun at the serine 73. This phosphorylation of c-jun was inhibited by staurosporine. These results suggest that a high level of Hg2+-mediated protein phosphorylation-linked signal induces rapid cell death bypassing DNA fragmentation, whereas a lower level induces cell death accompanying DNA fragmentation. This conclusion in turn implies that DNA fragmentation is not always a prerequisite for the signal transduction-dependent cell death of T-lymphocytes. J. Cell. Biochem. 71:243-253, 1998. © 1998 Wiley-Liss, Inc.
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    Hepatocyte growth factor/scatter factor and hepatocytes are potent downregulators of tyrosinase expression in B16 melanoma cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 264-276 
    Details
    ISSN: 0730-2312
    Keywords: HGF/SF ; MSH ; c-met ; tyrosinase ; B16 melanoma ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Reiterated selection in vivo of B16 murine melanoma cells for enhanced liver metastatic ability yielded a cell line (B16-LS9) dramatically overexpressing a constitutively active hepatocyte growth factor/scatter factor (HGF/SF) receptor, the product of the c-met proto-oncogene. Most likely because of their overexpressing c-met, B16-LS9 cells appear to be more responsive than parental B16-F1 cells to HGF stimulation, in terms of motility, invasion, and growth. They are also more pigmented, and express higher levels of tyrosinase as compared to parental B16-F1 cells. Therefore, we set out to explore whether HGF/SF and the liver might influence the differentiation state of B16 cells. We found that HGF/SF and MSH, two factors which reportedly have a strong influence on the phenotype and the malignant behavior of melanoma cells, may act at different levels, and with opposite results, on the regulation of gene expression. In fact, while MSH induces, at the transcriptional level, an increase in the production of both c-met and tyrosinase, HGF/SF, in contrast, promotes a decrease in the expression of both c-met and tyrosinase, however at a posttranscriptional level. These two opposite effects can counter-balance each other, when the cells are treated with both factors at the same time, apparently through a mechanism involving MAP kinase activation. The effects were, however, additive when morphological changes were considered. Most intriguingly, we also describe a very strong downregulatory activity, limited to tyrosinase expression, by hepatocytes in coculture with B16 cells. This activity, also at the posttranscriptional level, is much stronger than that exerted by HGF/SF, and appears to be due to a labile soluble factor produced by the hepatocytes. J. Cell. Biochem. 71:264-276, 1998. © 1998 Wiley-Liss, Inc.
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    Evidence of a direct role for Bcl-2 in the regulation of articular chondrocyte apoptosis under the conditions of serum withdrawal and retinoic acid treatmentThis article is a US Government work and, as such, is in the public domain in the United States of America. (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 302-309 
    Details
    ISSN: 0730-2312
    Keywords: cartilage ; aging ; osteoarthritis ; programmed cell death ; cell culture ; human ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The regulation of chondrocyte apoptosis in articular cartilage may underlay age-associated changes in cartilage and the development of osteoarthritis. Here we demonstrate the importance of Bcl-2 in regulating articular chondrocyte apoptosis in response to both serum withdrawal and retinoic acid treatment. Both stimuli induced apoptosis of primary human articular chondrocytes and a rat chondrocyte cell line as evidenced by the formation of DNA ladders. Apoptosis was accompanied by decreased expression of aggrecan, a chondrocyte specific matrix protein. The expression of Bcl-2 was downregulated by both agents based on Northern and Western analysis, while the level of Bax expression remained unchanged compared to control cells. The importance of Bcl-2 in regulating chondrocyte apoptosis was confirmed by creating cell lines overexpressing sense and antisense Bcl-2 mRNA. Multiple cell lines expressing antisense Bcl-2 displayed increased apoptosis even in the presence of 10% serum as compared to wild-type cells. In contrast, chondrocytes overexpressing Bcl-2 were resistant to apoptosis induced by both serum withdrawal and retinoic acid treatment. Finally, the expression of Bcl-2 did not block the decreased aggrecan expression in IRC cells treated with retinoic acid. We conclude that Bcl-2 plays an important role in the maintenance of articular chondrocyte survival and that retinoic acid inhibits aggrecan expression independent of the apoptotic process. J. Cell. Biochem. 71:302-309, 1998. © 1998 Wiley-Liss, Inc.
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    Collagen in tissue-engineered cartilage: Types, structure, and crosslinks (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 313-327 
    Details
    ISSN: 0730-2312
    Keywords: articular cartilage repair ; tissue engineering ; collagen type II ; collagen type IX ; collagen network ; pyridinium crosslinks ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The function of articular cartilage as a weight-bearing tissue depends on the specific arrangement of collagen types II and IX into a three-dimensional organized collagen network that can balance the swelling pressure of the proteoglycan/ water gel. To determine whether cartilage engineered in vitro contains a functional collagen network, chondrocyte-polymer constructs were cultured for up to 6 weeks and analyzed with respect to the composition and ultrastructure of collagen by using biochemical and immunochemical methods and scanning electron microscopy. Total collagen content and the concentration of pyridinium crosslinks were significantly (57% and 70%, respectively) lower in tissue-engineered cartilage that in bovine calf articular cartilage. However, the fractions of collagen types II, IX, and X and the collagen network organization, density, and fibril diameter in engineered cartilage were not significantly different from those in natural articular cartilage. The implications of these findings for the field of tissue engineering are that differentiated chondrocytes are capable of forming a complex structure of collagen matrix in vitro, producing a tissue similar to natural articular cartilage on an ultrastructural scale. J. Cell. Biochem. 71:313-327, 1998. © 1998 Wiley-Liss, Inc.
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    Insulin-regulated protein kinases during postnatal development of rat heart (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 328-339 
    Details
    ISSN: 0730-2312
    Keywords: insulin ; heart ; development ; PI 3-kinase ; protein kinase B ; S6 kinase ; casein kinase 2 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The control of glucose uptake and glycogen metabolism by insulin in target organs is in part mediated through the regulation of protein-serine/ threonine kinases. In this study, the expression and phosphotransferase activity levels of some of these kinases in rat heart ventricle were measured to investigate whether they might mediate the shift in the energy dependency of the developing heart from glycogen to fatty acids. Following tail-vein injection of overnight fasted adult rats with 2 U of insulin per kg body weight, protein kinase B (PKB), the 70-kDa ribosomal S6 kinase (S6K), and casein kinase 2 (CK2) were activated (30-600%), whereas the MAP/ extracellular regulated kinases (ERK)1 and ERK2 were not stimulated under these conditions. When the expression levels of the insulin-activated kinases were probed with specific antibodies in ventricular extracts from 1-, 10-, 20-, 50-, and 365-day-old rats, phosphatidylinositol 3-kinase (PI3K), PKB, S6K, and CK2 were downregulated (40-60%) with age. By contrast, ventricular glycogen synthase kinase-3β (GSK3β) protein levels were maintained during postnatal development. Similar findings were obtained when the expression of these kinases was investigated in freshly isolated ventricular myocytes, where they were detected predominantly in the cytosolic fraction of the myocytes. Compared to other adult rat tissues such as brain and liver, the levels of PI3K, PKB, S6K, and GSK3β were relatively low in the heart. Even though CK2 protein and activity levels were reduced by ∼60% in 365 day as compared to 1-day-old rats, expression of CK2 in the adult heart was as high as detected in any of the other rat tissues. The high basal activities of CK2 in early neonatal heart may be associated with the proliferating state of myocytes. J. Cell. Biochem. 71:328-339, 1998. © 1998 Wiley-Liss, Inc.
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    Regulation of intracellular membrane interactions: Recent progress in the field of neurotransmitter release (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 103-110 
    Details
    ISSN: 0730-2312
    Keywords: secretion ; SNARE hypothesis ; priming, fusion competence ; phosphoinositides ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Maintenance of compartmental independence and diversity is part of the blueprint of the eukaryotic cell. The molecular composition of every organelle membrane is custom tailored to fulfill its unique tasks. It is retained by strict sorting and directional transport of newly synthesized cellular components by the use of specific transport vesicles. Temporally and spatially controlled membrane fission and fusion steps thus represent the basic process for delivery of both, membrane-bound and soluble components to their appropriate destination. This process is fundamental to cell growth, organelle inheritance during cell division, uptake and intracellular transport of membrane-bound and soluble molecules, and neuronal communication. The latter process has become one of the best studied examples in terms of regulatory mechanisms of membrane interactions. It has been dissected into the stages of transmitter vesicle docking, priming, and fusion: Specificity of membrane interactions depends on interactions between sets of organelle-specific membrane proteins. Priming of the secretory apparatus is an ATP-dependent process involving proteins and membrane phospholipids. Release of vesicle content is triggered by a rise in intracellular free Ca2+ levels that relieves a block previously established between the membranes poised to fuse. Neurotransmitter release is a paradigm of highly regulated intracellular membrane interaction and molecular mechanisms for this phenomenon begin to be delineated. J. Cell. Biochem. Suppls. 30/31:103-110, 1998. © 1998 Wiley-Liss, Inc.
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    Signal transduction by transforming growth factor-β: A cooperative paradigm with extensive negative regulation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 111-122 
    Details
    ISSN: 0730-2312
    Keywords: TGF-β cooperative signaling ; SMADs ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Transforming growth factor-β (TGF-β) represents an evolutionarily conserved family of secreted factors that mobilize a complex signaling network to control cell fate by regulating proliferation, differentiation, motility, adhesion, and apoptosis. TGF-β promotes the assembly of a cell surface receptor complex composed of type I (TβRI) and type II (TβRII) receptor serine/threonine kinases. In response to TGF-β binding, TβRII recruits and activates TβRI through phosphorylation of the regulatory GS-domain. Activated TβRI then initiates cytoplasmic signaling pathways to produce cellular responses. SMAD proteins together constitute a unique signaling pathway with key roles in signal transduction by TGF-β and related factors. Pathway-restricted SMADs are phosphorylated and activated by type I receptors in response to stimulation by ligand. Once activated, pathway-restricted SMADs oligomerize with the common-mediator Smad4 and subsequently translocate to the nucleus. Genetic analysis in Drosophila melanogaster and Caenorhabditis elegans, as well as TβRII and SMAD mutations in human tumors, emphasizes their importance in TGF-β signaling. Mounting evidence indicates that SMADs cooperate with ubiquitous cytoplasmic signaling cascades and nuclear factors to produce the full spectrum of TGF-β responses. Operating independently, these ubiquitous elements may influence the nature of cellular responses to TGF-β. Additionally, a variety of regulatory schemes contribute temporal and/or spatial restriction to TGF-β responses. This report reviews our current understanding of TGF-β signal transduction and considers the importance of a cooperative signaling paradigm to TGF-β-mediated biological responses. J. Cell. Biochem. Suppls. 30/31:111-122, 1998. © 1998 Wiley-Liss, Inc.
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    G-protein regulatory pathways: Rocketing into the twenty-first century (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 137-146 
    Details
    ISSN: 0730-2312
    Keywords: G proteins ; signal transduction ; protein tyrosine kinases ; PMN ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Complex cellular responses involve the integration of heterotrimeric G protein systems with protein kinase signal transduction pathways. Key in this integration is the control of small GTP-binding proteins including Ras and Rho family members. In this paper, we discuss the control of signal transduction pathways by G proteins and their integration with specific tyrosine kinases. The integration of G proteins, kinases, and small GTP-binding proteins in controlling cellular responses is illustrated through the newly defined Gα12/13-regulated pathways. Furthermore, the polymorphonuclear leukocyte provides a primary cell system for analyzing the integration of G proteins, kinases, and small GTP-binding proteins in controlling cellular functions such as superoxide production, adherence, chemotaxis, and granule secretion. J. Cell. Biochem. Suppls. 30/31:137-146, 1998. © 1998 Wiley-Liss, Inc.
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    Peroxisomes in lipid metabolism (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 158-167 
    Details
    ISSN: 0730-2312
    Keywords: peroxisomes ; lipid metabolism ; H2O2 metabolism ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Gene targeting and the elucidation of mutations underlying inherited peroxisomal diseases have provided new insights in peroxisomal lipid metabolism in vivo. The work led to the identification of a novel peroxisomal β-oxidation pathway and established clearly that genes, which are required for efficient peroxisomal oxidation of fatty acids, at the same time are key regulators of PPARα function in vivo. The new mouse models may provide helpful tools in the search for unknown natural PPARα agonists and in screening for in vivo PPARα antagonists. J. Cell Biochem. Suppls. 30/31:158-167, 1998. © 1998 Wiley-Liss, Inc.
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    Nucleosome and chromatin structures and functions This article is a U.S. Government work and, as such, is in the public domain in the United States of America. (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 177-184 
    Details
    ISSN: 0730-2312
    Keywords: nucleosome ; chromosomes ; DNA ; 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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    Regulation and regulatory parameters of histone modifications (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 203-213 
    Details
    ISSN: 0730-2312
    Keywords: histone acetylation and phosphorylation ; coactivators ; corepressors ; transcriptional activation and repression ; histone acetyltransferase ; histone deacetylase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Histone acetylation and phosphorylation destablizes nucleosome and chromatin structure. Relaxation of the chromatin fiber facilitates transcription. Coactivator complexes with histone acetyltransferase activity are recruited by transcription factors bound to enhancers or promoters. The recruited histone acetyltransferases may acetylate histone or nonhistone chromosomal proteins, resulting in the relaxation of chromatin structure. Alternatively, repressors recruit corepressor complexes with histone deacetylase activity, leading to condensation of chromatin.This review highlights the recent advances made in our understanding of the roles of histone acetyltransferases, histone deacetylases, histone kinases, and protein phosphatases in transcriptional activation and repression. Exciting reports revealing mechanistic connections between histone modifying activities and the RNA polymerase II machinery, the coupling of histone deacetylation and DNA methylation, the possible involvement of histone deacetylases in the organization of nuclear DNA, and the role of chromatin modulators in oncogenesis are discussed. J. Cell. Biochem. Suppls. 30/31:203-213, 1998. © 1998 Wiley-Liss, Inc.
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    Linkages of nuclear architecture to biological and pathological control of gene expression (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 220-231 
    Details
    ISSN: 0730-2312
    Keywords: nuclear architecture ; gene expression ; tumor cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Functional interrelationships between components of nuclear architecture and control of gene expression are becoming increasingly evident. There is growing appreciation that multiple levels of nuclear organization integrate the regulatory cues that support activation and suppression of genes as well as the processing of gene transcripts. The linear organization of genes and promoter elements provide the potential for responsiveness to physiological regulatory signals. Parameters of chromatin structure and nucleosome organization support synergism between activities at independent regulatory sequences and render promoter elements accessible or refractory to transcription factors. Association of genes, transcription factors, and the machinery for transcript processing with the nuclear matrix facilitates fidelity of gene expression within the three-dimensional context of nuclear architecture. Mechanisms must be defined that couple nuclear morphology with enzymatic parameters of gene expression. The recent characterization of factors that mediate chromatin remodeling and intranuclear targeting signals that direct transcription factors to subnuclear domains where gene expression occurs, reflect linkage of genetic and structural components of transcriptional control. Nuclear reorganization and aberrant intranuclear trafficking of transcription factors for developmental and tissue-specific control that occurs in tumor cells and in neurological disorders provides a basis for high resolution diagnostics and targeted therapy. J. Cell. Biochem. Suppls. 30/31:220-231, 1998. © 1998 Wiley-Liss, Inc.
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    Intranuclear targeting of DNA replication factors (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 243-249 
    Details
    ISSN: 0730-2312
    Keywords: functional organization ; nucleus ; targeting sequence ; DNA replication ; nuclear matrix ; cell cycle ; DNA methyltransferase ; DNA ligase I ; PCNA ; DNA replication factors ; GFP ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Mammalian nuclei are highly organized into functional compartments. Major nuclear processes like DNA replication and RNA processing take place in distinct foci. These microscopically visible foci are formed by the assembly of, for example, DNA replication factors and associated proteins into megadalton complexes often referred to as protein machines or factories. Thus far, two proteins, DNA ligase I and DNA methyltransferase (DNA MTase), have been analyzed in greater detail. In both cases, the assembly process appears to be controlled by distinct targeting sequences that were attached to the catalytic protein core in the course of evolution and mediate the association with replication factories in mammalian cells. The dynamics of these nuclear structures throughout the cell cycle are analyzed using green fluorescent protein (GFP). Further studies are needed to elucidate the architecture, regulation, and role of these subnuclear structures. J. Cell. Biochem. Suppls. 30/31:243-249, 1998. © 1998 Wiley-Liss, Inc.
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    Color section (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 313-336 
    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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    High throughput analysis of differential gene expression (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 286-296 
    Details
    ISSN: 0730-2312
    Keywords: EST ; cDNA microarray ; RDA ; osteoblast differentiation ; pax-6 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Elucidation of the changes in gene expression associated with biological processes is a central problem in biology. Advances in molecular and computational biology have led to the development of powerful, high-thoughput methods for the analysis of differential gene expression. These tools have opened up new opportunities in disciplines ranging from cell and developmental biology to drug development and pharmacogenomics. In this review, the attributes of five commonly used differential gene expression methods are discussed: expressed sequence tag (EST) sequencing, cDNA microarray hybridization, subtractive cloning, differential display, and serial analysis of gene expression (SAGE). The application of EST sequencing and microarray hybridization is illustrated by the discovery of novel genes associated with osteoblast differentiation. The application of subtractive cloning is presented as a tool to identify genes regulated in vivo by the transcription factor pax-6. These and other examples illustrate the power of genomics for discovering novel genes that are important in biology and which also represent new targets for drug development. The central theme of the review is that each of the approaches to identifying differentially expressed genes is useful, and that the experimental context and subsequent evaluation of differentially expressed genes are the critical features that determine success. J. Cell. Biochem. Suppls. 30/31:286-296, 1998. © 1998 Wiley-Liss, Inc.
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    Author-subject index (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 338-340 
    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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    Oxidation of glutamine in HeLa cells: Role and control of truncated TCA cycles in tumour mitochondria (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 213-225 
    Details
    ISSN: 0730-2312
    Keywords: glutamine ; glutamate ; mitochondria ; metabolism ; HeLa cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The oxidative metabolism of glutamine in HeLa cells was investigated using intact cells and isolated mitochondria. The concentrations of the cytoplasmic amino acids were found to be aspartate, 8.0 mM; glutamate, 22.2 mM; glutamine, 11.3 mM; glycine, 9.8 mM; taurine, 2.3 mM; and alanine, 〈1 mM. Incubation of the cells with [14C]glutamine gave steady-state recoveries of 14C-label (estimated as exogenous glutamine) in the glutamine, glutamate, and aspartate pools, of 103%, 80%, and 25%, respectively, indicating that glutamine synthetase activity was absent and that a significant proportion of glutamate oxidation proceeded through aspartate aminotransferase. No label was detected in the alanine pool, suggesting that alanine aminotransferase activity was low in these cells. The clearance rate of [14C]glutamine through the cellular compartment was 65 nmol/min per mg protein. There was a 28 s delay after [14C]glutamine was added to the cell before 14C-label was incorporated into the cytoplasm, while the formation of glutamate commenced 10 s later.Aspartate was the major metabolite formed when the mitochondria were incubated in a medium containing either glutamine, glutamate, or glutamate plus malate. The transaminase inhibitor AOA inhibited both aspartate efflux from the mitochondria and respiration. The addition of 2-oxoglutarate failed to relieve glutamate plus malate respiration, indicating that 2-oxoglutarate is part of a well-coupled truncated cycle, of which aspartate aminotransferase has been shown to be a component [Parlo and Coleman (1984): J Biol Chem 259:9997-10003]. This was confirmed by the observation that, although it inhibited respiration, AOA did not affect the efflux of citrate from the mitochondria. Thus citrate does not appear to be a cycle component and is directly transported to the medium. Therefore, it was concluded that the truncated TCA cycle in HeLa cells is the result of both a low rate of citrate synthesis and an active citrate transporter. DNP (10 μM) induced a state III-like respiration only in the presence of succinate, which supports the evidence that NAD-linked dehydrogenases were not coupled to respiration, and suggests that these mitochondria may have a defect in complex I of the electron transport chain. Arising from the present results with HeLa cells and results extant in the literature, it has been proposed that a major regulating mechanism for the flux of glutamate carbon in tumour cells is the competitive inhibition exerted by 2-oxoglutarate on aspartate and alanine aminotransferases. This has been discussed and applied to the data. J. Cell. Biochem. 68:213-225, 1998. © 1998 Wiley-Liss, Inc.
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    Basic fibroblast growth factor decreases type V/XI collagen expression in cultured bovine aortic smooth muscle cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 247-258 
    Details
    ISSN: 0730-2312
    Keywords: SMCs ; bFGF ; collagen fibril structure ; mRNA ; atherosclerotic lesion ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Vascular smooth muscle cells (SMCs), the major cellular constituent of an artery, synthesize the bulk of fibrillar collagens, including type V/XI, which regulates heterotypic collagen fibril assembly. Basic fibroblast growth factor (bFGF) is a heparin-binding polypeptide growth factor that has been implicated in important events during the development of atherosclerosis, such as early intimal SMC proliferation. Here we have investigated the effects of bFGF on aortic SMC expression of type V/XI collagen. Treatment of exponentially growing or serum-deprived subconfluent cultures of bovine aortic SMCs with bFGF decreased the steady-state levels of the mRNAs for collagen type V/XI, including α1(V), α2(V), and α1(XI). The effect of bFGF was time dependent with a two- and a fourfold decrease in α2(V) mRNA observed after treatment for 24 and 48 h, respectively. This decrease resulted from a drop in the rate of α2(V) gene transcription; no change was observed in the stability of the α2(V) mRNA. Furthermore, accumulation of collagen protein decreased upon bFGF treatment. As expected, treatment with bFGF increased the rate of proliferation of serum-deprived SMCs, as judged by DNA content in the cultures, thymidine incorporation, and steady-state mRNA levels of the S-phase-expressed histone H3.2. These results suggest that bFGF plays an important role in the regulation of collagen fibril structure, with potential implications for the development and organization of an atherosclerotic lesion. J. Cell. Biochem. 68:247-258, 1998. © 1998 Wiley-Liss, Inc.
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    Effects of conformationally restricted synthetic retinoids on ovarian tumor cell growth (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 378-388 
    Details
    ISSN: 0730-2312
    Keywords: apoptosis ; growth suppression ; retinoic acid receptors ; ovarian cancer ; AHPN ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have used conformationally restricted retinoids to investigate the role of individual RAR subtypes and RXR in mediating the growth response of ovarian tumor cells to retinoids. Our results show that treatment of all-trans-RA-sensitive CAOV-3 cells with retinoids that bind and activate a single RAR or RXR led to a partial inhibition of growth. Treatment of all-trans-RA- resistant SKOV-3 cells did not alter growth. Maximum inhibition of growth, comparable to that observed following treatment with natural retinoids such as all-trans-RA and 9-cis-RA, was obtained only following treatment with a combination of an RAR-selective compound and an RXR-selective one. These results suggest that activation of both RAR and RXR classes is required in order to obtain maximum inhibition of ovarian tumor cell growth by retinoids. In addition, one compound, AHPN, was found to inhibit both RA-sensitive CAOV-3 and RA-resistant SKOV-3 cells. Further study of the effects of this retinoid showed that AHPN acts through an apoptotic pathway. Taken together, our results suggest that retinoids may serve as effective anti-proliferative agents in the treatment of ovarian cancer. J. Cell. Biochem. 68:378-388, 1998. © 1998 Wiley-Liss, Inc.
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    Tissue, cell type, and breast cancer stage-specific expression of a TGF-β inducible early transcription factor gene (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 226-236 
    Details
    ISSN: 0730-2312
    Keywords: TGF-β ; transcription factor ; rapid regulation ; tumor suppressor ; osteoblasts ; immunohistochemistry ; breast cancer stage ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This laboratory has previously identified a novel TGF-β inducible early gene (TIEG) in human osteoblasts [Subramaniam et al. (1995): Nucleic Acids Res 23:4907-4912]. Using TIEG specific polyclonal antibody and immunoprecipitation methods in normal human fetal osteoblast cells (hFOB cells), we have now demonstrated that TIEG encodes a 72-kDa protein whose levels are transiently increased at as early as 2 h of TGF-β treatment. Polarized confocal microscopic analysis of hFOB cells shows a nuclear localized TIEG protein in untreated cells under the conditions described under Methods. Interestingly, the levels of TIEG protein in the nuclei increase when the cells are treated with TGF-β1 for 2 h. In contrast, similar analyses of untreated human keratinocytes show a cytoplasmic localized TIEG protein that appears to be translocated to the nucleus after H2O2 treatment. Additional immunohistochemical studies have demonstrated that TIEG protein is expressed in epithelial cells of the placenta, breast, and pancreas, as well as in osteoblast cells of bone and selected other cells of the bone marrow and cerebellum with some cells showing a cytoplasmic localization and others a nuclear localization. All cells of the kidney display negative staining for this protein. Interestingly, a stage specific expression of TIEG protein is found in a dozen breast cancer biopsies, using immunohistochemistry. The cells in normal breast epithelium displays a high expression of TIEG protein, those in the in situ carcinoma display less than one-half of the levels, and those in the invasive carcinoma show a complete absence of the TIEG protein. TIEG has been localized to chromosome 8q22.2 locus, the same locus as the genes involved in osteopetrosis and acute myeloid leukemia and close to the c-myc gene locus and a locus of high polymorphism in cancer biopsies. The correlation between the levels of TIEG protein and the stage of breast cancer, its prime location in human chromosome 8q22.2, and past studies with pancreatic carcinoma, suggests that TIEG may play a role in tumor suppressor gene activities, apoptosis, or some other regulatory function of cell cycle regulation. J. Cell. Biochem. 68:226-236, 1998. © 1998 Wiley-Liss, Inc.
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    Differentiation-dependent expression of cardiac δ-CaMKII isoforms (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 259-268 
    Details
    ISSN: 0730-2312
    Keywords: multifunctional Ca2+/calmodulin-dependent protein kinase ; cardiac isoforms ; muscle differentiation ; cell line Hgc2 ; adult rat heart ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Despite their important role in controlling the cardiac Ca2+ homeostasis, presence and functions of individual isoforms of the multifunctional Ca2+/calmodulin-dependent protein kinase in the heart are not well studied. Here we report on expression of isoforms of the δ class in two differentiation states of the embryonic rat heart-derived cell line H9c2 compared to adult rat heart. Reverse transcription coupled polymerase chain reaction analysis revealed specific expression patterns of four variants of the δ class (δB, δC, δ4, δ9) in adult rat heart, H9c2 myoblasts, and skeletal muscle-like H9c2 myotubes. δC was identified as a common isoform with higher amounts in H9c2 cells and the prominent one in myoblasts. In contrast, expression of δ9 accompanied cardiac as well as skeletal muscle differentiation. Expression of δB, however, was representative for differentiated cardiac muscle, whereas δ4 expression coincided with differentiation into the skeletal muscle-like state. Our results demonstrate differentiation-dependent isoform expression of the δ class of the multifunctional Ca2+/calmodulin-dependent protein kinase of muscle. The identification of cardiac target proteins for this kinase, e.g. the α1-subunit of the L-type Ca2+ channel, the sarcoplasmic reticulum Ca2+-ATPase, phospholamban and the ryanodine receptor define H9c2 myoblasts as a suitable model system for further functional characterization of the identified cardiac δ isoforms. J. Cell. Biochem. 68:259-268, 1998. © 1998 Wiley-Liss, Inc.
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    Relationship between alkaline phosphatase levels, osteopontin expression, and mineralization in differentiating MC3T3-E1 osteoblasts (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 269-280 
    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: We are using viral oncogene probes to study the pathways by which osteoblast-specific gene expression is induced in ascorbic acid-treated MC3T3-E1 cells. The 12S product of the adenovirus E1A gene binds directly to key cellular regulators and, as a result, represses tissue specific gene expression and blocks differentiation in a wide variety of cell types. The main cellular targets of the E1A 12S product are the pRB family and p300/CBP family. The p300 family appears to be the primary target for E1A-mediated repression of tissue-specific gene expression in a variety of cell types. We have generated MC3T3-E1 cell lines that stably express either the wild-type 12S product or a mutant that targets p300/CBP, but not the pRB family. Using these constructs to dissect osteoblast differentiation, we found that targeting of p300/CBP appears to be sufficient to repress alkaline phosphatase expression, although a low but functional level of expression can be maintained if the pRB family is not targeted as well. Induction of alkaline phosphatase expression and activity can be dissociated from expression of late-stage markers such as osteocalcin and osteopontin. Surprisingly, cell lines exhibiting severe repression of alkaline phosphatase activity differentiate to a mineral-secreting phenotype much like normal MC3T3-E1 cells. Osteopontin induction is dependent on at least a minimal level of alkaline phosphatase activity, although it is not dependent on induction of alkaline phosphatase at the RNA level. If alkaline phosphatase is supplied exogenously, osteopontin expression can be induced in conditions in which endogenous alkaline phosphatase is severely repressed. J. Cell. Biochem. 68:269-280, 1998. © 1998 Wiley-Liss, Inc.
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    Glucocorticoids repress induction by thiazolidinediones, fibrates, and fatty acids of phosphoenolpyruvate carboxykinase gene expression in adipocytes (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 298-308 
    Details
    ISSN: 0730-2312
    Keywords: PEPCK ; adipocytes ; transcription ; fatty acids ; fibrates ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Phosphoenolpyruvate carboxykinase (PEPCK) exerts a glyceroneogenic function in adipocytes in which transcription of its gene is increased by unsaturated fatty acids and fibrates. We used cultured rat adipose tissue fragments and 3T3-F442A adipocytes to show that the antidiabetic thiazolidinedione BRL 49653, a ligand and an activator of the γ isoform of peroxisome proliferator activated receptors (PPARγ), is a potent inducer of PEPCK mRNA. In 3T3-F442A adipocytes, the effect of BRL 49653 is rapid and concentration dependent, with a maximum reached at 1 μM and a half-maximum at 10-100 nM. PEPCK mRNA is similarly induced by the natural ligand of PPARγ, the 15-deoxy-Δ12-14 prostaglandin J2. These observations strongly suggest that PPARγ is a primary regulator of PEPCK gene expression in adipocytes. Dexamethasone at 10 nM repress induction of PEPCK mRNA by 1 μM BRL 49653, 0.32 mM oleate, or 1 mM clofibrate, in a cycloheximide-independent manner. The antiglucocorticoid RU 38486 prevents dexamethasone action, demonstrating involvement of the glucocorticoid receptor. Stable transfectants of 3T3-F442A adipocytes bearing -2100 to +69 base pairs of the PEPCK gene promoter fused to the chloramphenicol acetyltransferase (CAT) gene respond to 1 μM BRL 49653 or 1 mM clofibrate by a large increase in CAT activity, which is prevented by the simultaneous addition of 10 nM dexamethasone. Hence, in adipocytes, glucocorticoids act directly through the 5′-flanking region of the PEPCK gene to repress, in a dominant fashion, the stimulation of PEPCK gene transcription by thiazolidinediones and fibrates. J. Cell. Biochem. 68:298-308, 1998. © 1998 Wiley-Liss, Inc.
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    Thiol redox modulation of tumor necrosis factor-α responsiveness in cultured AIDS-related Kaposi's sarcoma cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 339-354 
    Details
    ISSN: 0730-2312
    Keywords: glutathione ; reactive oxygen intermediates ; HIV ; signal transduction ; cytokines ; redox state ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Both clinical and experimental evidence indicates that AIDS-related Kaposi's sarcoma (AIDS-KS) has a multifactorial pathogenesis with factors such as HIV viral load, latent virus induction, and opportunistic infections contributing to disease progression. However, a consistent feature that unites these apparently diverse putative etiologic agents is sustained serum elevations of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α). While virtually every cell responds to TNF-α with gene activation, the extent of TNF-α-mediated cellular signaling is regulated by a delicate balance between signal activation and signal arresting events. Reactive oxygen intermediates (ROI), which are generated as a consequence of TNF-α membrane interaction, are part of this TNF-α-initiated cellular activation cascade. Previous studies in our laboratory have shown that AIDS-KS cells possess impaired oxygen intermediate scavenging capacities, thereby establishing conditions permissive for the intracellular retention of ROI. In this study, we used cellular capacity to upregulate the cytoprotective enzyme superoxide dismutase (SOD) to address the extent of cellular response to TNF-α. Concurrent with the SOD analyses, nucleotide profiles were obtained to assess cellular bioenergetic responses during TNF-α challenge. Proliferative growth levels of mitochondrial (Mn)SOD activities showed an activity spectrum ranging from lowest activity in AIDS-KS cells, to intermediate levels in matched, nonlesional cells from the AIDS-KS donors, to highest activities in HIV- normal fibroblasts. In contrast, following TNF-α challenge, the AIDS-KS and KS donor nonlesional cells showed a 11.89- and 5.86-fold respective increase in MnSOD activity, while the normal fibroblasts demonstrated a 1.35-fold decrease. Subsequent thiol redox modulation studies showed that only the normal fibroblast cultures showed a potentiation of TNF-α-mediated MnSOD upregulation following GSH depletion. In addition, provision of the GSH precursor, N-acetylcysteine during TNF-α challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population. Our data, which show that a perturbation in their cellular thiol redox status accentuates AIDS-KS cellular responsiveness to TNF-α, suggest a biochemical rationale for the recognized TNF-α AIDS-KS clinical correlation. J. Cell. Biochem. 68:339-354, 1998. © 1998 Wiley-Liss, Inc.
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    Overexpression of membrane glycoprotein PC-1 can influence insulin action at a post-receptor site (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 366-377 
    Details
    ISSN: 0730-2312
    Keywords: PC-1 ; insulin action ; insulin resistance ; insulin receptor ; tyrosine kinase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: An elevated content of membrane glycoprotein PC-1 has been observed in cells and tissues of insulin resistant patients. In addition, in vitro overexpression of PC-1 in cultured cells induces insulin resistance associated with diminished insulin receptor tyrosine kinase activity. We now find that PC-1 overexpression also influences insulin receptor signaling at a step downstream of insulin receptor tyrosine kinase, independent of insulin receptor tyrosine kinase. In the present studies, we employed Chinese hamster ovary cells that overexpress the human insulin receptor (CHO IR cells; ∼106 receptors per cell), and transfected them with human PC-1 c-DNA (CHO IR PC-1). In CHO IR PC-1 cells, insulin receptor tyrosine kinase activity was unchanged, following insulin treatment of cells. However, several biological effects of insulin, including glucose and amino acid uptake, were decreased. In CHO IR PC-1 cells, insulin stimulation of mitogen-activated protein (MAP) kinase activity was normal, suggesting that PC-1 overexpression did not affect insulin receptor activation of Ras, which is upstream of MAP kinase. Also, insulin-stimulated phosphatidylinositol (PI)-3-kinase activity was normal, suggesting that PC-1 overexpression did not interfere with the activation of this enzyme by insulin receptor substrate-1. In these cells, however, insulin stimulation of p70 ribosomal S6 kinase activity was diminished. These studies suggest, therefore, that, in addition to blocking insulin receptor tyrosine kinase activation, PC-1 can also block insulin receptor signaling at a post-receptor site. J. Cell. Biochem. 68:366-377, 1998. © 1998 Wiley-Liss, Inc.
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    Fluorescent analogues of myosin II for tracking the behavior of different myosin isoforms in living cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 389-401 
    Details
    ISSN: 0730-2312
    Keywords: cytoskeleton ; cell motility ; intracellular dynamics ; stress fibers ; heavy chain ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Fluorescently labeled smooth muscle myosin II is often used to study myosin II dynamics in non-muscle cells. In order to provide more specific tools for tracking non-muscle myosin II in living cytoplasm, fluorescent analogues of non-muscle myosin IIA and IIB were prepared and characterized. In addition, smooth and non-muscle myosin II were labeled with both cy5 and rhodamine so that comparative, dynamic studies may be performed. Non-muscle myosin IIA was purified from bovine platelets, non-muscle myosin IIB from bovine brain, and smooth muscle myosin II from turkey gizzards. After being fluorescently labeled with tetramethylrhodamine-5-iodoacetamide or with a succinimidyl ester of cy5, they retained the following properties: (1) reversible assembly into thick filaments, (2) actin-activatable MgATPase, (3) phosphorylation by myosin light chain kinase, (4) increased MgATPase upon light-chain phosphorylation, (5) interconversion between 6S and 10S conformations, and (6) distribution into endogenous myosin II-containing structures when microinjected into cultured cells. These fluorescent analogues can be used to visualize isoform-specific dynamics of myosin II in living cells. J. Cell. Biochem. 68:389-401, 1998. © 1998 Wiley-Liss, Inc.
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    Analysis of activin A gene expression in human bone marrow stromal cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 8-21 
    Details
    ISSN: 0730-2312
    Keywords: activin A ; bone marrow stromal cells ; gene regulation ; promoter activity ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Activin A, a member of the TGF-β superfamily, plays roles in differentiation and development, including hematopoiesis. Our previous studies indicated that the expression of activin A by human bone marrow cells and monocytes is highly regulated by inflammatory cytokines and glucocorticoids. The present study was undertaken to investigate the regulation of activin A gene expression in the human bone marrow stromal cell lines L87/4 and HS-5, as well as in primary stromal cells. Northern blots demonstrated that, like primary stromal cells, the cell lines expressed four activin A RNA transcripts (6.4, 4.0, 2.8, and 1.6 kb), although distribution of the RNA among the four sizes varied. The locations of the 5′ ends of the RNAs were investigated by Northern blots and RNase protection assays. The results identified a transcription start site at 212 nucleotides upstream of the translation start codon. In addition, luciferase expression assays of a series of deletion constructs were used to identify regulatory sequences upstream of the activin A gene. A 58 bp upstream sequence exhibits promoter activity. However, severalfold higher expression requires a positive element consisting of an additional 71 bp of the upstream region. Promoter activity was also identified between 2.5 and 3.6 kb upstream of the start codon. These findings suggest that expression of activin A at the transcriptional level follows complex patterns of regulation. J. Cell. Biochem. 70:8-21, 1998. © 1998 Wiley-Liss, Inc.
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    Cloning and characterization of a Dictyostelium gene encoding a small GTPase of the Rab11 family (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 29-37 
    Details
    ISSN: 0730-2312
    Keywords: small GTPase ; membrane traffic ; vesicles ; transport ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Eukaryotic cells achieve complexity by compartmentalizing a subset of cellular functions into membrane-bound organelles. Maintaining this high level of cellular organization requires precise regulation of traffic between membranes. This task is accomplished, in part, by rab proteins. How these small GTPases regulate membrane traffic between cellular compartments is not clear. Here we report the characterization of a novel rab GTPase from the soil amoebae Dictyostelium discoideum. The predicted coding sequence of the new rab gene, Dictyostelium rab11b, encodes a protein of 25 kD containing all the structural hallmarks of a rab GTPase. Comparison of the sequence with the GenBank database and cladistic analysis demonstrated Dictyostelium rab11b to be a divergent member of the rab11 branch of rab proteins. Southern analysis revealed the presence of related genes in Dictyostelium. RNAse protection assays showed the Dictyostelium rab11b gene to be expressed at uniform levels throughout growth and development. Gene deletion experiments revealed that Dictyostelium rab11b was not essential for growth or development. Conceivably, the function of rab11b may be redundant with that of related genes in this organism. J. Cell. Biochem. 70:29-37, 1998. © 1998 Wiley-Liss, inc.
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    Phosphorylation of phospholamban correlates with relaxation of coronary artery induced by nitric oxide, adenosine, and prostacyclin in the pig (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 49-59 
    Details
    ISSN: 0730-2312
    Keywords: coronary artery ; NO/EDRF ; adenosine ; prostacyclin ; phospholamban ; myosin light chain ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The intracellular mechanisms underlying the action of the endogenous vasodilators such as NO/EDRF, adenosine, and prostacyclin acting through cGMP and cAMP, respectively, are not well understood. One important action of cyclic nucleotides in smooth muscle relaxation is to lower the cytosolic Ca2+ concentration by enhanced sequestration into the sarcoplasmic reticulum. The present study was undertaken to elucidate the potential role of phosphorylation of phospholamban, the regulator of sarcoplasmic reticulum Ca2+ pump, for the control of coronary vascular tone by NO/EDRF, adenosine, and prostacyclin. Phospholamban was identified in pig coronary artery preparations by immunofluorescence microscopy, Western blotting and in vitro phosphorylation. Segments of pig coronary artery, with either intact or denuded endothelium, were precontracted with prostaglandin F2α (PGF2α). In endothelium-denuded preparations 3-morpholinosydnonimine (SIN-1), 5′-N-ethylcarboxiamidoadenosine (NECA), and iloprost (ILO) caused both relaxation and phospholamban phosphorylation with the potency: SIN-1 〉 NECA 〉 ILO. The regulatory myosin light chain was significantly dephosphorylated only by SIN-1. In endothelium-intact pig coronary artery, L-NAME caused additional vasoconstriction and a decrease in phospholamban phosphorylation, while phosphorylation of myosin light chain remained unchanged. An inverse relationship between phospholamban phosphorylation and vessel tone was obtained. Our findings demonstrate significant phospholamban phosphorylation during coronary artery relaxation evoked by NO, prostacyclin, and adenosine receptor activation. Because of the close correlation between phosphorylation of phospholamban and vessel relaxation, we propose that phospholamban phosphorylation is an important mechanism by which endogenous vasodilators, especially endothelial NO/EDRF, control coronary vascular smooth muscle tone. J. Cell. Biochem. 70:49-59, 1998. © 1998 Wiley-Liss, Inc.
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    L7 protein is a coregulator of vitamin D receptor-retinoid X receptor-mediated transactivation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 1-12 
    Details
    ISSN: 0730-2312
    Keywords: two-hybrid system ; vitamin D receptor ; retinoid X receptor ; vitamin D ; protein L7 ; basic region leucine zipper domain ; coregulation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The vitamin D receptor (VDR) heterodimerizes with the retinoid X receptor (RXR) and requires additional protein-protein interactions to regulate the expression of target genes. Using the yeast two-hybrid system, we identified the previously described protein L7, that specifically interacted with the VDR in the presence of vitamin D. Deletion analysis indicated, that the N-terminus of L7, which harbours a basic region leucine zipper like domain, mediated interaction with the VDR. Binding assays with purified GST-L7 demonstrated, that L7 specifically pulled down the VDR, that was either expressed in yeast or endogenously contained in the cell line U937. Interestingly, L7 inhibited ligand-dependent VDR-RXR heterodimerization, when constitutively expressed in yeast. We also demonstrate that L7 repressed binding of VDR-RXR heterodimers to a vitamin D response element. Surprisingly, L7 recruited RXR to the same response element in the presence of 9-cis retinoic acid. Ligand-dependent protein-protein interaction in the yeast two-hybrid system confirmed, that binding of L7 also was targeted at the RXR. Our data suggest, that protein L7 is a coregulator of VDR-RXR mediated transactivation of genes, that modulates transcriptional activity by interfering with binding of the receptors to genomic enhancer elements. J. Cell. Biochem. 69:1-12, 1998. © 1998 Wiley-Liss, Inc.
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    Ras-associated nuclear structural change appears functionally significant and independent of the mitotic signaling pathway (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 130-140 
    Details
    ISSN: 0730-2312
    Keywords: signal transduction ; chromatin structure ; cytology ; histones ; metastasis ; Ras ; MAPKK ; NIH3T3 cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: An altered nuclear morphology has been previously noted in association with Ras activation, but little is known about the structural basis, functional significance, signaling pathway, or reproducibility of any such change. We first tested the reproducibility of Ras-associated nuclear change in a series of rodent fibroblast cell lines. After independently developing criteria for recognizing Ras-associated nuclear change in a Papanicolaou stained test cell line with an inducible H(T24)-Ras oncogene, two cytopathologists blindly and independently assessed 17 other cell lines. If the cell lines showed Ras-associated nuclear change, a rank order of increasing nuclear change was independently scored. Ras-associated nuclear changes were identified in v-Fes, v-Src, v-Mos, v-Raf, and five of five H(T24)-Ras transfectants consisting of a change from a flattened, occasionally undulating nuclear shape to a more rigid spherical shape and a change from a finely textured to a coarse heterochromatic appearance. Absent or minimal changes were scored in six control cell lines. The two cytopathologists' independent morphologic rank orders were similar (P〈 .0002). The mitogen signaling pathway per se does not appear to transduce the change since no morphologic alterations were identified in cell lines with activations of downstream components of this pathway - MAPKK or c-Myc - and the rank orders did not correlate with markers of mitotic rate (P 〉 .11). The rank order correlated closely with metastatic potential (P 〈 .0014 and P 〈 .0003) but not with histone H1 composition or global nuclease sensitivity. Based on published studies of five of the cell lines, there may be a correlation between increases in certain nuclear matrix proteins and the Ras-associated nuclear change. J. Cell. Biochem. 70:130-140, 1998. © 1998 Wiley-Liss, Inc.
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    Nuclear neighbours: The spatial and functional organization of genes and nuclear domains (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 159-171 
    Details
    ISSN: 0730-2312
    Keywords: nucleus ; nuclear domain ; genome ; nucleolus ; coiled body ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: It is becoming clear that the cell nucleus is not only organized in domains but that these domains are also organized relative to each other and to the genome. Specific nuclear domains, enriched in different proteins and RNAs, are often found next to each other and next to specific gene loci. Several lines of investigation suggest that nuclear domains are involved in facilitating or regulating gene expression. The emerging view is that the spatial relationship between different domains and genes on different chromosomes, as found in the nucleolus, is a common organizational principle in the nucleus, to allow an efficient and controlled synthesis and processing of a range of gene transcripts. J. Cell. Biochem. 70:159-171. © 1998 Wiley-Liss, Inc.
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    Of coiled bodies, gems, and salmon (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 181-192 
    Details
    ISSN: 0730-2312
    Keywords: coiled bodies (CBs) ; gems ; p80 coilin ; RNPs ; RNA processing ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Coiled bodies (CBs) are nuclear organelles whose morphology and composition have been conserved from plants to animals. They are highly enriched in components of three different RNA processing pathways. Small nuclear RNAs (snRNAs) involved in pre-mRNA splicing, rRNA processing, and histone mRNA 3′ end maturation all take up residence in CBs. However, CB function(s) remain obscure. This review will focus on recent developments in several aspects of CB structure and function, including exciting new results on their twin organelles, called gems. In particular, the reader will be introduced to a novel hypothesis called the “salmon theory of snRNP biogenesis.” Questions arising from and experiments necessary to test this hypothesis will be discussed. J. Cell. Biochem. 70:181-192, 1998. © 1998 Wiley-Liss, Inc.
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    Functional subnuclear partitioning of transcription factors (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 213-221 
    Details
    ISSN: 0730-2312
    Keywords: transcription ; nucleus ; cell architecture ; nuclear matrix ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: After many years of reductionistic approaches to characterize molecular mechanisms involved in transcription, the number of factors recognized to take part in this process has increased remarkably and continues to grow. When considering posttranslational modifications in conjunction with the large number of factors involved in modulating the activity of transcription complex components, the overall intricacy becomes staggering. After two decades of intensive molecular investigations, there has been a concerted effort to integrate these findings with cellular approaches to understand transcription on a more global level. This sort of reasoning actually revisits studies of approximately 20 years ago that considered the functional consequences of steroid receptor association with nuclear structure. With an abundance of new molecular probes and increasingly powerful instruments to detect them in fixed and, more recently, live cells, the issue of functional subnuclear organization is receiving increased attention. In this report, we focus on advances in characterizing the functional significance of transcription factor association with the nucleoskeleton. In particular, we consider recent biochemical and “molecular morphology” data that point to the importance of dynamic spatial and solubility partitioning of gene regulators with nuclear architecture. J. Cell. Biochem. 70:213-221, 1998. © 1998 Wiley-Liss, Inc.
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    DNA topoisomerase II can drive changes in higher order chromosome architecture without enzymatically modifying DNA (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 127-142 
    Details
    ISSN: 0730-2312
    Keywords: chromosome architecture ; disassembly ; reassembly ; proteases ; in vitro model ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Topoisomerase II has been suggested to play a major role in chromosome organization based on its DNA decatenating activity and its ability to mediate direct binding interactions between DNA and nuclear matrix. However, this latter point remains controversial. Here we address the question of whether the chromatin binding activity of Topoisomerase II is sufficient to modify chromosome form using whole mammalian chromosomes in vitro. Intact chromosomes were microsurgically removed from living cells and disassembled by treatment with protease or heparin. When these disassembled chromosomes were incubated with recombinant human Topoisomerase II, the enzyme became incorporated into chromatin and reassembly resulted, leading to almost complete restoration of pre-existing chromosome shape and position within minutes. Chromosome reconstituition by Topoisomerase II was dose-dependent, saturable, and appeared to be controlled stoichiometrically, rather than enzymatically. Similar reassembly was observed in the absence of ATP and when a catalytically inactive thermosensitive Topoisomerase II mutant was used at the restrictive temperature. Chromosome recondensation also could be induced after the strand-passing activity of Topoisomerase II was blocked by treatment with an inhibitor of its catalytic activity, amsacrine. When a non-hydrolyzable β,γ-imido analog of ATP (AMP-PNP) was used to physiologically fix bound Topoisomerase II enzyme in a closed form around DNA, subsequent chromosome disassembly was prevented in the presence of high salt. These data suggest that Topoisomerase II may control higher order chromatin architecture through direct binding interactions, independently of its well-known catalytic activity. J. Cell. Biochem. 69:127-142, 1998. © 1998 Wiley-Liss, Inc.
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    Pulse application of platelet-derived growth factor enhances formation of a mineralizing matrix while continuous application is inhibitory (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 169-180 
    Details
    ISSN: 0730-2312
    Keywords: growth factor ; bone ; osteoblast ; inflammation ; alkaline phosphatase ; differentiation ; proliferation ; PDGF ; mineralized nodules ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Platelet-derived growth factor (PDGF) stimulates chemotaxis and proliferation of osteoblasts, and induces bone formation in vivo. To determine how PDGF might regulate these cells, the effect of PDGF on long-term mineralizing cultures of fetal rat osteoblastic cells was examined. Although PDGF increased cell proliferation in these cultures, continuous treatment with PDGF caused a dose-dependent decrease in mineralized nodule formation. When cells were treated with multiple, brief (1 day) exposures to PDGF at the osteoblast differentiation stage, there was a significant 50% increase in mineralized nodule area. Based on modulation of alkaline phosphatase activity it appears that longer-term exposure to PDGF reduces mineralized nodule formation largely by inhibiting differentiated osteoblast function, while short-term exposure enhances proliferation without inhibiting the differentiated phenotype. Thus, the ultimate affect of PDGF on bone formation is likely to reflect two processes: a positive effect through enhancing cell number or a negative effect by inhibiting differentiated function. The inhibitory effect of PDGF on formation of a mineralized matrix is unlikely to be simply a result of enhanced proliferation of “fibroblastic” cells since cultures treated with PDGF for 3 days and then transferred to new plastic dishes exhibited a 70% increase in mineralized nodule area compared to controls. These results would predict that multiple, brief exposures to PDGF would enhance bone formation in vivo, while prolonged exposure to PDGF, which is likely to occur in chronic inflammation, would inhibit differentiated osteoblast function and limit bone regeneration. J. Cell. Biochem. 69:169-180, 1998. © 1998 Wiley-Liss, Inc.
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    Inhibition of PPARα/RXRα-mediated direct hyperplasia pathways during griseofulvin-induced hepatocarcinogenesis (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 189-200 
    Details
    ISSN: 0730-2312
    Keywords: peroxisome proliferator activated receptor ; retinoid x receptor ; retinoic acid receptor ; liver hyperplasia ; hepatocarcinoma ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Chronic griseofulvin (GF) feeding induces preneoplastic foci followed by hepatocellular carcinoma in the mouse liver. Our previous study suggested that GF-induced hepatocellular proliferation had a different mechanism from that of peroxisome proliferator (PP)-induced direct hyperplasia. The GF-induced hepatocellular proliferation was mediated through activation of immediate early genes such as Fos, Jun, Myc, and NFκB. In contrast, PP-induced direct hyperplasia does not involve activation of any of these immediate early genes. It has been shown that nuclear hormone receptors including peroxisome proliferator activated receptors (PPARs) and retinoid x receptors (RXRs) play important roles in mediating the pleiotropic effects of PPs. To examine the possible roles of PPARs and RXRs during non-PP-induced hepatocellular proliferation and the interaction between PP and non-PP-induced proliferation, we have studied the expression of the PPAR and RXR genes in the GF model using northern blot hybridizations and gel retardation assays. The data showed that the expression of PPARα and RXRα genes was down-regulated in the livers containing preneoplastic nodules and in the liver tumors induced by GF. The mRNA down-regulation was accompanied by a decrease in the amount of nuclear protein-bound to peroxisome proliferator and retinoic acid responsive elements. Down-regulation was also associated with the suppressed expression of the PPARα/RXRα target genes (i.e., acyl-Co oxidase and cytochrome P450 4A1) and the catalase gene. The RXRγ gene was also down-regulated, but the RARα, β, and γ and PPARβ and γ genes were up-regulated. These results indicated that the hepatocarcinogenesis induced by GF is accompanied by suppression of the PPARα/RXRα-mediated direct hyperplasia pathway. The differential expression of these nuclear hormone receptors reveals a new aspect for understanding the individual roles and intercommunication of PPAR, RXR, and RAR isoforms in the liver. J. Cell. Biochem. 69:189-200, 1998. © 1998 Wiley-Liss, Inc.
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    Potent interaction of histamine and polyamines at microsomal cytochrome P450, nuclei, and chromatin from rat hepatocytes (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 233-243 
    Details
    ISSN: 0730-2312
    Keywords: histamine ; polyamines ; cytochrome P450 ; cell growth ; cell proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Histamine and polyamines have been implicated in the mediation of cell proliferation. Our previous work linked the growth-modulatory effects of histamine with its binding to intracellular sites in microsomes and nuclei of various tissues. In this study, we identify cytochrome P450 enzymes as a major component of microsomal intracellular sites in hepatocytes and demonstrate that polyamines compete with high affinity for histamine binding to them. Spectral measurement of histamine binding to P450 in liver microsomes resolved high and intermediate affinity binding sites (Ks1 = 2.4 ± 1.6 μM; Ks2 = 90 ± 17 μM) that corresponded to microsomal binding sites (Kd1 = 1.0 ± 0.9 μM; Kd2 = 57 ± 13 μM) resolved by 3H-histamine binding; additional low affinity (Kd3 ∼ 3 mM), and probably physiologically irrelevant, sites were resolved only by 3H-histamine radioligand studies. As determined spectrally, treatment of microsomes with NADPH/carbon monoxide decreased histamine binding to P450 by about 90% and, as determined by 3H-histamine binding, abolished the high affinity sites and reduced by 85% the number of intermediate sites. Spermine competed potently for 3H-histamine binding: in microsomes, Ki = 9.8 ± 5.8 μM; in nuclei, Ki = 13.7 ± 3.1 μM; in chromatin, Ki = 46 ± 33 nM. Polyamines inhibited the P450/histamine absorbance complex with the rank order of potency: spermine 〉 spermidine ≫ putrescine. In contrast, histamine did not compete for 3H- spermidine binding in nuclei or microsomes, suggesting that polyamines modulate histamine binding allosterically. We propose that certain P450 isozymes that modulate gene function by controlling the level of oxygenated lipids, represent at least one common intracellular target of growth-regulatory endogenous bioamines and, as shown previously, of exogenous growth-modulatory drugs including antiestrogens, antiandrogens, and certain antidepressants and antihistamines. J. Cell. Biochem. 69:233-243, 1998. © 1998 Wiley-Liss, Inc.
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    Tiludronate inhibits interleukin-6 synthesis in osteoblasts: Inhibition of phospholipase D activation in MC3T3-E1 cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 252-259 
    Details
    ISSN: 0730-2312
    Keywords: bisphosphonate ; prostaglandin F2α ; interleukin-6 ; phospholipase D ; osteoblast ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In previous studies, we have reported that PGF2α stimulates phosphoinositide hydrolysis by phospholipase C and phosphatidylcholine hydrolysis by phospholipase D through heterotrimeric GTP-binding protein in osteoblast-like MC3T3-E1 cells, and that PGF2α and PGE1 induce interleukin-6 (IL-6) synthesis via activation of protein kinase C and protein kinase A, respectively. In the present study, we investigated the effect of tiludronate, a bisphosphonate known to inhibit bone resorption, on the PGF2α- and PGE1-induced IL-6 synthesis in these cells. Tiludronate significantly suppressed the PGF2α-induced IL-6 secretion in a dose-dependent manner in the range between 0.1 and 30 μM. However, the IL-6 secretion induced by PGE1 or (Bu)2cAMP was hardly affected by tiludronate. The choline formation induced by PGF2α was reduced by tiludronate dose-dependently in the range between 0.1 and 30 μM. On the contrary, tiludronate had no effect on PGF2α-induced formation of inositol phosphates. Tiludronate suppressed the choline formation induced by NaF, known as an activator of heterotrimeric GTP-binding protein. However, tiludronate had little effect on the formation of choline induced by TPA, a protein kinase C activator. Tiludronate significantly inhibited the NaF-induced IL-6 secretion in human osteoblastic osteosarcoma Saos-2 cells. These results strongly suggest that tiludronate inhibits PGF2α-induced IL-6 synthesis via suppression of phosphatidylcholine-hydrolyzing phospholipase D activation in osteoblasts, and that the inhibitory effect is exerted at the point between heterotrimeric GTP-binding protein and phospholipase D. J. Cell. Biochem. 69:252-259, 1998. © 1998 Wiley-Liss, Inc.
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    Estrogen modulation of osteoblastic cell-to-cell communication (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 282-290 
    Details
    ISSN: 0730-2312
    Keywords: estrogen modulation ; osteoblastic cells ; plasma membrane receptors ; nuclear receptors ; gap junction communication ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Two osteoblastic cell populations, calvarial and marrow stromal cells, were exposed to estrogen derivatives in vitro. The hormonal effect was monitored by following intracellular Ca+2 levels [Ca+2]i and gap-junction communication. We measured fast changes in intracellular Ca+2 levels in response, of these cells, to the steroid hormones. The changes were dose dependent revealing maximal activity at 100 pM by 17-β-Estradiol and 1 nM by estradiol-CMO. Additionally, the effect of estrogen, on functional coupling of the cells, was measured using fluorescence dye migration and counting the number of neighboring cells coupled by gap junctions. An uncoupling effect was demonstrated in response of these cells to estrogen treatment. The quick stereospecific effect was achieved in the presence of 17-β-estradiol but not in the presence of 17-α-estradiol. These results suggest the involvement of plasma membrane receptors in addition to the already known nuclear receptors in transducing the hormone effects in the osteoblastic cells. J. Cell. Biochem. 69:282-290, 1998. © 1998 Wiley-Liss, Inc.
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    Butyrate analogue, isobutyramide, inhibits tumor growth and time to androgen-independent progression in the human prostate LNCaP tumor model (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 271-281 
    Details
    ISSN: 0730-2312
    Keywords: butyrate ; isobutyramide ; prostate cancer ; LNCaP ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Progression to androgen independence remains the main obstacle to improving survival and quality of life in patients with advanced prostate cancer. Induction of differentiation may serve as a rational basis for prevention of progression to androgen independence by modulating gene expression activated by castration or upregulated during androgen-independent progression. The objectives of this study were to characterize the in vitro effects of sodium butyrate on human prostate cancer cell growth, PSA gene expression, and differentiation in the LNCaP tumor model and to determine whether tumor progression in vivo is delayed by isobutyramide, an orally bioavailable butyrate analogue with a longer half-life. The effects of isobutyramide on LNCaP tumor growth and serum PSA levels in both intact and castrate male mice were compared to controls. At concentrations 〉 1 mM, butyrate induced dose-dependent changes towards a more differentiated phenotype, G1 cell cycle arrest, and an 80% decrease in LNCaP cell growth rates. PSA gene expression was increased threefold by butyrate, indicative of differentiation-enhanced gene expression. The half-life of isobutyramide in athymic mice was determined by gas chromatography to be 4 h. During a 4 week period in intact-placebo mice, tumor volume and serum PSA increased 4.1- and 6.6-fold, respectively, compared to twofold and 2.7-fold increases in tumor volume and serum PSA in intact-treated mice. During a 7 week period in castrate-placebo mice, tumor volume and serum PSA levels increased 2.4-fold and fourfold, respectively, compared to a 50% reduction in tumor volume and a twofold increase in serum PSA above nadir levels in castrate mice treated with adjuvant isobutyramide. Isobutyramide treatment induced pronouced morphological changes in LNCaP tumor cells, with loss of defined nucleoli and dispersion of chromatin distribution. LNCaP tumor PSA mRNA levels actually increased threefold, indicative of differentiation-enhanced gene expression. This study demonstrates that butyrate causes LNCaP cell cycle arrest and increased PSA gene expression, both indicative of differentiation. The combination of castration and adjuvant isobutyramide was synergistic in delaying tumor progression. Decreased tumor cell proliferation and increased PSA gene expression induced by isobutyramide results in disconcordant changes in serum PSA and tumor volume and reduces the utility of serum PSA as a marker of response to therapy. J. Cell. Biochem. 69:271-281, 1998. © 1998 Wiley-Liss, Inc.
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    Copper stimulates proliferation of human endothelial cells under culture (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 326-335 
    Details
    ISSN: 0730-2312
    Keywords: copper ; human endothelial cells ; angiogenesis ; growth factors ; cell proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Copper ions stimulate proliferation of human umbilical artery and vein endothelial cells but not human dermal fibroblasts or arterial smooth muscle cells. Incubation of human umbilical vein endothelial cells for 48 h with 500 μM CuSO4 in a serum-free medium in the absence of exogenous growth factors results in a twofold increase in cell number, similar to the cell number increase induced by 20 ng/ml of basic fibroblast growth factor under the same conditions. Copper-induced proliferation of endothelial cells is not inhibited by 10% fetal bovine serum or by the presence of antibodies against a variety of angiogenic, growth, and chemotactic factors including angiogenin, fibroblast growth factors, epidermal growth factor, platelet-derived growth factor, tumor necrosis factor-α, transforming growth factor-β, macrophage/monocyte chemotactic and activating factor, and macrophage inflammatory protein-1α. Moreover, despite the previous observations that copper increased total specific binding of 125I-angiogenin to endothelial cells, binding to the 170 kDa receptor is not changed; hence, the mitogenic activity of angiogenin is not altered by copper. Copper-induced proliferation, along with early reports that copper induces migration of endothelial cells, may suggest a possible mechanism for the involvement of copper in the process of angiogenesis. J. Cell. Biochem. 69:326-335, 1998. © 1998 Wiley-Liss, Inc.
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    Src protein and tyrosine-phosphorylated protein profiles in marrow stroma during osteogenic stimulation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 316-325 
    Details
    ISSN: 0730-2312
    Keywords: osteoprogenitors ; mineralization ; marrow stroma ; Src ; tyrosine kinase dexamethasone ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Src protein is essential for the regulation of bone turnover primarily via bone resorption because it is required in osteoclast differentiation and function. We followed temporal changes of Src protein abundance in marrow stromal cells induced to mineralize by dexamethasone (DEX), growth in cold temperature, or both. Given the tyrosine kinase function of Src and its numerous substrates, profiles of phosphotyrosine-containing proteins were followed as well. On day 11 of stimulation, specific alkaline phosphatase (ALP) activity at 30°C decreased under DEX relative to 37°C cultures, in accord with increased cell counts. Mineralization per well under DEX increased by 25% at 37°C, whereas at 30°C it increased by more than threefold regardless of the DEX stimulation. At 30°C, on a per cell basis mineralization increased 2.5 and 3 times with and without DEX, respectively. Cultures at 37°C showed a general drop per cell of many phosphotyrosine-containing proteins on day 3 relative to days 1 and 2 in both DEX-stimulated and nonstimulated cultures; several proteins did recover (recuperate) thereafter. On days 1 and 2, the phosphotyrosine signal was higher in several proteins under DEX stimulation; this trend became inverted after day 3. The changes in abundance per cell of Src protein (pp60src) followed a similar trend, and in addition a truncated Src molecule, p54/52src, was detected as a putative cleavage product presumably representing its carboxy terminus. The pp60src was most abundant, relative to its truncated product, in day 7 nonstimulated cultures, whereas under DEX stimulation the truncated species pp54/52src showed the highest relative abundance on days 7. At 30°C, DEX stimulation accentuated the increase in Src protein on day 3, showed no change on day 7, and returned to increase Src protein on day 10. Potassium ionophorvalinomycin, considered to select against mineralizing osteoprogenitors at 30°C, showed on day 10 in the absence of DEX a relative increase in truncated Src protein compared to both DEX-stimulated and nonstimulated cultures in the absence of valinomycin. On day 7 of DEX stimulation, the presence of valinomycin resulted in low p54/52src. Among phosphotyrosine-containing proteins, a 32-34 kDa band, as yet unidentified, showed the most concordant changes with mineralization induction. P32-34 decreased by DEX on days 2 and 8 and increased by low temperature alone or combined with DEX on day 3. On day 7, p32-34 did not change under DEX, but valinomycin selected cells with less phoshpotyrosine-containing p32-34. Taken together, high Src abundance at the start of osteogenic induction followed by a decrease 1 week later is probably related to energy metabolism-dependent induction of mineralization. This is in temporal accord with the increase in Src truncation and fluctuation in mitochondrial membrane potential (which affects mineralization). The reported binding of amino-terminal Src oligopeptide to p32 ADP/ATP carrier in the mitochondrial inner membrane raises the question of its possible involvement in mitochondria-regulated mineralization. J. Cell. Biochem. 69:316-325, 1998. © 1998 Wiley-Liss, Inc.
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    CBFa(AML/PEBP2)-related elements in the TGF-β type I receptor promoter and expression with osteoblast differentiation (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 353-363 
    Details
    ISSN: 0730-2312
    Keywords: AML/CBF/PEBP2 ; CBFa1 ; differentiation ; osteoblasts ; regulatory elements ; transforming growth factor-β ; receptor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Organization of the transforming growth factor-β (TGF-β) type I receptor (TRI) promoter predicts constitutive transcription, although its activity increases with differentiation status in cultured osteoblasts. Several sequences in the rat TRI promoter comprise cis-acting elements for CBFa (AML/PEBP2α) transcription factors. By gel mobility shift and immunological analyses, a principal osteoblast-derived nuclear factor that binds to these sites is CBFa1(AML-3/PEBP2αA). Rat CBFa1 levels parallel expression of the osteoblast phenotype and increase under conditions that promote mineralized bone nodule formation in vitro. Fusion of CBFa binding sequence from the TRI promoter to enhancer-free transfection vector increases reporter gene expression in cells that possess abundant CBFa1, and overexpression of CBFa increase the activity of transfected native TRI promoter/reporter plasmid. Consequently, phenotype-restricted use of cis-acting elements for CBFa transcription factors can contribute to the high levels of TRI that parallel osteoblast differentiation and to the potent effects of TGF-β on osteoblast function. J. Cell. Biochem. 69:353-363. © 1998 Wiley-Liss, Inc.
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    Multivalent cations depress ligand affinity of insulin-like growth factor-binding proteins-3 and -5 on human GM-10 fibroblast cell surfaces (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 364-375 
    Details
    ISSN: 0730-2312
    Keywords: IGF ; IGFBP ; zinc ; IGFBP-3 ; IGFBP-5 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The effect of multivalent cations on [125I]-IGF binding to cell-associated IGFBPs was investigated using human fibroblasts. The major cell-associated binding site for [125I]-IGF-I is IGFBP-3 and for [125I]-IGF-II are IGFBP-3 and IGFBP-5. Lanthanum and chromium did not affect either [125I]-IGF-I or [125I]-IGF-II binding to cell-associated IGFBPs. By contrast, zinc (Zn2+), gold (Au3+), and cadmium (Cd2+) depressed binding of both ligands. Ligand binding resulted in nonlinear Scatchard plots. Assuming a pre-existent asymmetric model with high- (KaHi) and low- (KaLo) affinity sites, Zn2+ lowered both KaHi and KaLo. Au3+ eliminated KaHi. Assuming that the nonlinear plots were caused by ligand-induced negative cooperativity, Zn2+ and Cd2+ lowered both Ke and Kf (affinity of unoccupied and saturated IGFBPs, respectively). Au3+ eliminated Ke and reduced Kf. Zn2+ was active at serum levels in lowering IGF binding. Zinc, gold, and cadmium bind to similar regions within proteins (a zinc-binding motif) indicating similar mechanisms of action. A zinc-binding motif is present in the IGFBPs, but not in the IGFs. We demonstrate for the first time that the trace nutrient zinc and related multivalent cations decrease IGF binding to fibroblast-associated IGFBPs by lowering the affinity of the IGF-IGFBP interaction. J. Cell. Biochem. 69:364-375, 1998. © 1998 Wiley-Liss, Inc.
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    Arrest of the cell cycle reduces susceptibility of target cells to perforin-mediated lysis (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 425-435 
    Details
    ISSN: 0730-2312
    Keywords: perforin ; cell cycle ; apoptosis ; T lymphocyte ; DNA synthesis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cytotoxic T lymphocytes secrete a pore-forming cytolysin, perforin, that damages membranes of target cells. They also ligate Fas receptors on target cells and provoke apoptotic death. A20 (B lymphoma) and P815 (mastocytoma) cell lines were examined for their susceptibility to perforin-mediated lysis and to Fas-induced apoptosis after blockade of the cell cycle at the G1/S interface. Cells were arrested at the G1/S interface by inhibition of DNA synthesis with thymidine or aphidicolin. Subsequently, the treated cells were incubated either with CTL cytotoxic granules or the Fas-specific monoclonal antibody Jo-2. We show that arrest of the cell cycle at the G1/S interface markedly reduced the susceptibility of target cells to perforin-mediated lysis. In contrast, growth arrest with thymidine or aphidicolin increased susceptibility of A20 and P815 cells to Fas-mediated apoptosis. Susceptibility to lysis by intact CTLs was not affected significantly by blockade of target cells with aphidicolin or thymidine. When cells surviving exposure to perforin-containing granules were isolated on Ficoll density gradients and cell-cycle profiles were examined by flow cytometry, the ratio of G1 to G2cells increased among the survivors exposed to granules in contrast to controls incubated with buffer alone. The data suggest that cells in G1 phase of the cell cycle are less susceptible to the perforin pathway than cells in G2and S phases but are more susceptible to the Fas pathway. J. Cell. Biochem. 69:425-435, 1998. © 1998 Wiley-Liss, Inc.
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    Purification of guinea pig YKl40 and modulation of its secretion by cultured articular chondrocytes (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 414-424 
    Details
    ISSN: 0730-2312
    Keywords: YKL40 ; purification ; guinea pig ; chondrocytes ; biochemical characterization ; regulation ; insulin-like growth factors ; osteoarthritis ; 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 study was to purify, characterize, and study the regulation at the chondrocyte level of the guinea pig (gp) homologue of human (R) YKL40, a putative marker of arthritic disorders. Studying YKL40 in guinea pigs is of particular interest, as age-related osteoarthritis develops in this species spontaneously. Both N-terminal sequencing and total amino acid composition of gpYKL40 purified from the secretion medium of cultured articular chondrocytes indicate a high degree of identity with hYKL40. gpYKL40 was found to contain complex N-linked carbohydrate, as demonstrated by N-glycosidase F and endoglycosidase F digestion. Isoelectric focusing demonstrated the presence of a major band at pI 6.7. The secretion of gpYKL40 by confluent articular chondrocytes in the extracellular medium was studied by immunoblotting. gpYKL40 was released by chondrocytes continuously over a 7 day period and did not appear to be degraded by proteinases, as its signal intensity in cell-free medium at 37°C did not decrease with time. Thus, gpYKL40 displays high stability and accumulates in extracellular medium without reaching a steady-state level. Among the main factors known to regulate cartilage metabolism, IL-1β, TNF-α, bFGF, or 1,25(OH)2D3 did not alter the basal level of gpYKL40, and retinoic acid had a slight inhibitory effect; TGF-β and IGF-I and -II dose-dependently and inversely modulated this basal level. TGF-β at 5 ng/ml decreased extracellular gpYKL40 2.9-fold, whereas IGF-I and IGF-II at 50 ng/ml increased extracellular gpYKL40 3.6- and 3.4-fold, respectively. The present biochemical and biological findings give new insights for studying the function of YKL40 in cartilage. J. Cell Biochem. 69:414-424, 1998. © 1998 Wiley-Liss, Inc.
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    Upregulation of P-glycoprotein in rat hepatoma ρ° cells: Implications for drug-DNA interactions (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 463-469 
    Details
    ISSN: 0730-2312
    Keywords: Adriamycin ; rat hepatoma ; ρ° cells ; multidrug resistance ; P-glycoprotein ; Sandoz SDZ PSC 833 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Rat hepatoma cells lacking mitochondrial DNA (ρ° cells) were used as a model system to examine the possible roles of mitochondrial DNA as a target for the DNA-acting anticancer drug Adriamycin (doxorubicin). The ρ° cells were 45-fold less sensitive to Adriamycin than the parental ρ+ cells containing mitochondrial DNA. Other non-DNA-acting drugs also exhibited similar behaviour, and this was shown to be due to a multidrug resistance (MDR) phenotype in the ρ° cells. This was indicated by confocal microscopy where ρ+ cells exhibited thirteenfold higher cellular levels of Adriamycin than ρ° cells. Upregulation (tenfold) of P-glycoprotein in ρ° cells was also confirmed by Northern dot blot analysis. Since the MDR phenotype is present in ρ° cells and upregulation of P-glycoprotein is maintained in these cells, ρ° cells are not a good model system for drug-DNA studies (where the drug is susceptible to extrusion by P-glycoprotein), and any such results obtained with this system must be treated with considerable caution. J. Cell. Biochem. 69:463-469, 1998. © 1998 Wiley-Liss, Inc.
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    1α,25(OH)2-Vitamin D3 signaling in chick enterocytes: Enhancement of tyrosine phosphorylation and rapid stimulation of mitogen-activated protein (MAP) kinase (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 470-482 
    Details
    ISSN: 0730-2312
    Keywords: enterocytes ; 1,25(OH)2-vitamin D3 ; tyrosine phosphorylation ; MAP kinase activation ; VDRnuc ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The steroid hormone 1α,25(OH)2-vitamin D3 (1α,25(OH)2D3) generates biological responses in intestinal and other cells via both genomic and rapid, nongenomic signal transduction pathways. We examined the hypothesis that 1α,25(OH)2D3 action in chick enterocytes may be linked to pathways involving tyrosine phosphorylation. Brief exposure of isolated chick enterocytes to 1α,25(OH)2D3 demonstrated increased tyrosine phosphorylation of several cellular proteins (antiphosphotyrosine immunoblots of whole cell lysates) with prominent bands at 42-44, 55-60, and 105-120 Kda. The 42-44 Kda bands comigrated with mitogen-activated protein (MAP) kinase (immunoblotting with anti-MAP kinase antibody) The response occurred within 30 s, peaked at 1 min, and was dose-dependent (0.01-10 nM), with maximal stimulation at 1 nM (three- to fivefold). This effect was specific for 1α,25(OH)2D3 since its metabolic precursors 25(OH)D3and vitamin D3 did not increase MAP kinase tyrosine phosphorylation. The tyrosine kinase inhibitor, genistein, blocked 1α,25(OH)2D3-induced tyrosine phosphorylation of MAP kinase, while staurosporine, a PKC inhibitor, attenuated the hormone's effects by 30%. We have evaluated the ability of 1α,25(OH)2D3 analogs, which have complete flexibility around the 6,7 carbon-carbon bond (6F) or which are locked in either the 6-s-cis (6C) or the 6-s-trans(6T) shape(s), to activate MAP kinase. Thus, two 6F and one 6C analog stimulated while one 6T analog did not stimulate MAP kinase tyrosine phosphorylation. In addition, 1β,25(OH)2D3, a known antagonist of 1α,25(OH)2D3-mediated rapid responses, blocked the hormone effects on MAP kinase. We conclude that 1α,25(OH)2D3 and analogs which can achieve the 6-s-cis shape (6F and 6C) can increase tyrosine phosphorylation and activation of MAP kinase in chick enterocytes. J. Cell. Biochem. 69:470-482, 1998. © 1998 Wiley-Liss, Inc.
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    Nucleolar targeting of 5S RNA in Xenopus laevis oocytes: Somatic-type nucleotide substitutions enhance nucleolar localization (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 490-505 
    Details
    ISSN: 0730-2312
    Keywords: nucleolus ; nuclear import ; ribosomal protein L5 ; ribonucleoprotein particles ; ribosome assembly ; TFIIIA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In Xenopus laevis oocytes, 5S RNA is stored in the cytoplasm until vitellogenesis, at which time it is imported into the nucleus and targeted to nucleoli for ribosome assembly. This article shows that throughout oogenesis there is a pool of nuclear 5S RNA which is not nucleolar-associated. This distribution reflects that of oocyte-type 5S RNA, which is the major 5S RNA species in oocytes; only small amounts of somatic-type, which differs by six nucleotides, are synthesized. Indeed, 32P-labeled oocyte-type 5S RNA showed a degree of nucleolar localization similar to endogenous 5S RNA (33%) after microinjection. In contrast, 32P-labeled somatic-type 5S RNA showed significantly enhanced localization, whereby 70% of nuclear RNA was associated with nucleoli. A chimeric RNA molecule containing only one somatic-specific nucleotide substitution also showed enhanced localization, in addition to other somatic-specific phenotypes, including enhanced nuclear import and ribosome incorporation. The distribution of 35S-labeled ribosomal protein L5 was similar to that of oocyte-type 5S RNA, even when preassembled with somatic-type 5S RNA. The distribution of a series of 5S RNA mutants was also analyzed. These mutants showed various degrees of localization, suggesting that the efficiency of nucleolar targeting can be influenced by many discrete regions of the 5S RNA molecule. J. Cell. Biochem. 69:490-505, 1998. © 1998 Wiley-Liss, Inc.
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    Cell cycle: Molecular targets for diagnosis and therapy: Tumor suppressor genes and cell cycle progression in cancerThis symposium was held on November 7-8, 1997, at the Roswell Park Cancer Institute, Buffalo, New York. (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 1-7 
    Details
    ISSN: 0730-2312
    Keywords: apoptosis ; p53 ; pRb2/p130 ; E2F ; transcriptional control ; leukemia ; protein phosphatases ; colon cancer ; retinoblastoma ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A significant portion of published literature is dedicated to describing the cloning and the characterization of proteins involved in the progression of the cell cycle, which govern cell growth both in cancer and normal ontogenesis. With this abundance of information, the cascading pathways of molecular events that occur in the cell cycle are proving to be exceedingly complicated. The purpose of this conference was to attract the leading clinical and basic science investigators in the growth control field with a final goal to determine how this current wealth of knowledge can be used to impact upon patient care and management by the design of novel adjuvant therapeutics specifically targeted at tumor cells and the identification of molecular diagnostic and/or prognostic markers in an efficient and cost effective manner. J. Cell. Biochem. 70:1-7, 1998. © 1998 Wiley-Liss, Inc.
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    Msh homeobox genes regulate cadherin-mediated cell adhesion and cell-cell sorting (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 22-28 
    Details
    ISSN: 0730-2312
    Keywords: Msx-1 ; Msx-2 ; homeobox ; adhesion ; sorting ; cadherin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Msx-1 and Msx-2 are two closely related homeobox genes expressed in cephalic neural crest tooth buds, the optic cup endocardial cushions, and the developing limb [Hill and Davidson, 1991; Monaghan et al., 1991; Robert et al., 1991]. These sites correspond to regions of active cell segregation and proliferation under the influence of epithelial-mesenchymal cell interactions [Brown et al., 1993; Davidson et al., 1991], suggesting that Msx-1 and Msx-2 regulate cell-cell interactions. We have investigated the potential relationship between expression of the Msh homeobox genes (Msx-1 and Msx-2) and cadherin-mediated cell adhesion and cell sorting. We report that cell lines stably expressing Msx-1 or Msx-2 differentially sort on the basis of Msh gene expression. We demonstrate in vitro that initial cell aggregation involves calcium-dependent adhesion molecules (cadherins) and that Msh genes regulate cadherin-mediated adhesion. These results support the hypothesis that Msh genes play a role in the regulation of cell-cell adhesion and provide a link between the genetic phenomena of homeobox gene expression and cellular events involved in morphogenesis, including cell sorting and proliferation. J. Cell. Biochem. 70:22-28, 1998. © 1998 Wiley-Liss, Inc.
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    Downregulation and subcellular redistribution of the γ-aminobutyric acidA receptor induced by tunicamycin in cultured brain neurons (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 38-48 
    Details
    ISSN: 0730-2312
    Keywords: GABAA receptor ; N-glycosylation ; radioligand binding ; in situ trypsinization ; galactosylation ; mannosylation ; immunoblotting ; immunocytochemistry ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The significance of N-linked glycosylation and oligosaccharide processing was examined for the expression of γ-aminobutyric acidA receptor (GABAAR) in cultured neurons derived from chick embryo brains. Incubation of cultures with 5 μg/ml of tunicamycin for 24 h blocked the binding of 3H-flunitrazepam and 3H-muscimol, probes for the benzodiazepine and GABA sites on the receptor, by about 20% and 28%, respectively. The loss of ligand binding was due to a reduction in the number of binding sites with no significant changes in receptor affinity. Light microscopic immunocytochemistry also revealed that the treatment reduced approximately 13% of the intensity of GABAAR immunoreactivity in the neuronal somata. Furthermore, the fraction of intracellular receptors was decreased to 24% from 34% of control in the presence of the agent, as revealed by trypsinization of cells in situ followed by 3H-flunitrazepam binding. The molecular weight of the receptor subunit protein was lowered around 0.5 kDa after tunicamycin treatment, in accordance with that following N-glycosidase F digestion, indicating the blockade of N-linked glycosylation of GABAAR by tunicamycin. Moreover, intense inhibitions of 91% and 44%, respectively, were detected to the general galactosylation and mannosylation in the tunicamycin-treated cells, whereas the protein synthesis was hindered by 13%, through assaying the incorporation of 3H-sugars and 3H-leucine. Nevertheless, treatment with castanospermine or swainsonine (10 μg/ml, 24 h), inhibitors to maturation of oligosaccharides, failed to produce significant changes in the ligand binding. In addition, in situ hybridization analysis showed that these three inhibitors did not perturb the mRNA of GABAAR α1-subunit. The data suggest that tunicamycin causes the downregulation and subcellular redistribution of GABAAR by producing irregularly glycosylated receptors and modifying their localization. Both galactosylation and mannosylation during the process of N-linked glycosylation may be important for the functional expression and intracellular transport of GABAAR. J. Cell. Biochem. 70:38-48, 1998. © 1998 Wiley-Liss, Inc.
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    Early alterations of actin cytoskeleton in OK cells by opioids (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 60-69 
    Details
    ISSN: 0730-2312
    Keywords: opossum kidney cells ; opioid receptors ; actin ; microfilament reorganization ; cell proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Recently we identified and characterized opioid binding sites in OK (opossum kidney) cells and observed decreased proliferation of these cells in response to opioids. In the present study we investigated the effects of opioids on the actin cytoskeleton and explored whether their antiproliferative action may relate to alterations in the distribution or the dynamics of actin microfilaments. Exposure of OK cells to the opioids αS1 casomorphin and ethylketocyclazocine resulted in a rapid and substantial actin microfilament reorganization. This was documented by a significant dose-dependent decrease in the amounts of F-actin, determined by measurements of quantitative fluorescence, by immunoblot analysis and by a concomitant increase of the G/total-actin ratio measured by the DNase I inhibition assay. These changes were verified by confocal laser scanning microscopy, which showed marked redistribution of the microfilamentous structures in the presence of the opioids without affecting the organization of microtubules or vimentin intermediate filaments. The effect of opioids on actin polymerization dynamics occurred within 15 min and persisted for at least 2 h, while their restoration to control levels was accomplished 6 h later, indicating a reversible phenomenon. Northern blot analysis showed that the concentration of the actin transcript was unaffected. The addition of diprenorphine, a general opioid antagonist, prevented the effects of opioids on the actin cytoskeleton. The inhibition of OK cell proliferation, induced by ethylketocyclazocine and αS1 casomorphin was partially prevented in the presence of phallacidin, which stabilizes microfilaments. Our findings demonstrate that opioids, acting via kappa 1 binding sites, induce rapidly modifications in the dynamics of actin polymerization, and in the organization of microfilaments in OK cells, which may relate to their antiproliferative effect on these cells. J. Cell. Biochem. 70:60-69, 1998. © 1998 Wiley-Liss, Inc.
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    Estrogen stimulates PTHrP but not PTH/PTHrP receptor gene expression in the kidney of ovariectomized rat (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 84-93 
    Details
    ISSN: 0730-2312
    Keywords: PTHrP ; PTH/PTHrP receptor ; estrogen ; ovariectomy ; kidney ; rat ; in vivo ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The aim of the present study was to test the hypothesis that the decreased renal tubular reabsorption of calcium observed in estrogen deficiency is associated with a local regulation of either PTHrP or PTH/PTHrP receptor genes in the kidney. Rats were randomly sham-operated (S) or ovariectomized receiving either vehicule (OVX) or 4 μg E2/kg/day (OVX+E4) or 40 μg E2/kg/d (OVX+E40) during 14 days using alzet minipumps. Plasma PTH and calcium levels were lower in untreated OVX animals than in all other groups (P 〈 0.01). Plasma PTH was higher in OVX+E40 than in OVX+E4 (P 〈 0.05). PTHrP mRNA expression in the kidney was unaffected by ovariectomy but was increased in OVX+E40 (0.984 ± 0.452 for PTHrP/GAPDH mRNAs expression vs. 0.213 ± 0.078 in sham, P 〈 0.01). PTH/PTHrP receptor mRNA expression and the cAMP response of renal membranes to PTH were unaffected by ovariectomy and estrogen substitution. In conclusion, renal PTHrP and PTH/PTHrP receptor mRNAs are not modified by ovariectomy. However, 17β-estradiol increases renal expression of PTHrP mRNA without evident changes in its receptor expression and function. This may help to explain the pharmacological action of estrogen in the kidney, especially how it prevents the renal leak of calcium in postmenopausal women. J. Cell. Biochem. 70:84-93, 1998. © 1998 Wiley-Liss, Inc.
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    Characterization of naturally occurring myosin heavy chain antisense mRNA in rat heart (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 110-120 
    Details
    ISSN: 0730-2312
    Keywords: myosin heavy chains ; rat heart ; naturally occurring antisense mRNA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Analysis of mRNA by Northern blot and reverse transcription-polymerase chain reaction demonstrated the expression of sense and considerable amounts of naturally occurring antisense mRNA for β-myosin heavy chain (MHC) and α-MHC in the neonatal rat heart: antisense MHC mRNA expression of α-MHC and β-MHC was approximately half of the corresponding sense MHC mRNA expression. Using a computational approach, we could identify a reverse Pol II promoter in the β-MHC gene. Both sense and antisense MHC mRNA demonstrated similar sizes of approximately 6,000 bp in the Northern blot. Alpha-MHC antisense mRNA consisted of approximately 3,700 bp of complementary exon sequences and β-MHC consisted of approximately 2,700 bp, suggesting a higher probability of α-MHC mRNA dimerization. Hence, sense mRNA transcripts and protein of α-MHC should exist at different relative levels in the neonatal state. In fact, the relative proportion of α-MHC was 52.0 ± 2.6% on the sense mRNA but only 36.3 ± 1.8% on the protein level. Because of its high abundance in the heart, we suggest that in the neonatal heart naturally occurring antisense mRNA may play a role in the regulation of MHC expression and, therefore, in the control of the energetical and contractile behaviour of the heart. J. Cell. Biochem. 70:110-120, 1998. © 1998 Wiley-Liss, Inc.
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    Interrelationships of nuclear architecture with gene expression: Functional encounters on a long and winding road (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 157-158 
    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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    Regulation of endothelial cell myosin light chain phosphorylation and permeability by vanadate (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 141-155 
    Details
    ISSN: 0730-2312
    Keywords: endothelial cell ; tyrosine phosphatase ; vanadate ; permeability ; MLCK ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The involvement of tyrosine protein phosphorylation in the regulation of endothelial cell (EC) contraction and barrier function is poorly understood. We have previously shown that myosin light chain (MLC) phosphorylation catalyzed by a novel 214 kDa EC myosin light chain kinase (MLCK) isoform is a key event in EC contraction and barrier dysfunction [Garcia et al. (1995): J Cell Physiol 163:510-522; Garcia et al. (1997): Am J Respir Cell Mol Biol 16:487-491]. In this study, we tested the hypothesis that tyrosine phosphatases participate in the regulation of EC contraction and barrier function via modulation of MLCK activity. The tyrosine phosphatase inhibitor, sodium orthovanadate (vanadate), significantly decreased electrical resistance across bovine EC monolayers and increased albumin permeability consistent with EC barrier impairment. Vanadate significantly increased EC MLC phosphorylation in a time-dependent manner (maximal increase observed at 10 min) and augmented both the MLC phosphorylation and permeability responses produced by thrombin, an agonist which rapidly increases tyrosine kinase activities. The vanadate-mediated increase in MLC phosphorylation was not associated with alterations in either phosphorylase A Ser/Thr phosphatase activities or in cytosolic [Ca2+] but was strongly associated with significant increases in EC MLCK phosphotyrosine content. These data suggest that tyrosine phosphatase activities may participate in EC contractile and barrier responses via the regulation of the tyrosine phosphorylation status of EC MLCK. J. Cell. Biochem. 70:141-155, 1998. © 1998 Wiley-Liss, Inc.
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    Nuclear dreams: The malignant alteration of nuclear architecture (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 172-180 
    Details
    ISSN: 0730-2312
    Keywords: nuclear matrix ; nuclear structure ; cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cancer is diagnosed by examining the architectural alterations to cells and tissues. Changes in nuclear structure are among the most universal of these and include increases in nuclear size, deformities in nuclear shape, and changes in the internal organization of the nucleus. These may all reflect changes in the nuclear matrix, a non-chromatin nuclear scaffolding determining nuclear form, higher order chromatin folding, and the spatial organization of nucleic acid metabolism. Malignancy-induced changes in this structure may have profound effects on chromatin folding, on the fidelity of genome replication, and on gene expression. Elucidating the mechanisms and the biological consequences of nuclear changes will require the identification of the major structural molecules of the internal nuclear matrix and an understanding of their assembly into structural elements. If biochemical correlates to malignant alterations in nuclear structure can be identified then nuclear matrix proteins and, perhaps nuclear matrix-associated structural RNAs, may be an attractive set of diagnostic markers and therapeutic targets. J. Cell. Biochem. 70:172-180, 1998. © 1998 Wiley-Liss, Inc.
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    The nucleus: A target site for parathyroid hormone-related peptide (PTHrP) action (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 193-199 
    Details
    ISSN: 0730-2312
    Keywords: parathyroid hormone-related peptide ; nucleus ; nucleolus ; intracrine actions ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: It is becoming increasingly apparent that parathyroid hormone-related peptide (PTHrP) modulates cellular function in a dual mode of action: first, by binding and activating its cognate cell surface G-protein-coupled receptor and, second, by direct intracellular effects following translocation to the nucleus and/or nucleolus of the target cell. Little is presently known about the mechanisms and events that determine the timing and degree of PTHrP nuclear translocation or the role it may serve in normal or dysregulated cellular function. Clarifying the nuclear actions of PTHrP would add significantly to our present understanding of this protein as a signaling molecule during embryonic development and as an oncoprotein whose expression in many tumors correlates with increased tumor aggressiveness and propensity for metastasis. J. Cell. Biochem. 70:193-199, 1998. © 1998 Wiley-Liss, Inc.
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    Interrelationships of nuclear structure and transcriptional control: Functional consequences of being in the right place at the right time (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 200-212 
    Details
    ISSN: 0730-2312
    Keywords: gene expression ; AML/CBF transcription factors ; nuclear matrix ; cancer ; nuclear domains ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Functional interrelationships between components of nuclear architecture and control of gene expression are becoming increasingly evident. In this article we focus on the concept that association of genes and cognate transcription factors with the nuclear matrix may support the formation and/or activities of nuclear domains that facilitate transcriptional regulation. Several lines of evidence are consistent with the concept that association of transcription factors with the nuclear matrix may be obligatory for fidelity of gene expression and maximal transcriptional activity. The identification of specific regions of transcription factors that are responsible for intranuclear trafficking to nuclear matrix-associated sites that support transcription, reinforces the linkage of nuclear structure to regulation of genes. CBFA2/AML-1 and CBFA1/AML-3 provide paradigms for directing gene regulatory factors to RNA polymerase II containing foci within the nucleus. The implications of modifications in the intranuclear trafficking of transcription factors for developmental and tissue-specific control, as well as for aberrations in gene expression that are associated with cancer and neurological disorders, are addressed. J. Cell. Biochem. 70:200-212, 1998. © 1998 Wiley-Liss, Inc.
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    Inhibition of proliferation and induction of differentiation of osteoblastic cells by a novel 1,25-dihydroxyvitamin D3 analog with an extensively modified side chain (CB1093) (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 414-424 
    Details
    ISSN: 0730-2312
    Keywords: analog ; bone ; growth inhibition ; differentiation ; vitamin D ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: 1,25-Dihydroxyvitamin D3 (1,25D) is involved in the regulation of proliferation and differentiation of a variety of cell types including cancer cells. In recent years, numerous new vitamin D3 analogs have been developed in order to obtain favorable therapeutic properties. The effects of a new 20-epi analog, CB1093 (20-epi-22-ethoxy-23-yne-24a,26a,27a-trihomo-1α,25(OH)2D3), on the proliferation and differentiation of human MG-63 osteosarcoma cell line were compared here with those of the parent compound 1,25D. Proliferation of the MG-63 cells was inhibited similarly by 22%, 50% and 59% after treatment with 0.1 μM 1,25D or CB1093 for 48 h, 96 h, and 144 h, respectively. In transfection experiments, the compounds were equipotent in stimulating reporter gene activity under the control of human osteocalcin gene promoter. In cell culture experiments, however, CB1093 was more potent than 1,25D at low concentrations and more effective for a longer period of time in activating the osteocalcin gene expression at mRNA and protein levels. Also, a 6-h pretreatment and subsequent culture for up to 120 h without 1,25D or CB1093 yielded higher osteocalcin mRNA and protein levels with analog-treated cells than with 1,25D-treated cells. The electrophoretic mobility shift assay (EMSA) revealed stronger VDR-VDRE binding with analog-treated MG-63 cells than with 1,25D-treated cells. The differences in the DNA binding of 1,25D-bound vs. analog-bound VDR, however, largely disappeared when the binding reactions were performed with recombinant hVDR and hRXRβ proteins. These results demonstrate that the new analog CB1093 was equally or even more effective than 1,25D in regulating all human osteosarcoma cell functions ranging from growth inhibition to marker gene expression and that the differences in effectivity most probably resulted from interactions of the hVDR:hRXRβ-complex with additional nuclear proteins. J. Cell. Biochem. 70:414-424, 1998. © 1998 Wiley-Liss, Inc.
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    Translocation and activation of AKT2 in response to stimulation by insulin (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 433-441 
    Details
    ISSN: 0730-2312
    Keywords: AKT2 ; serine-threonine kinase ; oncogene ; insulin ; phosphatidylinositol 3-kinase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The AKT2 oncogene encodes a protein-serine/threonine kinase that was recently shown to be activated by a variety of growth factors. In addition, we previously showed that AKT2 is abundant in brown fat and skeletal muscle, tissues that are highly insulin responsive and that play a role in glucose metabolism. In this study, we demonstrate that AKT2 is activated in response to stimulation by insulin in a dose- and time-dependent manner in human ovarian carcinoma cells and that activation of AKT2 is abolished in cells pretreated with wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI 3-kinase). Activation of AKT2 is manifested by changes in its phosphorylation state. Immunofluorescence experiments demonstrate that AKT2 is translocated to the plasma membrane after insulin stimulation, and this translocation is abolished by wortmannin. Both wild-type AKT2 activated by insulin and constitutively active AKT2, which has been targeted to the membrane by the addition of a myristoylation signal, were found to inactivate glycogen synthase kinase-3 (GSK-3) in vitro. GSK-3 was not inactivated by a catalytically inactive AKT2 mutant. Collectively, these data indicate that activation of AKT2 by insulin is mediated by PI 3-kinase and that GSK-3 is a downstream target of AKT2, suggesting a potentially important role of AKT2 in glycogen synthesis and other GSK-3 signaling pathways. J. Cell. Biochem. 70:433-441, 1998. © 1998 Wiley-Liss, Inc.
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    NGF induces transient but not sustained activation of ERK in PC12 mutant cells incapable of differentiating (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 425-432 
    Details
    ISSN: 0730-2312
    Keywords: nerve growth factor ; tyrosine kinase receptors ; differentiation ; PC12 cells ; mitogen-activated protein kinase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Activation of receptor tyrosine kinases stimulates a diverse array of cellular responses such as proliferation and differentiation. The first events in the signal transduction pathways mediated by different receptor tyrosine kinases are similar and include activation of the mitogen-activated protein kinase (MAPK) pathway and the induction of immediate early genes. The precise signaling pathways leading to each of the cellular responses mediated by receptor tyrosine kinases are still unknown, although it has been proposed that sustained activation of the MAPK pathway by receptor tyrosine kinases such as the nerve growth factor (NGF) receptor TrkA is sufficient to induce differentiation in PC12 cells. In the present study we examined the effect of NGF on mutant PC12 cells that were derived spontaneously in our cultures. NGF induced normal activation of immediate early genes in these cells, whereas the activation of some delayed response genes, as well as neurite outgrowth, was impaired. Furthermore, activation of the NGF-induced extracellular signal-regulated kinase (ERK) in these cells was transient, not sustained. These results support the hypothesis that sustained activation of ERK plays an important role in activating the induction of delayed response genes. However, sustained ERK activation is not a mandatory condition for the promotion of all the features of differentiated PC12 cells, as NGF could induce transcription of the delayed response gene, transin, in PC12 mutant cells. Taken together, our results suggest that NGF induces differentiation of PC12 cells via several signaling pathways, an important one of which is the MAPK pathway. J. Cell. Biochem. 70:425-432, 1998. © 1998 Wiley-Liss, Inc.
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    Characterization of two distinct families of transcription factors that bind to the CCAAT box region of the human COL1A2 gene (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 455-467 
    Details
    ISSN: 0730-2312
    Keywords: collagen ; gene regulation ; DNA-binding proteins ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Both the mouse and human α2(I) procollagen promoters contain an inverted CCAAT box at -80, but only the human promoter contains an additional regulatory element, the collagen modulating element (CME), immediately downstream of the CCAAT box [Collins et al. (1997): Biochem J 322:199-206]. In this study, the transcription factors that bind to the G/CBE and CME within the human promoter were characterized in SVWI-38 and CT-1 nuclear extracts. Two distinct proteins bind to the CME, and both were identified as heat-labile factors that were sensitive to high ionic strengths and required Zn2+ for DNA-binding activity. These proteins had Stokes radii of 4.12 and 3.15 nm, sedimentation coefficients of 3.9 and 3.2 S and native molecular weights of 66 and 41 kDa, respectively. On the basis of biochemical and DNA-binding properties, the CME binding proteins are probably novel factors involved in the regulation of the human α2(I) procollagen gene. By contrast, the G/CBE binding proteins were more resistant to heat, ionic strength, and divalent metal ion chelators, demonstrating that the G/CBE and CME binding proteins had distinct DNA-binding properties. The above properties suggest that this factor is a member of the previously characterized family of CCAAT box-binding factors, CBF, NF-Y, CP-1 and α-CP1. Taken together, these physicochemical properties of the COL1A2 CCAAT box and CME-binding proteins demonstrated that they were distinct unrelated transcription factors. These results also suggest that there is a distinct difference in the DNA-binding activity between the equivalent region of the mouse and human α2(I) procollagen promoters. J. Cell. Biochem. 70:455-467, 1998. © 1998 Wiley-Liss, Inc.
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    Proteolytic cleavage and activation of PAK2 during UV irradiation-induced apoptosis in A431 cells (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 442-454 
    Details
    ISSN: 0730-2312
    Keywords: UV irradiation ; PAK2 ; apoptosis ; CPP32/caspase-3 ; A431 cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Exposure of mammalian cells to ultraviolet (UV) light elicits a cellular response and can also lead to apoptotic cell death. In this report, we show that a 36-kDa myelin basic protein (MBP) kinase detected by an in-gel kinase assay can be dramatically activated during the early stages of UV irradiation-triggered apoptosis of A431 cells. Immunoblot analysis revealed that this 36-kDa MBP kinase could be recognized by an antibody against the C-terminal regions of a family of p21Cdc42/Rac-activated kinases (PAKs). By using this antibody and a PAK2-specific antibody against the N-terminal region of PAK2 as studying tools, we further demonstrated that UV irradiation caused cleavage of PAK2 to generate a 36-kDa C-terminal catalytic fragment and a 30-kDa N-terminal fragment in A431 cells. The appearance of the 36-kDa C-terminal catalytic fragment of PAK2 matched exactly with the activation of the 36-kDa MBP kinase in A431 cells upon UV irradiation. In addition, UV irradiation also led to activation of CPP32/caspase-3, but not ICH-1L/caspase-2 and ICE/caspase-1, in A431 cells and the kinetics of activation of CPP32/caspase-3 appeared to correlate well with that of DNA fragmentation and of cleavage/activation of PAK2, respectively. Moreover, blockage of activation of CPP32/caspase-3 by pretreating the cells with two specific tetrapeptidic inhibitors for caspases (Ac-DEVD-cho and Ac-YVAD-cmk) could significantly attenuate the extent of cleavage/activation of PAK2 induced by UV irradiation. Collectively, the results demonstrate that cleavage and activation of PAK2 can be induced during the early stages of UV irradiation-triggered apoptosis and indicate the involvement of CPP32/caspase-3 in this process. J. Cell. Biochem. 70:442-454, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
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