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  • 1
    Electronic Resource
    Electronic Resource
    The Inositol Lipids of Paramecium tetraurelia and Preliminary Characterizations of Phosphoinositide Kinase Activity in the Ciliary Membrane (1989)
    Oxford, UK : Blackwell Publishing Ltd
    The @journal of eukaryotic microbiology 36 (1989), S. 0 
    Details
    ISSN: 1550-7408
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Inositol glycerolipids make up less than 10% of total phospholipids of Paramecium tetraurelia cells. Unlike inositol lipids found in mammalian and other cell types, these lipids from Paramecium lack arachidonic acid. It was demonstrated that kinase and possibly phosphatase enzymes that interconvert phosphatidylinositol (PI), phosphatidylinositol phosphate (PI-P) and phosphati-dylinositol-bis-phosphate (PI-P2) exist in ciliary membranes of this ciliate. When exogenous soybean PI and [γ-32P]ATP were provided as substrates, isolated cilia preparations exhibited PI and PI-P kinase activities as demonstrated by the incorporation of radiolabel into PI-P and PI-P2. Kinase activity was activated by millimolar [Mg2+] and inhibited by millimolar [Ca2+]. Significant inhibition of kinase activity in the presence of unlabeled excess ATP suggested that ATP is the preferred phosphate donor for this reaction. Of 4 suborganellar fractions of isolated cilia, the membrane fraction had the greatest kinase activity indicating that the enzyme(s) is membrane-associated
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1550-7408.1989.tb01072.x
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  • 2
    Electronic Resource
    Electronic Resource
    Microtubule-dependent transport of secretory granules during stalk secretion in a peritrich ciliate (1982)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 2 (1982), S. 47-71 
    Details
    ISSN: 0886-1544
    Keywords: microtubules ; transport ; secretion ; peritrich ciliate ; directional turnover ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The role of microtubules in secretory granule translocation was studied during stalk secretion in the peritrich ciliate, Zoothamnium arbuscula. In each cell, the release of stalk-forming secretory materials is restricted to a specialized region of the cytoplasm, the scopula. Many of the membrane-bound secretory granules that dominate the scopular cytoplasm appear to be aligned along cortical microtubules that converge on the scopular surface. This arrangement is consistent with the hypothesis that microtubules transport granules relative to the sites of exocytosis. To establish the role of microtubules in stalk secretion, telotrochs were exposed to agents with different disruptive effects on microtubule function. Exocytosis itself is not prevented by these drugs, and granules positioned for secretion prior to treatment are released. Maytansine and isopropyl-n-phenyl carbamate (IPC) completely inhibit stalk elongation. In maytansine-treated cells, microtubules are absent from the scopular cytoplasm, and granules are absent from the scopular surface. Microtubules are present in IPC-treated cells, but the granules are misdirected to the cytoplasm lateral to the scopula where no secretory sites exist. Even though the rate of stalk secretion is decreased by deuterium oxide (D2O), a control length stalk is eventually produced. In D2O-treated cells microtubules are present and in their normal orientation. The inhibition of secretion when microtubules are absent (maytansine) or misdirected (IPC) and the retardation of secretion when microtubule turnover is reduced (D2O) supports a mechanism of granule transport based on the directional turnover of microtubule subunits.
    Additional Material: 17 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970020105
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  • 3
    Electronic Resource
    Electronic Resource
    Isolation of Thy-1 caps and analysis of their phospholipid composition in mouse T-lymphoma cells (1988)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 134 (1988), S. 67-77 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In this study we have used a density perturbation method to isolate anti-Thy-1 antibody-induced Thy-1 caps from mouse T-lymphoma cells in the absence of detergents, and then compared the phospholipid composit on of these capped membranes with that of uncapped membranes. Initial phospholipid analysis by two-dimensional thin layer chromatography (2-D TLC) reveals a significant increase in the amount of 32P-labeled phosphatidylcholine in the Thy-1 capped membrane. In contrast, no significant changes are observed in the labeling of phosphatidylserine, phosphatidylethanolamine, or the sphingomyelins. Therefore, it is suggested that phosphatidylcholine may be involved in the organization and/or regulation of Thy-1 antigen redistribution. The composition of phosphoinositide in uncapped and capped membranes was analysed separately using one-dimensional thin layer chromatography (1-D TLC) to resolve phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), and phosphatidylinositol 4, 5-bisphosphate (PIP2) from all other phospholipids. This analysis reveals a significant reduction in levels of PIP and PIP2, but not PI, in Thy-1 caps. Through the use of ion exchange column chromatography, we have found an increased production of all three species of inositol phosphates during anti-Thy-1 antibody-induced capping. Inositol 1, 4, 5 -triphosphate (IP3) shows the most significant increase, compared to the much smaller increases in inositol 4, 5-bisphosphate (IP2) and inositol monophosphate (IP). These results suggest that the binding of anti-Thy-1 antibody to Thy-1 antigen activates phospholipase C which, in turn, initiates polyphosphoinositide turnover and IP3 production. It is proposed that these observed effects are the result of early signal transducing events which are prerequisite steps in Thy-1 receptor cap formation.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041340108
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  • 4
    Electronic Resource
    Electronic Resource
    Endocytosis of mannose-6-phosphate binding sites by mouse T-lymphoma cells (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 127 (1986), S. 146-161 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The endocytosis and intracellular transport of mannose-6-phosphate conjugated to bovine serum albumin (Man-6-P:BSA) by mouse T-lymphoma cells were investigated in detail using several methods of analysis, both morphological and biochemical. Man-6-P:BSA was labeled with fluorescein or 125I and used to locate both surface and intracellular Man-6-P binding sites by light or electron microscopy, respectively. Incubation of cells with either fluorescent or 125I-labeled Man-6-P:BSA at 0°C revealed a uniform distribution of the Man-6-P binding sites over the cell surface. Competition experiments indicate that the Man-6-P:BSA binding sites on the cell surface are the same receptors that can recognize lysosomal hydrolases. After as little as 1 min incubation at 37°C, endocytosis of Man-6-P binding sites was clearly observed to occur through regions of the plasma membrane and via vesicles that also bound anticlathrin antibody. After a 5-15-min incubation of cells at 37°C, the internalized ligand was detected first in the cis region of the Golgi apparatus and then in the Golgi stacks using both autoradiography and immunocytochemistry to visualize the ligand. The appearance of Man-6-P:BSA in the Golgi region after 15-30 min was confirmed by subcellular fractionation, which demonstrated an accumulation of Man-6-P:BSA in light membrane fractions that corresponded with the Golgi fractions. After a 30-min incubation at 37°C, the internalized Man-6-P binding sites were localized primarily in lysosomal structures whose membrane but not lumen co-stained for acid phosphatase. These results demonstrate a temporal participation of clathrin-containing coated vesicles during the initial endocytosis of Man-6-P binding sites and that one step in the Man-6-P:BSA transport pathway between plasma membrane and the lysosomal structure can involve a transit through the Golgi stacks.
    Additional Material: 15 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041270118
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  • 5
    Electronic Resource
    Electronic Resource
    Thrombospondin mediates migration and potentiates platelet-derived growth factor-dependent migration of calf pulmonary artery smooth muscle cells (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 157 (1993), S. 24-32 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A precipitating factor in the development of atherosclerotic lesions is the inappropriate migration and proliferation of vascular smooth muscle cells (SMC) within the intima of the vessel wall. Focusing on the role of extracellular matrix proteins in SMC migration, we have demonstrated that thrombospondin (TSP) itself is a potent modulator of SMC motility and acts to potentiate platelet-derived growth factor (PDGF)-mediated SMC migration as well. Migration of SMC to TSP was dose dependent. Interestingly, maximal SMC migration to TSP exceeded that to either PDGF or basic fibroblast growth factor (bFGF). The distal COOH terminus of TSP was shown to mediate SMC migration as demonstrated by complete inhibition of the response by monoclonal antibody (mAb) C6.7. Nevertheless, proteolytic fragments of TSP were not as potent as intact TSP in mediating SMC migration. Only by combining the heparin-binding domain (HBD) with the 140 kD COOH terminal fragment was SMC migration restored to levels seen with intact TSP. Based on antibody inhibition studies, an αv-containing integrin receptor, but not αvβ1 or αvβ3, appeared to be involved in SMC migration to TSP. The coincidental expression of PDGF and TSP at sites of vascular injury and inflammation led us to evaluate the effect of suboptimal levels of TSP on SMC responsiveness to PDGF. SMC migration in response to PDGF was enhanced nearly 60% in the presence of suboptimal concentrations of TSP. This effect was specific for PDGF and dependent on the concentration of TSP with maximal potentiation obtained between 50-100 nM TSP, concentrations tenfold lower than those necessary for SMC migration to TSP itself. mAb C6.7 completely inhibited enhancement but, as with SMC migration to TSP alone, TSP proteolytic fragments did not possess the effectiveness of the intact molecule. Additional experiments assessing SMC migration to PDGF demonstrated that PDGF stimulated SMC motility indirectly by inducing TSP synthesis. These studies suggested that TSP functions as an autocrine motility factor to modulate SMC migration, which in conjunction with PDGF could serve to aggravate and accelerate development of atherosclerotic lesions at sites of vascular injury or inflammation. © 1993 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041570104
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