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  • 1
    Electronic Resource
    Electronic Resource
    Dexamethasone-induced adhesion in hepatoma cells: the role of plasminogen activator (1979)
    [s.l.] : Nature Publishing Group
    Nature 277 (1979), S. 312-313 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Fig. 1 Wild-type HTC cells were incubated overnight m radioactive medium containing 3% plasmmogen-depleted fetal calf serum in the presence () or absence (O) of 0 1 ,? dexamethasone, or in the same medium reconstituted with 4 8 jxg ml"1 plasminogen in the presence (A) or absence (?) of 0 1 ,? ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/277312a0
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Isolation of rat hepatoma cell variants selectively resistant to dexamethasone inhibition of plasminogen activator (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 99 (1979), S. 333-341 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Glucocorticoids induce several phenotypic changes in rat hepatoma cells in tissue culture, including the inhibition of plasminogen activator activity. Variant cell lines resistant to dexamethasone inhibtion of plasminogen activator activity have been isolated using an agar-fibrin overlay technique to identify colonies with fibrinolytic (plasminogen activator) activity. The variants are resistant to concentrations of dexamethasone 1,000 times that necessary to completely inhibit plasminogen activator activity in wild-type cells. The variant phenotype has been inherited in a stable manner for more than 300 generations in continuous culture in the absence of dexamethasone. These variants are unique in that the resistance is not secondary to defective or absent glucocorticoid receptors but is due to a lesion specific for regulation of plasminogen activator. Fluctuation analyses support the hypothesis that resistance to dexamethasone arises randomly and is not induced by dexamethasone. Because HTC cells are heteroploid and karyotypically highly variable, variants are thought to arise primarily by chromosomal segregation events. These variants provide a valuable tool for studying the mechanism of hormonal regulation of plasminogen activator as well as the role of proteases in hormonal regulation of membrane functions.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040990308
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  • 3
    Electronic Resource
    Electronic Resource
    Hormonal regulation of membrane phenotype (1977)
    New York, N.Y. : Wiley-Blackwell
    Journal of Supramolecular Structure 6 (1977), S. 325-331 
    Details
    ISSN: 0091-7419
    Keywords: plasminogen activator ; hepatoma cells ; transformed membrane phenotype ; glucocorticoid-resistant variants ; glucocorticoids ; amino acid transport ; hormonal regulation ; glucocorticoid regulation ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Incubation of rat hepatoma cells (HTC) in tissue culture with glucocorticoids alters several membrane properties characteristic of transformed cells, without affecting the growth rate of these cells. Variant cell lines resistant to dexamethasone inhibition of plasminogen activator production have been isolated using an agar-fibrin overlay technique to detect plasminogen activator production by individual colonies of HTC cells. The resistance to dexamethasone is not secondary to abnormal or absent glucocorticoid receptors, but due to a lesion in a later step in hormone action specific for plasminogen activator. These variants should prove useful for the study of the mechanism of steroid action as well as for the analysis of the role of proteases in the hormonal regulation of membrane function.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jss.400060305
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    Paper (German National Licenses)
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