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  • 1
    ISSN: 1432-1335
    Keywords: Metastatic variants ; Membrane glycoproteins ; Lectins ; Hypoxanthine-guanine phosphoribosyltransferase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The isolation of deoxyguanosine-resistant 10T 1/2 mouse cell lines following stepwise selection in the presence of increasing concentrations of drug led to the identification of a highly metastatic line, as measured by the ability to form secondary tumors in syngenic mice after intravenous injection. This metastatic deoxyguanosine-resistant mutant was determined to be deficient in hypoxanthine-guanine phosphoribosyltransferase activity, accounting for the resistance to deoxyguanosine. Lectin-binding studies determined that the metastatic potential of high- and low-metastatic revertant clones of this deoxyguanosine-resistant mutant was negatively correlated to soybean agglutinin binding, but not to concanavalin A or wheat germ agglutinin binding. Examination of labelled cell-surface glycoproteins led to the identification of two glycoproteins, gp80 and gp48, which were present on the low-metastatic wild-type cell line but absent from the highly metastatic drug-resistant cells. Our studies suggest that these cell-surface glycoprotein alterations play a role in determining the malignant properties of the cells, and indicate that metastatic variants with the properties described in this report would be useful biological tools for investigations into the roles played by specific cell-surface structures in mechanisms of tumor progression.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 92 (1990), S. 137-146 
    ISSN: 1573-4919
    Keywords: myoblast ; glycoprotein ; cell fusion ; ketoconazole
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of ketoconazole on the fusion of L6 myoblasts was studied. Ketoconazole was a potent inhibitor of myoblast fusion at concentrations as low as 0.1 μM, but fusion was restored when the inhibitor was removed. The inhibitor resulted in decreased binding of conA and WGA to cell surface oligosaccharides showing that it was inhibiting N-linked cell surface glycoproteins. Inhibition of fusion by ketoconazole was accompanied by reduced creatine phosphokinase activities showing that it is affecting biochemical differentiation. Incorporation of labelled mannose from GDP-mannose into lipid-sugar and lipid-oligosaccharide complexes involved in the synthesis of N-linked oligosaccharides was also inhibited by ketoconazole, but the inhibition was reversed by addition of exogenous dolichol phosphate to the incorporation mixture. The main conclusion from these studies was that ketoconazole inhibited fusion of L6 myoblasts by affecting the synthesis of dolichol-phosphate required for the synthesis of lipid-oligosaccharides needed for the synthesis of fusogenic cell surface N-linked glycoproteins.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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