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Cell Growth & Differentiation, Vol 2, Issue 1 51-58, Copyright © 1991 by American Association of Cancer Research
ARTICLES |
DA Talmage, C Riney and TL Benjamin
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.
Expression of antisense c-src RNAs in rat and mouse fibroblasts had a dramatic effect on the function of polyoma virus middle T (mT). Antisense c-src RNA decreased the amount of mT:pp60c-src complexes in de novo virus-infected cells and prevented expression of the transformed phenotype in rat F111 cells. Expression of antisense c-src RNA in infected NIH3T3 cells also reduced the formation of mT:pp60c-src complexes but did not affect the ability of polyoma virus to carry out a productive infection. Further analysis of the effects of antisense c-src RNA in uninfected cells revealed that pp60c-src is required for cell growth. When pp60c-src synthesis was reduced, F111 cells stopped proliferating and showed decreased S6 phosphorylation in response to serum. However, F111 cells expressing reduced pp60c-src could be efficiently transformed by v-rasHa, even in the presence of low serum. Thus, pp60c-src appears to function as a component of a signal transduction pathway which regulates cell proliferation in response to serum.
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Y.-Y. Ho, R. J. Deckelbaum, Y. Chen, T. Vogel, and D. A. Talmage Apolipoprotein E Inhibits Serum-stimulated Cell Proliferation and Enhances Serum-independent Cell Proliferation J. Biol. Chem., November 9, 2001; 276(46): 43455 - 43462. [Abstract] [Full Text] [PDF] |
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