EFFECT OF NOCODAZOLE ON THE ACTIVATION OF TRANSCRIPTION FACTORS STATl AND STAT3 IN A431 CELLS
K. P. Vasilenko,1 E. B. Burova, N. A. Vinogradova, N. N. Nikolsky
Institute of Cytology RAS, St. Petersburg, Russia;
1 e-mail: shambala@mail.cytspb.rssi.ru
The STAT transcription factors (signal transducers and activators of transcription), STATl and STAT3, are involved in
signal transduction from growth factors and different cytokine receptors. STATl and STAT3 activation mechanisms are not sufficiently
investigated, but they are known to depend upon both cell type and stimulus for either of them. Recently, we have shown that nocodazole
blocked EGF-induced STATl transport to the nucleus. Here, we have compared STATl and STATS activation in response to IFNy, IFNa and
epidermal growth factor (EOF) in A431 cells. We have shown the STATl activation by all these agents; unlike, STAT3 was activated by EOF
only. STATl and STAT3 activation upon EOF is blocked by both nocodazole and Src-kinase family inhibitor. STATl activation upon IFNy
influence is blocked by nocodazole, but does not depend on-the activity of Src-family kinases. The increased STAT3 phosphorylation
results from a combined action of Src-kinase inhibitor and IFNy. IFNa-induced activation of STATl was not inhibited by either nocodazole
or Src-kinase inhibitor. Taken together, the data obtained suggest that the activation of both STATl and STAT3 in A431 cells is
accomplished by different mechanisms.
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