Membrane protein kinase C activity rapidly increases in quiescent tsRSV-infected NRK cells upon reactivation of the mitogenic v-src protein kinase |
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Authors: | Jon P Durkin Balu Chakravarthy Roger Tremblay and James F Whitfield |
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Institution: | Cells Signal Group, Institute of Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada K1A 0R6 |
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Abstract: | The viral src protein kinase, pp60v-src, is a powerful intracellular mitogen which can initiate and maintain the proliferation of quiescent cells in the absence of any exogenous growth factors. In an attempt to understand how pp60v-src induces proliferation, we examined the early events in the G0 to G1 transition caused by the activation of a thermolabile v-src protein in quiescent, serum-starved tsRSV-transformed NRK cells. The reactivation of pp60v-src, in the presence of exogenous growth factors, triggered a rapid biphasic surge of membrane-associated protein kinase C (PKC) activity. Unlike TPA-stimulated PKC activity, the pp60v-src-induced increase in PKC was readily extracted from membranes by EGTA. The down-regulation of PKC activity in these quiescent cells by prolonged exposure to TPA strongly inhibited the ability of the reactivated v-src protein to stimulate DNA replication in serum-deficient medium, suggesting that PKC plays a role in the initial signal by which the viral enzyme induces the G0 to G1 transition in NRK cells. |
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Keywords: | v-src protein kinase C proliferation |
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