作者: I. D. Horak , R. E. Gress , P. J. Lucas , E. M. Horak , T. A. Waldmann
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摘要: Addition of interleukin 2 (IL-2) to IL-2-dependent T cells results in tyrosine protein kinase signal transduction events even though the IL-2 receptor alpha and beta chains lack intrinsic enzymatic activity. Here we report that addition human transiently stimulates specific activity p56lck, a member src family nonreceptor kinases expressed at high levels lymphocytes. The ability induce p56lck activation was found be independent capacity associate with either CD4 or CD8. Following treatment, undergo serine/threonine phosphorylation modifications resulted altered mobility lck gene product on polyacrylamide gels. These observations raise possibility participates IL-2-mediated cells.