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首页> 外文期刊>Molecular and Cellular Biology >Functional role of GTPase-activating protein in cell transformation by pp60v-src.
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Functional role of GTPase-activating protein in cell transformation by pp60v-src.

机译：GTPase激活蛋白在pp60v-src细胞转化中的功能作用。

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Morphological transformation of NIH 3T3 cells was observed following coexpression of a portion of the ras GTPase-activating protein (GAP) comprising the amino terminus (GAP-N) and a mutant of v-src (MDSRC) lacking the membrane-localizing sequence. Cells expressing either of these genes alone remained nontransformed. Coexpression of GAP-N with MDSRC did not alter the subcellular localization, kinase activity, or pattern of cellular substrates phosphorylated by the MDSRC product. In contrast to SHC, phospholipase C-gamma 1, and the p85 alpha phosphatidylinositol 3'-kinase subunit, the endogenous GAP product (p120GAP) was highly tyrosine-phosphorylated only in cells transformed by wild-type v-src. Furthermore, for transformation induced by wild-type v-src as well as by coexpression of MDSRC and GAP-N, a strict correlation was observed between cell transformation, elevated tyrosine phosphorylation of p62, p190, and a novel protein of 150 kDa, and complex formation between these proteins and p120GAP. As with cells transformed by wild-type v-src, the MDSRC plus GAP-N transformants remained dependent on endogenous Ras. The results suggest that tyrosine phosphorylation and complex formation involving p120GAP represent critical elements of cell transformation by v-src and that complementation of the cytosolic v-src mutant by GAP-N results, at least in part, from the formation of these complexes.
机译：共表达包含氨基末端（GAP-N）和缺少膜定位序列的v-src突变体（MDSRC）的部分ras GTPase-活化蛋白（GAP）后，观察到NIH 3T3细胞的形态转化。仅表达这些基因之一的细胞保持未转化。 GAP-N与MDSRC的共表达不会改变MDSRC产物磷酸化的亚细胞定位，激酶活性或细胞底物的模式。与SHC，磷脂酶C-γ1和p85α磷脂酰肌醇3'-激酶亚基相反，内源性GAP产物（p120GAP）仅在野生型v-src转化的细胞中被酪氨酸磷酸化。此外，对于野生型v-src以及MDSRC和GAP-N的共表达所诱导的转化，在细胞转化，p62，p190酪氨酸磷酸化和150 kDa的新蛋白升高之间存在严格的相关性，并且这些蛋白质与p120GAP之间形成复杂的复合物。与野生型v-src转化的细胞一样，MDSRC加GAP-N转化子仍然依赖于内源性Ras。结果表明，酪氨酸磷酸化和涉及p120GAP的复合物形成是v-src转化细胞的关键因素，而GAP-N对胞质v-src突变体的互补至少部分是由这些复合物的形成引起的。

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