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首页> 外文期刊>Molecular and Cellular Biology >A transforming ras gene can provide an essential function ordinarily supplied by an endogenous ras gene.
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A transforming ras gene can provide an essential function ordinarily supplied by an endogenous ras gene.

机译：转化ras基因可以提供通常由内源ras基因提供的基本功能。

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Microinjection of monoclonal antibody Y13-259, which reacts with all known mammalian and yeast ras-encoded proteins, has previously been shown to prevent NIH 3T3 cells from entering the S phase (L. S. Mulcahy, M. R. Smith, and D. W. Stacey, Nature [London] 313:241-243, 1985). We have now found several transformation-competent mutant v-rasH genes whose protein products in transformed NIH 3T3 cells are not immunoprecipitated by this monoclonal antibody. These mutant proteins are, however, precipitated by a different anti-ras antibody. Each of these mutants lacks Met-72 of v-rasH. In contrast to the result for cells transformed by wild-type v-rasH, Y13-259 microinjection of NIH 3T3 cells transformed by these mutant ras genes did not prevent the cells from entering the S phase. These results imply that a transformation-competent ras gene can supply a normal essential function for NIH 3T3 cells. When the proteins encoded by the mutant ras genes were overproduced in Escherichia coli, several mutant proteins that lacked Met-72 failed to bind Y13-259 in a Western blot. However, a ras protein from a mutant lacking amino antibody, but a ras protein from a mutant lacking amino acids 72 to 84 did not. These results suggest that Y13-259 may bind to a higher ordered structure that has been restored in the mutant lacking amino acids 72 to 82.
机译：显微注射单克隆抗体Y13-259可与所有已知的哺乳动物和酵母ras编码的蛋白发生反应，以前已被证明可以阻止NIH 3T3细胞进入S期（LS Mulcahy，MR Smith和DW Stacey，Nature [伦敦] 313：241-243，1985）。现在我们已经发现了几种具有转化能力的突变型v-rasH基因，这些基因的转化产物NIH 3T3细胞中的蛋白质产物不能被这种单克隆抗体免疫沉淀。但是，这些突变蛋白是由不同的抗ras抗体沉淀的。这些突变体均缺少v-rasH的Met-72。与野生型v-rasH转化的细胞的结果相反，这些突变ras基因转化的NIH 3T3细胞的Y13-259显微注射并未阻止细胞进入S期。这些结果表明，具有转化能力的ras基因可以为NIH 3T3细胞提供正常的基本功能。当在大肠杆菌中过量产生由突变ras基因编码的蛋白质时，一些缺少Met-72的突变蛋白质在Western blot中无法结合Y13-259。然而，来自缺乏氨基酸抗体的突变体的ras蛋白，但是缺乏缺乏氨基酸72至84的突变体的ras蛋白。这些结果表明，Y13-259可能与在缺少氨基酸72至82的突变体中已恢复的更高阶结构结合。

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