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Complementation by BCL2 and C-HA-RAS oncogenes in malignant transformation of rat embryo fibroblasts.

机译:BCL2和C-HA-RAS癌基因对大鼠胚胎成纤维细胞恶性转化的补充。

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The BCL2 (B cell lymphoma/leukemia-2) and C-HA-RAS oncogenes encode membrane-associated proteins of 26 and 21 kilodaltons, respectively. Although RAS proteins have long been known for their ability to bind and hydrolyze GTP, recent investigations suggest that BCL2 encodes a novel GTP-binding protein (S. Haldar, C. Beatty, Y. Tsujimoto, and C. M. Croce, Nature [London] 342:195-198, 1989). Cotransfection of BCL2 and HA-RAS oncogenes resulted in morphological transformation of early-passage rodent fibroblasts, rendering these cells tumorigenic in animals and enabling them to grow in semisolid medium. In contrast, cotransfection of BCL2 with oncogenes that encode nuclear proteins (E1A and C-MYC) did not produce malignant transformation, whereas HA-RAS did complement with these genes. These findings suggest that proteins encoded by oncogenes such as BCL2 and HA-RAS, although having similar subcellular locations and perhaps similar biochemical properties, can regulate distinct complementary pathways involved in cellular transformation.
机译:BCL2(B细胞淋巴瘤/白血病-2)和C-HA-RAS癌基因分别编码26和21千道尔顿的膜相关蛋白。尽管RAS蛋白具有结合GTP并水解GTP的能力,但近来的研究表明BCL2编码一种新的GTP结合蛋白(S. Haldar,C。Beatty,Y。Tsujimoto和CM Croce,Nature [London] 342 :195-198,1989)。 BCL2和HA-RAS癌基因的共转染导致了早期传代的啮齿动物成纤维细胞的形态转化,使这些细胞在动物体内具有致瘤性,并使它们能够在半固体培养基中生长。相反,BCL2与编码核蛋白(E1A和C-MYC)的癌基因共转染不会产生恶性转化,而HA-RAS确实能与这些基因互补。这些发现表明,由癌基因如BCL2和HA-RAS编码的蛋白质,尽管具有相似的亚细胞位置和可能相似的生化特性,但可以调节参与细胞转化的独特互补途径。

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