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Retroviral oncogenes and TOR.

机译:逆转录病毒致癌基因和TOR。

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摘要

Retroviruses have recruited the catalytic subunit of PI 3-kinase and its downstream target, Akt, as oncogenes. These viruses cause tumors in animals and induce oncogenic transformation in cell culture. The oncogenicity of these viruses is specifically inhibited by rapamycin; retroviruses carrying other oncogenes are insensitive to this macrolide antibiotic. Rapamycin is an inhibitor of the TOR (target of rapamycin) kinase whose downstream targets include p70 S6 kinase and the negative regulator of translation initiation 4E-BP. Emerging evidence suggests that the TOR signals transmitted to the translational machinery are essential for oncogenic transformation by the PI 3-kinase pathway.
机译:逆转录病毒已经募集了PI 3-激酶的催化亚基及其下游靶标Akt作为癌基因。这些病毒在动物中引起肿瘤,并在细胞培养中诱导致癌转化。这些病毒的致癌性受到雷帕霉素的特异性抑制。携带其他癌基因的逆转录病毒对这种大环内酯类抗生素不敏感。雷帕霉素是TOR(雷帕霉素的靶标)激酶的抑制剂,其下游靶标包括p70 S6激酶和翻译起始4E-BP的负调节剂。新兴证据表明,传递至翻译机制的TOR信号对于PI 3激酶途径致癌性转化至关重要。

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