视网膜母细胞瘤家族蛋白对内源性E2F1稳定性的调控。
Regulation of endogenous E2F1 stability by the retinoblastoma family proteins.
作者信息
Martelli F, Livingston D M
机构信息
The Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
出版信息
Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):2858-63. doi: 10.1073/pnas.96.6.2858.
Abstract
Certain E2F transcription factor species play a pivotal role in regulating cell-cycle progression. The activity of E2F1, a protein with neoplastic transforming activity when unregulated, is tightly controlled at the transcriptional level during G0 exit. In addition, during this interval, the stability of endogenous E2F1 protein increased markedly. E2F1 stability also was dynamically regulated during myogenic differentiation and in response to gamma irradiation. One or more retinoblastoma family proteins likely participate in the stability process, because simian virus 40 T antigen disrupted E2F1 stability regulation during G1 exit in a manner dependent on its ability to bind to pocket proteins. Thus, endogenous E2F1 function is regulated by both transcriptional and posttranscriptional control mechanisms.
摘要
某些E2F转录因子在调节细胞周期进程中起关键作用。E2F1是一种在未受调控时具有肿瘤转化活性的蛋白质，其活性在G0期退出过程中在转录水平受到严格控制。此外，在此期间，内源性E2F1蛋白的稳定性显著增加。E2F1的稳定性在肌源性分化过程中以及对γ射线照射的反应中也受到动态调节。一种或多种视网膜母细胞瘤家族蛋白可能参与了稳定性过程，因为猿猴病毒40 T抗原以依赖于其与口袋蛋白结合能力的方式破坏了G1期退出过程中E2F1的稳定性调节。因此，内源性E2F1的功能受转录和转录后控制机制的调节。
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