Simian virus 40 large T overcomes p300 repression of c-Myc.
Simian virus 40 large T overcomes p300 repression of c-Myc.
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猿猴病毒 40 大 T 克服了 p300 对 c-Myc 的抑制。
DOI：
10.1016/j.virol.2008.04.042
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发表时间：
2008
期刊：
影响因子：
3.7
通讯作者：
Thimmapaya,Bayar
中科院分区：
文献类型：
--
作者：
Singhal,Ghata;Kadeppagari,RaviKumar;Sankar,Natesan;Thimmapaya,Bayar
我们以前的研究表明，在静止期细胞中，p300/CBP通过使c-Myc保持在抑制状态来负调节细胞周期G1-S转换，并且腺病毒E1 A通过与p300/CBP结合来诱导c-Myc。研究表明，p300/CBP与猴病毒40大T的结合是间接的，并由p53介导。通过使用一系列的大T突变体，无法结合到各种细胞蛋白，包括p53以及细胞中的p300过表达或p53被敲低，我们表明，协会的大T与p300有助于诱导c-Myc和细胞周期。通过这种机制诱导c-Myc可能在大T介导的细胞周期诱导和细胞转化中是重要的。
We previously showed that in quiescent cells p300/CBP negatively regulates the cell cycle G1-S transition by keeping c-Myc in a repressed state and that adenovirus E1A induces c-Myc by binding to p300/CBP. Studies have shown that p300/CBP binding to simian virus 40 large T is indirect and mediated by p53. By using a series of large T mutants that fail to bind to various cellular proteins including p53 as well as cells where p300 is overexpressed or p53 is knocked down, we show that the association of large T with p300 contributes to the induction of c-Myc and the cell cycle. The induction of c-Myc by this mechanism is likely to be important in large T mediated cell cycle induction and cell transformation.