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BID as a double agent in cell life and death.

机译:BID是细胞生与死的双重作用。

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摘要

DNA damage leads to the activation of ATM and ATR, which in turn either cause cell cycle arrest and DNA repair or apoptosis. We have demonstrated that DNA damage leads to ATM-mediated BID phosphorylation, and that this phosphorylation regulates a novel, pro-survival function of BID important for S phase arrest. Thus, BID, a member from the core apoptotic regulatory machinery (BCL-2 family) receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death.
机译:DNA损伤导致ATM和ATR激活,进而引起细胞周期停滞和DNA修复或凋亡。我们已经证明DNA损伤导致ATM介导的BID磷酸化,并且这种磷酸化调节BID对S期停滞重要的新型生存功能。因此,BID是核心细胞凋亡调控机制(BCL-2家族)的成员,它从细胞周期阻滞/ DNA修复机制(ATM)的关键调控子接受直接输入,因此是协调遗传毒性应激反应和凋亡细胞死亡。

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