Proapoptotic Bid mediates the Atr-directed DNA damage response to replicative stress.
Proapoptotic Bid mediates the Atr-directed DNA damage response to replicative stress.
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DOI：
10.1038/cdd.2010.151
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发表时间：
2011-05
影响因子：
12.4
通讯作者：
中科院分区：
文献类型：
--
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Pro-apoptotic Bid, a BH3-only Bcl-2 family member, is situated at the interface between the DNA damage response and apoptosis, with roles in death receptor-induced apoptosis as well as cell cycle checkpoints following DNA damage. Here we demonstrate that Bid acts at the level of the sensor complex in the Atm and Rad3-related (Atr)-directed DNA damage response. Bid is found with Replication protein A (RPA) in nuclear foci and associates with the Atr/Atr-interacting protein (Atrip)/RPA complex following replicative stress. Furthermore, Bid-deficient cells demonstrate an impaired response to replicative stress manifest by reduced accumulation of Atr and Atrip on chromatin and at DNA damage foci, reduced recovery of DNA synthesis following replicative stress, and decreased Chk1 activation and RPA phosphorylation. These results establish a direct role for the BH3-only Bcl-2 family member, Bid, acting at the level of the damage sensor complex to amplify the Atr-directed cellular response to replicative DNA damage.
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