期刊
CELL
卷 122, 期 4, 页码 579-591出版社
CELL PRESS
DOI: 10.1016/j.cell.2005.06.022
关键词
-
资金
- NCI NIH HHS [CA098394, P01 CA92625, R37 CA50239] Funding Source: Medline
The BCL-2 family of apoptotic proteins encompasses key regulators proximal to irreversible cell damage The BH3-only members of this family act as sentinels interconnecting specific death signals to the core apoptotic pathway. Our previous data demonstrated a role for BH3-only BID in maintaining myeloid homeostasis and suppressing leukemogenesis. In the absence of Bid, mice accumulate chromosomal aberrations and develop a fatal myeloproliferative disorder resembling chronic myelomonocytic leukemia. Here, we describe a role for BID in preserving genomic integrity that places BID at an early point in the path to determine the fate of a cell. We show that BID plays an unexpected role in the intra-S phase checkpoint downstream of DNA damage distinct from its proapoptotic function. We further demonstrate that this role is mediated through BID phosphorylation by the DNA-damage kinase ATM. These results establish a link between proapoptotic Bid and the DNA-damage response.
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