| First Author | Zinkel SS | Year | 2005 |
| Journal | Cell | Volume | 122 |
| Issue | 4 | Pages | 579-91 |
| PubMed ID | 16122425 | Mgi Jnum | J:101952 |
| Mgi Id | MGI:3605956 | Doi | 10.1016/j.cell.2005.06.022 |
| Citation | Zinkel SS, et al. (2005) A role for proapoptotic BID in the DNA-damage response. Cell 122(4):579-91 |
| abstractText | 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. |
