| First Author | Kamer I | Year | 2005 |
| Journal | Cell | Volume | 122 |
| Issue | 4 | Pages | 593-603 |
| PubMed ID | 16122426 | Mgi Jnum | J:115186 |
| Mgi Id | MGI:3690822 | Doi | 10.1016/j.cell.2005.06.014 |
| Citation | Kamer I, et al. (2005) Proapoptotic BID is an ATM effector in the DNA-damage response. Cell 122(4):593-603 |
| abstractText | The 'BH3-only' proapoptotic BCL-2 family members are sentinels of intracellular damage. Here, we demonstrated that the BH3-only BID protein partially localizes to the nucleus in healthy cells, is important for apoptosis induced by DNA damage, and is phosphorylated following induction of double-strand breaks in DNA. We also found that BID phosphorylation is mediated by the ATM kinase and occurs in mouse BID on two ATM consensus sites. Interestingly, BID-/- cells failed to accumulate in the S phase of the cell cycle following treatment with the topoisomerase II poison etoposide; reintroducing wild-type BID restored accumulation. In contrast, introducing a nonphosphorylatable BID mutant did not restore accumulation in the S phase and resulted in an increase in cellular sensitivity to etoposide-induced apoptosis. These results implicate BID as an ATM effector and raise the possibility that proapoptotic BID may also play a prosurvival role important for S phase arrest. |
