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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Proapoptotic BID is an ATM effector in the DNA-damage response.

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.[1]

References

  1. Proapoptotic BID is an ATM effector in the DNA-damage response. Kamer, I., Sarig, R., Zaltsman, Y., Niv, H., Oberkovitz, G., Regev, L., Haimovich, G., Lerenthal, Y., Marcellus, R.C., Gross, A. Cell (2005) [Pubmed]
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