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

A role for proapoptotic BID in the DNA-damage response.

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.[1]


  1. A role for proapoptotic BID in the DNA-damage response. Zinkel, S.S., Hurov, K.E., Ong, C., Abtahi, F.M., Gross, A., Korsmeyer, S.J. Cell (2005) [Pubmed]
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