| First Author | Zinkel SS | Year | 2013 |
| Journal | Oncogene | Volume | 32 |
| Issue | 27 | Pages | 3213-3219 |
| PubMed ID | 23069655 | Mgi Jnum | J:199973 |
| Mgi Id | MGI:5506694 | Doi | 10.1038/onc.2012.454 |
| Citation | Zinkel SS, et al. (2013) Rejuvenating Bi(d)ology. Oncogene 32(27):3213-9 |
| abstractText | The BH3-only Bid protein is a critical sentinel of cellular stress in the liver and the hematopoietic system. Bid's initial 'claim to fame' came from its ability-as a caspase-truncated product-to trigger the mitochondrial apoptotic program following death receptor activation. Today we know that Bid can response to multiple types of proteases, which are activated under different conditions such as T-cell activation, ischemical reperfusion injury and lysosomal injury. Activation of the mitochondrial apoptotic program by Bid-via its recently identified receptor mitochondrial carrier homolog 2-involves multiple mechanisms, including release of cytochrome c and second mitochondria-derived activator of caspase (Smac), alteration of mitochondrial cristae organization, generation of reactive oxygen species and engagement of the permeability transition pore. Bid is also emerging-in its full-length form-as a pivotal sentinel of DNA damage in the bone marrow regulated by the ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and Rad3-related (ATR) kinases. The ATM/ATR-Bid pathway is critically involved in preserving the quiescence and survival of hematopoietic stem cells both in the absence and presence of external stress, and a large part of this review will be dedicated to recent advances in this area of research. |
