Sandra Zinkel
Assistant Professor of Medicine
Last active: 3/26/2019

Rejuvenating Bi(d)ology.

Zinkel SS, Yin XM, Gross A
Oncogene. 2013 32 (27): 3213-3219

PMID: 23069655 · PMCID: PMC4037911 · DOI:10.1038/onc.2012.454

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.

MeSH Terms (6)

Animals Apoptosis BH3 Interacting Domain Death Agonist Protein Hematopoietic Stem Cells Humans Signal Transduction

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