Rejuvenating bi(d)ology

S. S. Zinkel, X. M. Yin, A. Gross

Research output: Contribution to journalReview article

10 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3213-3219
Number of pages7
JournalOncogene
Volume32
Issue number27
DOIs
StatePublished - Jul 4 2013

Keywords

  • Apoptosis
  • ATM/ATR
  • Bid
  • DNA damage
  • Mitochondria

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

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    Zinkel, S. S., Yin, X. M., & Gross, A. (2013). Rejuvenating bi(d)ology. Oncogene, 32(27), 3213-3219. https://doi.org/10.1038/onc.2012.454