Rejuvenating bi(d)ology

S. S. Zinkel, Xiao-Ming Yin, A. Gross

Research output: Contribution to journalArticle

8 Citations (Scopus)

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

Fingerprint

Ataxia Telangiectasia
Caspases
BH3 Interacting Domain Death Agonist Protein
Hematopoietic System
Death Domain Receptors
Hematopoietic Stem Cells
Cytochromes c
Reperfusion Injury
DNA Damage
Permeability
Reactive Oxygen Species
Mitochondria
Peptide Hydrolases
Phosphotransferases
Bone Marrow
T-Lymphocytes
Liver
Wounds and Injuries
Research
cyhalothrin

Keywords

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

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

Cite this

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

Rejuvenating bi(d)ology. / Zinkel, S. S.; Yin, Xiao-Ming; Gross, A.

In: Oncogene, Vol. 32, No. 27, 04.07.2013, p. 3213-3219.

Research output: Contribution to journalArticle

Zinkel, SS, Yin, X-M & Gross, A 2013, 'Rejuvenating bi(d)ology', Oncogene, vol. 32, no. 27, pp. 3213-3219. https://doi.org/10.1038/onc.2012.454
Zinkel SS, Yin X-M, Gross A. Rejuvenating bi(d)ology. Oncogene. 2013 Jul 4;32(27):3213-3219. https://doi.org/10.1038/onc.2012.454
Zinkel, S. S. ; Yin, Xiao-Ming ; Gross, A. / Rejuvenating bi(d)ology. In: Oncogene. 2013 ; Vol. 32, No. 27. pp. 3213-3219.
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