Regulation of mitochondrial morphological dynamics during apoptosis by Bcl-2 family proteins

A key in Bak?

Craig Brooks, Zheng Dong

Research output: Contribution to journalReview article

80 Citations (Scopus)

Abstract

Early during apoptosis, the mitochondrial network collapses into short punctate fragments. The seemingly morphological change, called mitochondrial fragmentation, contributes to mitochondrial injury. Mitochondrial morphology is dictated by two opposing processes, fission and fusion. It is unclear how the fission-fusion balance is tilted during apoptosis, resulting in mitochondrial fragmentation. Emerging evidence has now suggested a regulation of mitochondrial morphological dynamics by Bcl-2 family proteins. In this regulation, Bak appears to be a key. Through interaction with mitofusins, Bak may block mitochondrial fusion to induce fragmentation. By this function, Bak may collaborate with Bax to permeabilize mitochondrial outer membrane, leading to the release of apoptogenic factors.

Original languageEnglish (US)
Pages (from-to)3043-3047
Number of pages5
JournalCell Cycle
Volume6
Issue number24
DOIs
StatePublished - Dec 15 2007

Fingerprint

Mitochondrial Dynamics
Staphylococcal Protein A
Apoptosis
Mitochondrial Membranes
Wounds and Injuries
Proteins

Keywords

  • Apoptosis
  • Bak
  • Bax
  • Fission
  • Fusion
  • Mitochondria
  • Mitofusin

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Cite this

Regulation of mitochondrial morphological dynamics during apoptosis by Bcl-2 family proteins : A key in Bak? / Brooks, Craig; Dong, Zheng.

In: Cell Cycle, Vol. 6, No. 24, 15.12.2007, p. 3043-3047.

Research output: Contribution to journalReview article

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abstract = "Early during apoptosis, the mitochondrial network collapses into short punctate fragments. The seemingly morphological change, called mitochondrial fragmentation, contributes to mitochondrial injury. Mitochondrial morphology is dictated by two opposing processes, fission and fusion. It is unclear how the fission-fusion balance is tilted during apoptosis, resulting in mitochondrial fragmentation. Emerging evidence has now suggested a regulation of mitochondrial morphological dynamics by Bcl-2 family proteins. In this regulation, Bak appears to be a key. Through interaction with mitofusins, Bak may block mitochondrial fusion to induce fragmentation. By this function, Bak may collaborate with Bax to permeabilize mitochondrial outer membrane, leading to the release of apoptogenic factors.",
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