Bcl-2 regulation of mitochondrial energetics

Elizabeth Murphy, Ken Ichi Imahashi, Charles Jr Steenbergen

Research output: Contribution to journalArticle

Abstract

Recent data suggest that in addition to regulating apoptosis, Bcl-2 (an anti-apoptotic protein overexpressed in B-cell lymphoma) and Bcl-2 family members also regulate mitochondrial and cell physiology. t-Bid, a Bcl-2 family member, has been shown to modulate reorganization of mitochondrial cristae. Bcl-2 appears to regulate voltage-dependent anion channel permeability, which has important consequences for mitochondrial transport of adenine nucleotides, Ca2+, and other metabolites. BAD, a pro-apoptotic Bcl-2 family member, is required for the binding of glucokinase to a mitochondrial complex, and BAD null mice have altered glucose homeostasis. It has been suggested that Bcl-2 family members may regulate important mitochondrial/cell functions and serve as sentinels to detect abnormalities in these pathways and, when the abnormalities are severe enough, to initiate or facilitate cell death. Understanding the physiologic processes controlled by Bcl-2 will be important in understanding cell regulation, and it may also provide new insights into the regulation of apoptosis.

Original languageEnglish (US)
Pages (from-to)283-290
Number of pages8
JournalTrends in Cardiovascular Medicine
Volume15
Issue number8
DOIs
StatePublished - Nov 2005
Externally publishedYes

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Voltage-Dependent Anion Channels
Apoptosis
Glucokinase
Cell Physiological Phenomena
Apoptosis Regulatory Proteins
Adenine Nucleotides
B-Cell Lymphoma
Permeability
Homeostasis
Cell Death
Glucose
cyhalothrin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Bcl-2 regulation of mitochondrial energetics. / Murphy, Elizabeth; Imahashi, Ken Ichi; Steenbergen, Charles Jr.

In: Trends in Cardiovascular Medicine, Vol. 15, No. 8, 11.2005, p. 283-290.

Research output: Contribution to journalArticle

Murphy, Elizabeth ; Imahashi, Ken Ichi ; Steenbergen, Charles Jr. / Bcl-2 regulation of mitochondrial energetics. In: Trends in Cardiovascular Medicine. 2005 ; Vol. 15, No. 8. pp. 283-290.
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