BCL-2 improves oxidative phosphorylation and modulates adenine nucleotide translocation in mitochondria of cells harboring mutant mtDNA. Academic Article uri icon

Overview

abstract

  • Members of the BCL-2-related antiapoptotic family of proteins have been shown previously to regulate ATP/ADP exchange across the mitochondrial membranes and to prevent the loss of coupled mitochondrial respiration during apoptosis. We have found that BCL-2/BCL-x(L) can also improve mitochondrial oxidative phosphorylation in cells harboring pathogenic mutations in mitochondrial tRNA genes. The effect of BCL-2 overexpression in mutated cells was independent from apoptosis and was presumably associated with a modulation of adenine nucleotide exchange between mitochondria and cytosol. These results suggest that BCL-2 can regulate respiratory functions in response to mitochondrial distress by regulating the levels of adenine nucleotides.

publication date

  • November 12, 2002

Research

keywords

  • Apoptosis
  • DNA, Mitochondrial
  • Mitochondria
  • Mitochondrial ADP, ATP Translocases
  • Oxidative Phosphorylation
  • Proto-Oncogene Proteins c-bcl-2

Identity

Scopus Document Identifier

  • 0037458714

Digital Object Identifier (DOI)

  • 10.1074/jbc.M203080200

PubMed ID

  • 12431997

Additional Document Info

volume

  • 278

issue

  • 8