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-xL 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.
Original language | English (US) |
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Pages (from-to) | 5639-5645 |
Number of pages | 7 |
Journal | Journal of Biological Chemistry |
Volume | 278 |
Issue number | 8 |
DOIs | |
State | Published - Feb 21 2003 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology