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 |
|---|---|
| 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 |
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ASJC Scopus subject areas
- Biochemistry
Cite this
BCL-2 improves oxidative phosphorylation and modulates adenine nucleotide translocation in mitochondria of cells harboring mutant mtDNA. / Manfredi, Giovanni; Kwong, Jennifer Q.; Oca-Cossio, José A.; Woischnik, Markus; Gajewski, Carl D.; Martushova, Katherine; D'Aurelio, Marilena; Friedlichl, Avi L.; Moraes, Carlos T.
In: Journal of Biological Chemistry, Vol. 278, No. 8, 21.02.2003, p. 5639-5645.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - BCL-2 improves oxidative phosphorylation and modulates adenine nucleotide translocation in mitochondria of cells harboring mutant mtDNA
AU - Manfredi, Giovanni
AU - Kwong, Jennifer Q.
AU - Oca-Cossio, José A.
AU - Woischnik, Markus
AU - Gajewski, Carl D.
AU - Martushova, Katherine
AU - D'Aurelio, Marilena
AU - Friedlichl, Avi L.
AU - Moraes, Carlos T
PY - 2003/2/21
Y1 - 2003/2/21
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0037458714&partnerID=8YFLogxK
U2 - 10.1074/jbc.M203080200
DO - 10.1074/jbc.M203080200
M3 - Article
VL - 278
SP - 5639
EP - 5645
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 8
ER -