| First Author | Vahsen N | Year | 2004 |
| Journal | EMBO J | Volume | 23 |
| Issue | 23 | Pages | 4679-89 |
| PubMed ID | 15526035 | Mgi Jnum | J:134036 |
| Mgi Id | MGI:3784887 | Doi | 10.1038/sj.emboj.7600461 |
| Citation | Vahsen N, et al. (2004) AIF deficiency compromises oxidative phosphorylation. EMBO J 23(23):4679-89 |
| abstractText | Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein that, after apoptosis induction, translocates to the nucleus where it participates in apoptotic chromatinolysis. Here, we show that human or mouse cells lacking AIF as a result of homologous recombination or small interfering RNA exhibit high lactate production and enhanced dependency on glycolytic ATP generation, due to severe reduction of respiratory chain complex I activity. Although AIF itself is not a part of complex I, AIF-deficient cells exhibit a reduced content of complex I and of its components, pointing to a role of AIF in the biogenesis and/or maintenance of this polyprotein complex. Harlequin mice with reduced AIF expression due to a retroviral insertion into the AIF gene also manifest a reduced oxidative phosphorylation (OXPHOS) in the retina and in the brain, correlating with reduced expression of complex I subunits, retinal degeneration, and neuronal defects. Altogether, these data point to a role of AIF in OXPHOS and emphasize the dual role of AIF in life and death. |
