AIF deficiency compromises oxidative phosphorylation

By N. Vahsen, C. Candé, J. Briere, P. Bénit, N. Joza, N. Larochette, P. Mastroberardino, M. Péquignot, N. Casares, Vladimir Lazar and 10 more. EMBO Journal, 2004

634 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a784322bcfb536bd646e259dc23917eb6903aade

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Citations in the corpus

• NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, unknown): “However, AIF also plays a significant role in mitochondrial complex I activity (290).”
• Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, unknown): “These gene defects include deletion of the mitochondrial flavoprotein apoptosis-inducing factor, which can initiate progressive dysfunction of oxidative phosphorylation (260, 316), and deletion of mitochondrial transcription factor A, which results in mice with myopathy and progressively deteriorati”
• Functional and physical interaction between Bcl‐XL and a BH3‐like domain in Beclin‐1 (2007, unknown): “…T- sta rv ed eg l-1 (n 48 7) st ar ve d eg l-1 (o k1 41 8) -s ta rv ed 50 μm DsRED::LGG-1 The EMBO Journal VOL 26 | NO 10 | 2007 &2007 European Molecular Biology Organization2536 Solution medium (Sigma) (Vahsen et al, 2004), optionally supplemented with ABT737 (1mM; synthesized by Servier).”
• OXIDANT STRESS, MITOCHONDRIA AND CELL DEATH MECHANISMS IN DRUG-INDUCED LIVER INJURY: LESSONS LEARNED FROM ACETAMINOPHEN HEPATOTOXICITY (2012, background): “Recently, we demonstrated that apoptosis-inducing factor (AIF), which functions as nicotinamide adenine dinucleotide (NADH) oxidase in mitochondria and regulates complex I activity (Miramar et al., 2001; Vahsen et al., 2004), can promote APAP-induced oxidant stress (Bajt et al.”
• Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “AIF is essential for ETC complex I function (75). p53 deficiency leads to reduced SCO2 and AIF activity, resulting in mitochondrial OXPHOS impairment (76).”