Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 35, Issue 5, Pages 278-287Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2009.12.008
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Funding
- Ligue Nationale contre le Cancer
- Ligue Nationale contre le Cancer (Equipes labellisee)
- Agence Nationale pour la Recherche (ANR)
- European Commission
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Canceropole Ile-de-France
- Swedish Childhood Cancer Foundation (Barncancerfonden)
- Swedish Research Council
- Association Francaise contre l'Ataxie de Friedreich (AFAF)
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Apoptosis-inducing factor (AIF) was initially discovered as a caspase-independent death effector. AIF fulfills its lethal function after its release from mitochondria and its translocation to the nucleus of the dying cell. The contribution of AIF to programmed cell death is dependent upon the cell type and apoptotic insult. Recent in vivo data indicate that, in addition to its lethal activity, AIF plays a vital mitochondrial role in healthy cells. A segment of AIF which is dispensable for its apoptotic function carries an NADH-oxidase domain that regulates the respiratory chain complex I and is required for cell survival, proliferation and mitochondrial integrity. Mice that express reduced levels of AIF constitute a reliable model of complex I deficiency. Here we discuss recent reports on the survival-related function(s) of AIF.
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