Apoptosis Inducing Factor

A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.

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Networked: 299 relevant articles (5 outcomes, 23 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Blomgren, Klas: 10 articles (06/2012 - 06/2003)
2.	Zhu, Changlian: 9 articles (01/2012 - 06/2003)
3.	Kroemer, Guido: 7 articles (01/2015 - 06/2003)
4.	Szabó, Csaba: 7 articles (01/2007 - 07/2002)
5.	Plesnila, Nikolaus: 5 articles (07/2011 - 04/2004)
6.	Susin, Santos A: 5 articles (05/2010 - 09/2003)
7.	Chung, Jing-Gung: 4 articles (08/2012 - 10/2009)
8.	Yang, Jai-Sing: 4 articles (08/2012 - 10/2009)
9.	Wang, Xiaoyang: 4 articles (01/2012 - 07/2003)
10.	Yuste, Victor J: 4 articles (05/2010 - 09/2003)

Related Diseases

1.	Brain Ischemia (Cerebral Ischemia) 07/15/2011 - "In the current study we investigated the role of apoptosis-inducing factor (AIF), a major caspase-independent mitochondrial cell death protein, for neuronal cell death following global cerebral ischemia (GCI). " 07/15/2011 - "Role of apoptosis inducing factor (AIF) for hippocampal neuronal cell death following global cerebral ischemia in mice." 04/01/2004 - "Nuclear translocation of apoptosis-inducing factor after focal cerebral ischemia." 02/01/2009 - "Protective effects of scutellarin against cerebral ischemia in rats: evidence for inhibition of the apoptosis-inducing factor pathway." 05/01/2010 - "Contributions of poly(ADP-ribose) polymerase-1 and -2 to nuclear translocation of apoptosis-inducing factor and injury from focal cerebral ischemia."
2.	Ischemia 12/01/2013 - "In our latest studies, we revealed that GS-Rd could prevent mitochondrial release of apoptosis-inducing factor (AIF) and reduce inflammatory response following transient focal ischemia in rats. " 11/01/2006 - "In the present study, we focused on the localization of apoptosis-inducing factor (AIF), which is an important protein in the signal-transduction system through caspase-independent pathways, to investigate the possible mechanism for the protective effect of HGF after transient forebrain ischemia. " 01/01/2014 - "A deficiency of apoptosis inducing factor (AIF) in Harlequin mouse heart mitochondria paradoxically reduces ROS generation during ischemia-reperfusion." 06/14/2013 - "Cardioprotection by modulation of mitochondrial respiration during ischemia-reperfusion: role of apoptosis-inducing factor." 11/01/2007 - "Our findings suggested that treatment with HGF was capable of protecting hippocampal neurons against ischemia-induced cell death through the prevention of apoptosis-inducing factor translocation to the nucleus. "
3.	Leukemia 02/01/2012 - "CopA3-induced apoptosis in leukemia cells was mediated by apoptosis inducing factor (AIF), indicating induction of a caspase-independent signaling pathway." 10/01/2005 - "Eicosapentaenoic acid (EPA) was previously shown to induce caspase-independent apoptosis in rat basophilic leukemia cells (RBL2H3 cells) by translocation of apoptosis-inducing factor (AIF) [Free Radic Res (2005) 39, 225-235]. " 12/01/2005 - "Targeting PBR by hexaminolevulinate-mediated photodynamic therapy induces apoptosis through translocation of apoptosis-inducing factor in human leukemia cells." 12/01/2006 - "In this study, we found that treatment with 30 microM magnolol exhibited growth inhibition partly by inducing apoptosis in cultured human leukemia U937 cells and that the apoptosis was induced via the sequential ordering of molecular events; 1) a transient decrease of phosphorylated extracelluar signal-requlated kinase (ERK), 2) translocation of apoptosis inducing factor (AIF) from mitochondria to cytosol concurrent with a decreased membrane potential, and 3) downregulation of bcl-2 protein. " 09/01/2006 - "Although benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone inhibited caspase activity in Bcl-2-overexpressing U937 cells, it completely prevented neither the induction of apoptosis or the nuclear translocation of apoptosis-inducing factor, which suggests that evodiamine is, at least in part, able to bypass the resistance of leukemia cells via caspase-independent apoptotic pathways. "
4.	Cadaver (Cadavers) 01/01/2012 - "Here we show that the cytosolic release from mitochondria of apoptosis-inducing factor (AIF) is required for PS exposure during death receptor-induced apoptosis and for efficient clearance of cell corpses by primary human macrophages. "
5.	Necrosis 04/01/2012 - "In response to sympathetic stimuli, ETS2 is also up-regulated, and functionally, adenovirus-mediated over-expression of ETS2 promotes apoptosis-inducing factor-mediated, caspase-independent programmed necrosis exclusively in CMs that can be fully inhibited by the PARP-1 inhibitor DPQ. " 05/15/2009 - "Interestingly, we found that these cells became highly sensitive to TRAIL (tumour necrosis factor-related apoptosis-inducing factor) in comparison with K562 cells showing high resistance to TRAIL. " 11/01/2008 - "Little or no necrosis is observed, and cell death is caspase-independent and associated with nuclear translocation of the apoptosis-inducing factor, AIF. " 12/01/2006 - "HR cardiomyoblasts were affected by both necrosis and apoptosis, the latter involving the nuclear translocation of apoptosis-inducing factor. " 11/01/2005 - "Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apoptosis inducing factor."

Related Drugs and Biologics

1.	Cytochromes c (Cytochrome c)
2.	Poly(ADP-ribose) Polymerases (Poly ADP Ribose Polymerase)
3.	Caspase 3 (Caspase-3)
4.	nigranoic acid
5.	Hepatocyte Growth Factor (Growth Factor, Hepatocyte)
6.	Sodium
7.	Butyrates (Butyrate)
8.	scutellarin
9.	vorinostat (suberoylanilide hydroxamic acid)
10.	D 21266 (perifosine)

Related Therapies and Procedures

1.	Heterologous Transplantation (Xenotransplantation)
2.	Resuscitation
3.	Photochemotherapy (Photodynamic Therapy)
4.	Drug Therapy (Chemotherapy)
5.	Aftercare (After-Treatment)