HUGO ID Detailed Result 8768


HUGO ID 8768
Symbol AIFM1
Name apoptosis-inducing factor, mitochondrion-associated, 1
#Occurrence 34
#Paper 6

 


PMID Match String Actual String Score Flanking text Edited by Edit
16046141AIFAIF0.6For cytochrome c and AIF release experiments ETNA cells were harvested in hypotonic buffer (2 
16046141AIFAIF0.6that other mitochondrial factors involved in apoptotic pathways such as AIF ( Fig 4 and Fig 5 and EndoG (not not 
16046141AIFAIF0.6pore causing leakage of cytochrome c and apoptosis-inducing factor (AIF) AIF ( Friedlander 2003 were suggested to play a role in 
16046141AIFAIF0.6mutants were assessed for the presence of cytochrome c and AIF by Western blot 
16046141AIFAIF0.6untransfected ETNA cells were used as a positive control for AIF and cytochrome c expression 
16046141AIFAIF0.6Fig 5._amp_#xa0 ETNA cells retain mitochondrial AIF upon fALS-SOD1 expression 
16046141AIFAIF0.6confocal immunofluorescence microscopy staining of cytochrome c (green) green and AIF (red) red in ETNA cells 48 h after transfection with 
16050975AIFAIF0.6pro-apoptotic factors such as cytochrome c apoptosis inducing factor (AIF), AIF and endoG from individual mitochondria perhaps in response to local 
17150307AIFAIF0.6of GSH decreased mitochondrial function facilitated apoptosis inducing factor (AIF) AIF translocation cytochrome c release and caspase 3 activation and consequently 
17150307AIFAIF0.6the spinal cord and motor neuron cells is correlated with AIF translocation caspase 3 activation and motor neuron degeneration during ALS-like 
17150307AIFAIF0.6Western analysis was performed to analyze cytochrome c release and AIF translocation 
17150307AIFAIF0.6incubated with specific antibodies overnight at 4 _amp_#x000b0 C (AIF, AIF cytochrome c and active caspase 3 antibodies were all at 
17150307AIFAIF0.6Results GSH depletion promoted AIF redistribution cytochrome c release caspase 3 activation and apoptotic cell 
17150307AIFAIF0.6nuclear fractionations coupled with western analysis showed an increase of AIF translocation to nucleus following GSH depletion in NSC34 cells ( 
17150307AIFAIF0.6Immunohistochemical staining confirmed the increase of AIF translocation to the nucleus from the mitochondria upon GSH depletion 
17150307AIFAIF0.6Decreased GSH was associated with AIF nuclear translocation caspase 3 activation and motor neuron cell death 
17150307AIFAIF0.6Reduction in GSH was associated with redistribution of AIF from mitochondria to nuclei 3 
17150307AIFAIF0.6cell death mechanisms potentially induced by GSH depletion we assessed AIF redistribution and found that there was an increase in AIF 
17150307AIFAIF0.6AIF redistribution and found that there was an increase in AIF translocation from mitochondria to nuclei upon GSH depletion ( Figure 
17150307AIFAIF0.6AIF is a flavoprotein residing in mitochondrial intermembrane ( Cande et 
17150307AIFAIF0.6Translocation of AIF initiates cell apoptosis by cleavage internucleosomal DNA to relative large 
17150307AIFAIF0.6AIF nuclear translocation has been observed in a variety of cell 
17150307AIFAIF0.6The AIF redistribution detected in EA treated cells and also observed in 
17150307AIFAIF0.6coupled with increased oxidative stress by mutant G93A-SOD1 that facilitates AIF nuclear translocation may underlie some of the events linked to 
17150307AIFAIF0.6Figure 9 Redistribution of AIF and active caspase 3 in motor neuron cells of ALS-like 
17150307AIFAIF0.6AIF Apoptosis Inducing Factor ALS Amyotrophic Lateral Sclerosis BSO L-Buthionine Sulfoximine 
14739060apoptosis-inducing factorapoptosis inducing factor1.0hen it is released from the mitochondria into cytoplasm trigger the caspase chain _amp_#x2022; smac/diablo binds to inhibitors of activated caspases and causes further caspase activation _amp_#x2022; apoptosis inducing factor and endonuclease g mediate caspase independent cell death pathways  
16046141apoptosis-inducing factorapoptosis inducing factor1.0 leading to bioenergetic failure in the motor neurons bendotti et al. 2001 and jung et al. 2002 and to alteration in the mitochondrial permeability transition pore causing leakage of cytochrome c and apoptosis inducing factor aif friedlander 2003 were suggested to play a role in the mitochondrial dependent motor neuron death through the activation of a caspase mediated cascade leading to programmed cell death.  
16050975apoptosis-inducing factorapoptosis inducing factor1.0one may envision a scenario where mitochondrial dysfunction results in quantal releases of pro apoptotic factors such as cytochrome c apoptosis inducing factor aif and endog from individual mitochondria perhaps in response to local calcium mediated toxicity for example under excitatory synapses.  
16242643apoptosis-inducing factorapoptosis inducing factor1.0this blockade in turn inhibits the release of the proapoptotic factors cytochrome c smac diablo and apoptosis inducing factor from the mitochondria wang et al. 2003 and zhu et al. 2002 .  
17099894apoptosis-inducing factorapoptosis inducing factor1.0the mn death is independent of activation of caspases 1 3 and 8 or apoptosis inducing factor within mns with a blockade of apoptosis possibly mediated by aven up regulation.  
17150307apoptosis-inducing factorapoptosis inducing factor1.0furthermore depletion of gsh decreased mitochondrial function facilitated apoptosis inducing factor aif translocation cytochrome c release and caspase 3 activation and consequently led to motor neuron like cell apoptosis.  
17150307apoptosis-inducing factorapoptosis inducing factor1.0aif apoptosis inducing factor als amyotrophic lateral sclerosis bso l buthionine sulfoximine dcf dichlorofluorescin dmem dulbecco_amp_#x02019;s modified eagle_amp_#x02019;s medium ea ethacrynic acid fbs fetal bovine serum _amp_#x 
17150307apoptosis-inducing factorapoptosis inducing factor1.0apoptosis inducing factor|biological markers|enzyme inhibitors|reactive oxygen species|buthionine sulfoximine|ethacrynic acid|glutathione|superoxide dismutase 1|superoxide dismutase|