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Human Polyclonal AIFM1 Primary Antibody for WB - ABIN222988
Jayanthi, Deng, Noailles, Ladenheim, Cadet: Methamphetamine induces neuronal apoptosis via cross-talks between endoplasmic reticulum and mitochondria-dependent death cascades. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2004
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Human Polyclonal AIFM1 Primary Antibody for IF (p), IHC (p) - ABIN724010
Gong, Hua, Zhang, Zhao, Tang, Mei, Zhang, Cui, Li: Hypothermia-induced neuroprotection is associated with reduced mitochondrial membrane permeability in a swine model of cardiac arrest. in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2013
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Human Monoclonal AIFM1 Primary Antibody for ICC, FACS - ABIN968950
Son, Jang, Heo, Chung, Choi, Lee: Apoptosis-inducing factor plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells. in Apoptosis : an international journal on programmed cell death 2009
Human Polyclonal AIFM1 Primary Antibody for ELISA, WB - ABIN4278850
Lewis, Wilkinson, Jackson, Mehra, Varambally, Chinnaiyan, Wilkinson: The enzymatic activity of apoptosis-inducing factor supports energy metabolism benefiting the growth and invasiveness of advanced prostate cancer cells. in The Journal of biological chemistry 2012
we sought to investigate mechanisms mediated by Hsp70 (show HSP70 Antibodies) acetylation in relation to apoptotic and autophagic programmed cell death. Upon stress-induced apoptosis, Hsp70 (show HSP70 Antibodies) acetylation inhibits apoptotic cell death, mediated by Hsp70 (show HSP70 Antibodies) association with apoptotic protease-activating factor (Apaf)-1 (show APAF1 Antibodies) and apoptosis-inducing factor (AIF), key modulators of caspase (show CASP3 Antibodies)-dependent and -independent apoptotic pathways, respectively
Overexpression of full-length AIFM1 suppresses proliferation and induces apoptosis of HepG2 and Hep3B cells. Caspase 3 (show CASP3 Antibodies) and DRAM (show DRAM1 Antibodies) are involved in full-length AIFM1-induced apoptosis in HepG2 and Hep3B cells.
Real-time PCR results showed that apoptosis-inducing factor (AIF) and calpain-1 mRNAs were highly expressed in the transitional segmentof the Hirschsprung's disease bowel, whereas autophagy protein 5 (Atg5) was highly expressed in the narrow segment. Western blot results were consistent with mRNA levels, with increased AIF, calpain-1, and Atg5 expressions in the transitional segment compared with the dilated segment.
Data revealed that under a nutrient deficient condition, CD317 (show BST2 Antibodies) functions as an anti-apoptotic factor through AIF-mediated caspase (show CASP3 Antibodies) and autophagy-independent manner.
we report that AIF-independent PARP-1 (show PARP1 Antibodies)-dependent necrosis constitutes a major mechanism of RPE (show RPE Antibodies) cell death leading to retinal degeneration in dry age-related macular degeneration .
Downregulation of AIF by hypoxia causes oxidative inactivation of the lipid phosphatase activity of phosphatase and tensin homolog on chromosome 10 (PTEN), with ensuing activation of Akt (show AKT1 Antibodies) kinase, phosphorylation of the Akt (show AKT1 Antibodies) substrate GSK-3beta and activation of WNT (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling in colon cancer cells.
novel pathway for mda-7/IL-24 (show IL24 Antibodies)-induced caspase (show CASP3 Antibodies)-independent apoptosis in neuroblastoma (show ARHGEF16 Antibodies) cells mediated through modulation of AIF, ATM (show ATM Antibodies), and gamma-H2AX (show H2AFX Antibodies).
Study defines the mechanism whereby AIF is allosterically modulated by charge-complex formation with NADH. Two distinct molecular pathways couple AIF's active site to dimerization and release of its regulatory C-loop insert with implications for AIF allosteric switching in cell survival and death.
Whole exome sequencing indicated a single plausible candidate - the p.Asp237Gly variant in apoptosis inducing factor mitochondria associated 1 (AIFM1; chr. Xq26.1), and the p.Asp237Gly segregated with disease in two families.
Only a drastic decrease in the expression level or/and redox activity of AIF tends to cause an early and severe neurodegeneration, whereas less pronounced changes in the AIF properties could lead to a broad range of slowly progressive neurological disorders.
Drosophila Apoptosis-inducing factor (AIF) is a mitochondrial effector of cell death that plays roles in developmentally regulated cell death and normal mitochondrial function.
Mycobacterium bovis-induced macrophage cell death is caspase (show CASP3 Antibodies) independent with apoptosis-inducing factor participation.
Mitochondrial apoptosis-inducing factor was found to translocate to the nucleus during porcine epidemic diarrhea virus infection.
caspase-1 (show CASP1 Antibodies) regulates dopaminergic neuronal death in the pathogenesis of Parkinson's disease in mice via caspase-7 (show CASP7 Antibodies)/PARP1 (show PARP1 Antibodies)/AIF pathway.
flavonoids of Rosa roxburghii Tratt enhanced radioprotection at least partially by regulating PARP-1 (show PARP1 Antibodies)/AIF to reduce apoptosis.
X-ray irradiation induces apoptosis of mouse GC1 sperm cells via nuclear translocation of AIF.
The first structure of a pathogenic AIF variant in complex with NAD+ is reported. The G307E mutation leads to wrong positioning of NAD+ adenylate moiety.
AIF deficiency is a risk factor for the development of diabetic kidney disease.
In conclusion, calpain was involved in oxygen glucose deprivation-induced RGC-5 necroptosis with the increased expression of its downstream molecule tAIF.
The results identify new protein-protein interactions between AIF-Cx43 (show GJA1 Antibodies), ETFB (show ETFB Antibodies)-Cx43 (show GJA1 Antibodies) and AIF-ETFB (show ETFB Antibodies) as possible players in the regulation of the mitochondrial redox state.
our findings suggest that MIA40 (show CHCHD4 Antibodies) reduction contributes to the effects of AIF deficiency on OXPHOS, as it may impact on the correct assembly and maintenance of the respiratory subunits.
These results indicate that the adenylate moiety of NAD(+)/H is crucial for the association with AIF and for the subsequent structural reorganization of the complex, but not for protein dimerization.
Taken together, these data suggest that AIF is likely to play a region-specific role in AD-related caspase (show CASP3 Antibodies)-independent PCD (show PCBD1 Antibodies), which is consistent with aging-associated mitochondrial impairment and oxidative stress.
This gene encodes a flavoprotein essential for nuclear disassembly in apoptotic cells, and it is found in the mitochondrial intermembrane space in healthy cells. Induction of apoptosis results in the translocation of this protein to the nucleus where it affects chromosome condensation and fragmentation. In addition, this gene product induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Mutations in this gene cause combined oxidative phosphorylation deficiency 6, which results in a severe mitochondrial encephalomyopathy. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 10.
apoptosis-inducing factor 1, mitochondrial
, programmed cell death 8 (apoptosis-inducing factor)
, striatal apoptosis-inducing factor
, apoptosis inducing factor
, programmed cell death 8
, apoptosis-inducing factor, mitochondrion-associated, 1
, mammary apoptosis inducing factor
, flavoprotein and apoptosis inductor
, apoptosis-inducing factor 1, mitochondrial-like
, programmed cell death protein 8