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Here, the binding site of AIF(Delta1-121) and AIF(370-394) on CypA (show PPIA Proteins) has been mapped by NMR spectroscopy and biochemical studies, and a molecular model of the complex has been proposed. The authors show that AIF(370-394) interacts with CypA (show PPIA Proteins) on the same surface recognized by AIF(Delta1-121) protein and that the region is very close to the CypA (show PPIA Proteins) catalytic pocket.
new form of motor neuropathy expands the phenotypic spectrum of AIFM1 mutations and therefore, the AIFM1 gene should be considered in the diagnosis of hereditary motor neuropathies
X-linked hypomyelination with spondylometaphyseal dysplasia associated with mutations in AIFM1
report of a family carrying a novel missense mutation in AIFM1 that exhibits an isolated axonal polyneuropathy with misassembly of mitochondrial complex I and III.
we sought to investigate mechanisms mediated by Hsp70 (show HSP70 Proteins) acetylation in relation to apoptotic and autophagic programmed cell death. Upon stress-induced apoptosis, Hsp70 (show HSP70 Proteins) acetylation inhibits apoptotic cell death, mediated by Hsp70 (show HSP70 Proteins) association with apoptotic protease-activating factor (Apaf)-1 (show APAF1 Proteins) and apoptosis-inducing factor (AIF), key modulators of caspase (show CASP3 Proteins)-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 Proteins) and DRAM 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 Proteins) functions as an anti-apoptotic factor through AIF-mediated caspase (show CASP3 Proteins) and autophagy-independent manner.
we report that AIF-independent PARP-1 (show PARP1 Proteins)-dependent necrosis constitutes a major mechanism of RPE (show RPE Proteins) 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 Proteins) kinase, phosphorylation of the Akt (show AKT1 Proteins) substrate GSK-3beta and activation of WNT (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling in colon cancer cells.
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 Proteins) 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 Proteins) regulates dopaminergic neuronal death in the pathogenesis of Parkinson's disease in mice via caspase-7 (show CASP7 Proteins)/PARP1 (show PARP1 Proteins)/AIF pathway.
flavonoids of Rosa roxburghii Tratt enhanced radioprotection at least partially by regulating PARP-1 (show PARP1 Proteins)/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 Proteins), ETFB (show ETFB Proteins)-Cx43 (show GJA1 Proteins) and AIF-ETFB (show ETFB Proteins) as possible players in the regulation of the mitochondrial redox state.
our findings suggest that MIA40 (show CHCHD4 Proteins) 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-independent PCD, 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