ARG57162

anti-AIF antibody [22E9]

anti-AIF antibody [22E9] for ICC/IF,Western blot and Human

Overview

Product Description Mouse Monoclonal antibody [22E9] recognizes AIF
Tested Reactivity Hu
Tested Application ICC/IF, WB
Host Mouse
Clonality Monoclonal
Clone 22E9
Isotype IgG2a, kappa
Target Name AIF
Antigen Species Human
Immunogen Recombinant fragment around aa. 98-609 of Human AIF
Conjugation Un-conjugated
Alternate Names CMTX4; NAMSD; COWCK; Apoptosis-inducing factor 1, mitochondrial; CMT2D; EC 1.1.1.-; NADMR; PDCD8; COXPD6; AIF; Programmed cell death protein 8

Application Instructions

Application Suggestion
Tested Application Dilution
ICC/IFAssay-dependent
WBAssay-dependent
Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist.

Properties

Form Liquid
Purification Purification with Protein A.
Buffer PBS (pH 7.4), 0.02% Sodium azide and 10% Glycerol.
Preservative 0.02% Sodium azide
Stabilizer 10% Glycerol
Concentration 1 mg/ml
Storage Instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use.
Note For laboratory research only, not for drug, diagnostic or other use.

Bioinformation

Database Links

GeneID: 9131 Human AIFM1

Swiss-port # O95831 Human Apoptosis-inducing factor 1, mitochondrial

Gene Symbol AIFM1
Gene Full Name apoptosis-inducing factor, mitochondrion-associated, 1
Background 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 (COXPD6), a severe mitochondrial encephalomyopathy, as well as Cowchock syndrome, also known as X-linked recessive Charcot-Marie-Tooth disease-4 (CMTX-4), a disorder resulting in neuropathy, and axonal and motor-sensory defects with deafness and mental retardation. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 10. [provided by RefSeq, Aug 2015]
Function Functions both as NADH oxidoreductase and as regulator of apoptosis. In response to apoptotic stimuli, it is released from the mitochondrion intermembrane space into the cytosol and to the nucleus, where it functions as a proapoptotic factor in a caspase-independent pathway. In contrast, functions as an antiapoptotic factor in normal mitochondria via its NADH oxidoreductase activity. The soluble form (AIFsol) found in the nucleus induces 'parthanatos' i.e. caspase-independent fragmentation of chromosomal DNA. Interacts with EIF3G,and thereby inhibits the EIF3 machinery and protein synthesis, and activates casapse-7 to amplify apoptosis. Plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells. Binds to DNA in a sequence-independent manner. [UniProt]
Calculated MW 67 kDa
PTM Under normal conditions, a 54-residue N-terminal segment is first proteolytically removed during or just after translocation into the mitochondrial intermembrane space (IMS) by the mitochondrial processing peptidase (MPP) to form the inner-membrane-anchored mature form (AIFmit). During apoptosis, it is further proteolytically processed at amino-acid position 101 leading to the generation of the mature form, which is confined to the mitochondrial IMS in a soluble form (AIFsol). AIFsol is released to the cytoplasm in response to specific death signals, and translocated to the nucleus, where it induces nuclear apoptosis in a caspase-independent manner.
Ubiquitination by XIAP/BIRC4 does not lead to proteasomal degradation. Ubiquitination at Lys-255 by XIAP/BIRC4 blocks its ability to bind DNA and induce chromatin degradation, thereby inhibiting its ability to induce cell death.