Mouse Anti- AIF
调亡诱导因子抗体 / Anti- AIF
Apoptosis inducing factor; Harlequin; Hq; mAIF; MGC111425; MGC5706; PDCD 8; PDCD8; Programmed cell death 8; Programmed cell death 8 isoform 1; Programmed cell death 8 isoform 2; Programmed cell death 8 isoform 3; Programmed cell death protein 8 mitochondrial; Programmed cell death protein 8 mitochondrial precursor; Striatal apoptosis inducing factor; AIFM1_HUMAN; Apoptosis-inducing factor 1, mitochondrial.
0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide；Reconstitute with 0.1ml sterile distilled water.
免 疫 原：
KLH conjugated synthetic peptide derived from human AIF
Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Rabbit, Sheep
Lyophilized or Liquid
分 子 量：
Predicted molecular weight 56kDa
affinity purified by Protein A
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Use a manual defrost freezer and avoid repeated freezethaw cycles.
1 month from date of receipt, 2 to 8℃, reconstituted.
6 months from date of receipt, -20 to -70℃, reconstituted.
12 months from date of receipt, -20 to -70℃as supplied.
When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
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. [provided by RefSeq, May 2010].
Probable oxidoreductase that has a dual role in controlling cellular life and death; during apoptosis, it is translocated from the mitochondria to the nucleus to function as a proapoptotic factor in a caspase-independent pathway, while in normal mitochondria, it functions as an antiapoptotic factor via its 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.
Interacts with XIAP/BIRC4. Interacts (via N-terminus) with EIF3G (via C-terminus).
Mitochondrion intermembrane space. Mitochondrion inner membrane. Cytoplasm. Nucleus. Cytoplasm, perinuclear region. Note=Proteolytic cleavage during or just after translocation into the mitochondrial intermembrane space (IMS) results in the formation of an inner-membrane-anchored mature form (AIFmit). During apoptosis, further proteolytic processing leads to a 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. Colocalizes with EIF3G in the nucleus and perinuclear region.
Isoform 5 is frequently down-regulated in human cancers.
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.
Defects in AIFM1 are the cause of combined oxidative phosphorylation deficiency type 6 (COXPD6) [MIM:300816]. It is a mitochondrial disease resulting in a neurodegenerative disorder characterized by psychomotor delay, hypotonia, areflexia, muscle weakness and wasting.
Belongs to the FAD-dependent oxidoreductase family.