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AMID / AIFM2 Antibody (N-Terminus)
Goat Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, E |
|---|---|
| Primary Accession | Q9BRQ8 |
| Reactivity | Human |
| Host | Goat |
| Clonality | Polyclonal |
| Calculated MW | 41kDa |
| Dilution | ELISA (1:128000), IHC-P (4 µg/ml), |
| Gene ID | 84883 |
|---|---|
| Other Names | Apoptosis-inducing factor 2, 1.-.-.-, Apoptosis-inducing factor homologous mitochondrion-associated inducer of death, Apoptosis-inducing factor-like mitochondrion-associated inducer of death, p53-responsive gene 3 protein, AIFM2, AMID, PRG3 {ECO:0000303|PubMed:12135761} |
| Target/Specificity | Human AIFM2 / AMID. |
| Reconstitution & Storage | Store at -20°C. Minimize freezing and thawing. |
| Precautions | AMID / AIFM2 Antibody (N-Terminus) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | AIFM2 {ECO:0000303|PubMed:26689472, ECO:0000312|HGNC:HGNC:21411} |
|---|---|
| Function | A NAD(P)H-dependent oxidoreductase that acts as a key inhibitor of ferroptosis (PubMed:31634899, PubMed:31634900, PubMed:35922516). At the plasma membrane, catalyzes reduction of coenzyme Q/ubiquinone-10 to ubiquinol-10, a lipophilic radical-trapping antioxidant that prevents lipid oxidative damage and consequently ferroptosis (PubMed:31634899, PubMed:31634900). Acts in parallel to GPX4 to suppress phospholipid peroxidation and ferroptosis (PubMed:31634899, PubMed:31634900). This anti-ferroptotic function is independent of cellular glutathione levels (PubMed:31634899, PubMed:31634900). Also acts as a potent radical-trapping antioxidant by mediating warfarin-resistant vitamin K reduction in the canonical vitamin K cycle: catalyzes NAD(P)H-dependent reduction of vitamin K (phylloquinone, menaquinone-4 and menadione) to hydroquinone forms (PubMed:35922516). Hydroquinones act as potent radical-trapping antioxidants inhibitor of phospholipid peroxidation and ferroptosis (PubMed:35922516). May play a role in mitochondrial stress signaling (PubMed:26689472). Upon oxidative stress, associates with the lipid peroxidation end product 4-hydroxy-2-nonenal (HNE) forming a lipid adduct devoid of oxidoreductase activity, which then translocates from mitochondria into the nucleus triggering DNA damage and cell death (PubMed:26689472). Capable of DNA binding in a non-sequence specific way (PubMed:15958387). |
| Cellular Location | Lipid droplet. Cell membrane; Lipid-anchor Cytoplasm. Mitochondrion membrane. Nucleus |
| Tissue Location | Detected in most normal tissues as two transcripts of 1.8 and 4.0 kb in length, respectively. Highly expressed in heart, moderately in liver and skeletal muscles, and expressed at low levels in placenta, lung, kidney, and pancreas. Both transcripts expressed following p53/TP53 induction. The shorter 1.8 kb transcript seems to be the major transcript in EB1 colon cancer cells |
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Provided below are standard protocols that you may find useful for product applications.
Background
Oxidoreductase, which may play a role in mediating a p53/TP53-dependent apoptosis response. Probable oxidoreductase that acts as a caspase-independent mitochondrial effector of apoptotic cell death. Binds to DNA in a sequence-independent manner. May contribute to genotoxin-induced growth arrest.
References
Ohiro Y.,et al.FEBS Lett. 524:163-171(2002).
Wu M.,et al.J. Biol. Chem. 277:25617-25623(2002).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Deloukas P.,et al.Nature 429:375-381(2004).
Mural R.J.,et al.Submitted (JUL-2005) to the EMBL/GenBank/DDBJ databases.
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