Product nameMouse AIF Antibody Pair - BSA and Azide free
See all AIF kits
Assay typeELISA set
Range7.81 ng/ml - 500 ng/ml
Species reactivityReacts with: Mouse, Rat, Human
Antibody Pairs – BSA and Azide free include a capture and a detector antibody pair suitable for sandwich ELISA. The Antibody Pair can be used to quantify native and recombinant Mouse AIF.
For additional information on the performance of the antibody pair used in this kit, please see equivalent SimpleStep ELISA® Kit (ab235651), which use the same antibody pair. Both capture and detector antibodies are rabbit monoclonal antibodies delivering consistent, specific, and sensitive results.
Please note that the range provided is only an estimation based on the performance of a related product using the same antibody pair. Performance of the antibody pair will depend on the specific characteristics of your assay.
To receive an electronic copy of the Certificate of Analysis, please send an email with "CoA for matched antibody pair kit" in the subject line and the desired product number and lot number in the body of the email.
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Tested applicationsSuitable for: ELISAmore details
Storage instructionsStore at +4°C. Please refer to protocols.
Components 10 x 96 tests Mouse AIF Capture Antibody 1 x 100µg Mouse AIF Detector Antibody 1 x 100µg
FunctionProbable 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.
Involvement in diseaseDefects 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.
Sequence similaritiesBelongs to the FAD-dependent oxidoreductase family.
modificationsUnder 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.
Cellular localizationMitochondrion intermembrane space. Mitochondrion inner membrane. Cytoplasm. Nucleus. Cytoplasm > perinuclear region. 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.
- Information by UniProt
- Apoptosis inducing factor
Our Abpromise guarantee covers the use of ab244137 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ELISA||Use at an assay dependent concentration.|
ab244137 has not yet been referenced specifically in any publications.