Anti-Noxa Pmaip1 Antibody

Apoptosis is related to many diseases and development. The p53 tumor-suppressor protein induces apoptosis through transcriptional activation of several genes including p53R2, p53AIP1, and PUMA. A new p53 target gene, Noxa, was recently identified, which encodes a protein belonging to the subfamily of BH3-only proapoptic proteins. Noxa and PUMA are both transcriptional targets of p53 and BH3-only proteins. X-ray irradiation increased p53-dependent Noxa mRNA and protein levels. Noxa, when ectopically expressed, interacted with anti-apoptotic Bcl-2 family members, resulting in the activation of caspase-9. Noxa, like PUMA, localized to mitochondria and induces apoptosis in response to p53. Noxa and PUMA may represent direct mediators of p53-induced apoptosis. Increased levels of p53 and its target gene Noxa was found in the impaired tumor development.

Noxa antibody was raised against a synthetic peptide corresponding to 17 amino acids at the amino terminus of mouse Noxa. The immunogen is located within the first 50 amino acids of Noxa.

Detected in thymocytes after irradiation with X-rays. Not detectable in untreated thymocytes (at protein level) . Detected in embryonic neural precursor cells of the telencephalon Constitutively expressed at low levels in adult brain, testis, thymus, spleen, lung and kidney.

Promotes activation of caspases and apoptosis. Promotes mitochondrial membrane changes and efflux of apoptogenic proteins from the mitochondria. Contributes to p53/TP53-dependent apoptosis after radiation exposure. Promotes proteasomal degradation of MCL1. Competes with BIM/BCL2L11 for binding to MCL1 and can displace BIM/BCL2L11 from its binding site on MCL1 (By similarity) . Competes with BAK1 for binding to MCL1 and can displace BAK1 from its binding site on MCL1.

Noxa antibody can be stored at 4°C for three months and -20°C, stable for up to one year. Avoid repeated freeze-thaw cycles. Antibodies should not be exposed to prolonged high temperatures.