Anti-BNIP3 Antibody

At -20°C for one year. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for a longer time.Avoid repeated freezing and thawing.

BNIP3

The Bcl-2 nineteen kilodalton interacting protein 3(BNIP3 or NIP3), is a hypoxia-inducible proapoptotic member of the Bcl-2 family that induces cell death by associating with the mitochondria. BNIP3, expressed in skeletal muscle and in the brain at low levels, is primarily localized to the nucleus of glial cells of the normal human brain, as well as in the malignant glioma cell line U251. BNIP3 expression in the cytoplasm increases and localizes with the mitochondria, contributing to induction of cell death. Cellular protein BNIP3 interacts with E1B-19K, BCL-2, BCL-xL, and EBV-BHRF1. BNIP3 contains Bcl-2 homology 3(BH3) domain and COOH-terminal transmembrane(TM) domain. The BH3 domain of BNIP3 mediates Bcl-2/Bcl-X(L) heterodimerization and confers pro-apoptotic activity; whereas the TM domain is critical for homodimerization, pro-apoptotic function, and mitochondrial targeting.

Each vial contains 5 mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05 mg Thimerosal, 0.05 mg NaN3.

Add 0.2 ml of distilled water will yield a concentration of 500 ug/ml.

|cell biology|apoptosis|intracellular|bcl2 family| microbiology|interspecies interaction|host virus interaction| cell biology|mitochondrial| cardiovascular|heart| cancer|cancer metabolism|response to hypoxia| metabolism|pathways and processes|mitochondrial metabolism|mitochondrial markers|metabolism processes|types of disease|cell death

Apoptosis-inducing protein that can overcome BCL2 suppression. May play a role in repartitioning calcium between the two major intracellular calcium stores in association with BCL2. Involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, participates to mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. The physical interaction of SPATA18/MIEAP, BNIP3 and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane in order to mediate the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix. Plays an important role in the calprotectin (S100A8/A9)-induced cell death pathway.

Hamster