Rabbit Anti-BNIP3 Recombinant Antibody (D7U1T) (CBMAB-CP0012-LY)

Rabbit

Human

D7U1T

IgG

WB, IP, IHC-P, IF (ICC)

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human BNIP3 protein.

Human

IgG

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Liquid

100 µg/ml BSA, 50% glycerol

0.02% sodium azide

> 95% Purity determined by SDS-PAGE.

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

BCL2 interacting protein 3

This gene is encodes a mitochondrial protein that contains a BH3 domain and acts as a pro-apoptotic factor. The encoded protein interacts with anti-apoptotic proteins, including the E1B 19 kDa protein and Bcl2. This gene is silenced in tumors by DNA methylation.

NIP3

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 in 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.

Apoptotic process Source: MGI
Autophagic cell death Source: Ensembl
Autophagy of mitochondrion Source: ParkinsonsUK-UCL
Brown fat cell differentiation Source: Ensembl
Cardiac muscle cell apoptotic process Source: Ensembl
Cell death Source: UniProtKB
Cellular response to cobalt ion Source: BHF-UCL
Cellular response to hydrogen peroxide Source: Ensembl
Cellular response to hypoxia Source: BHF-UCL
Cellular response to mechanical stimulus Source: UniProtKB
Cerebral cortex development Source: Ensembl
Defense response to virus Source: UniProtKB
Granzyme-mediated programmed cell death signaling pathway Source: GO_Central
Intrinsic apoptotic signaling pathway in response to hypoxia Source: BHF-UCL
Mitochondrial fragmentation involved in apoptotic process Source: BHF-UCL
Mitochondrial outer membrane permeabilization Source: UniProtKB
Mitochondrial protein catabolic process Source: UniProtKB
Negative regulation of apoptotic process Source: UniProtKB
Negative regulation of cell death Source: MGI
Negative regulation of membrane potential Source: UniProtKB
Negative regulation of mitochondrial fusion Source: BHF-UCL
Negative regulation of mitochondrial membrane permeability involved in apoptotic process Source: Ensembl
Negative regulation of mitochondrial membrane potential Source: Ensembl
Negative regulation of reactive oxygen species metabolic process Source: Ensembl
Neuron apoptotic process Source: UniProtKB
Oligodendrocyte differentiation Source: Ensembl
Positive regulation of apoptotic process Source: UniProtKB
Positive regulation of autophagy Source: UniProtKB
Positive regulation of autophagy of mitochondrion Source: Ensembl
Positive regulation of cardiac muscle cell apoptotic process Source: Ensembl
Positive regulation of macroautophagy Source: MGI
Positive regulation of mitochondrial calcium ion concentration Source: Ensembl
Positive regulation of mitochondrial fission Source: BHF-UCL
Positive regulation of necrotic cell death Source: Ensembl
Positive regulation of programmed cell death Source: UniProtKB
Positive regulation of protein-containing complex disassembly Source: BHF-UCL
Positive regulation of release of cytochrome c from mitochondria Source: BHF-UCL
Reactive oxygen species metabolic process Source: UniProtKB
Regulation of aerobic respiration Source: Ensembl
Regulation of mitochondrial membrane permeability Source: UniProtKB
Regulation of programmed cell death Source: GO_Central
Response to axon injury Source: Ensembl
Response to bacterium Source: Ensembl
Response to hyperoxia Source: Ensembl
Response to hypoxia Source: UniProtKB
Response to oxygen-glucose deprivation Source: Ensembl
Toxin transport Source: Ensembl
Viral process Source: UniProtKB-KW

Mitochondrion; Mitochondrion outer membrane. Coexpression with the EIB 19-kDa protein results in a shift in NIP3 localization pattern to the nuclear envelope. Colocalizes with ACAA2 in the mitochondria. Colocalizes with SPATA18 at the mitochondrion outer membrane.

Helical: 229-249 aa