Anti-BNIP3L/Nix Rabbit Monoclonal Antibody

BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like; Adenovirus E1B19K-binding protein B5; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3A; NIP3-like protein X; NIP3L; BNIP3L; BNIP3A, BNIP3H, NIX

In fetal tissues, highly expressed in brain, detectable in lung and liver, but not in kidney. In adult tissues, expressed ubiquitously in the brain, detectable in the heart, liver, spleen, thymus, prostate, testis, ovary, small intestine and colon. The type A isoforms seem to be expressed predominantly in fetal brain whereas type B isoforms are expressed abundantly in both fetal and adult brain. .

Apoptosis, Apoptotic Markers, Cancer, Cardiovascular, Cell Biology, Cell Death, Intracellular, Invasion/Microenvironment, Metabolism, Metabolism Processes, Mitochondrial Metabolism, Oncoproteins/Suppressors, p53 Pathway, Pathways and Processes, Tumor Suppressors

Induces apoptosis. Interacts with viral and cellular anti-apoptosis proteins. Can overcome the suppressors BCL-2 and BCL-XL, although high levels of BCL-XL expression will inhibit apoptosis. Inhibits apoptosis induced by BNIP3. 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. May function as a tumor suppressor. .

Nucleus envelope. Endoplasmic reticulum. Mitochondrion outer membrane. Membrane ; Single-pass membrane protein . Colocalizes with SPATA18 at the mitochondrion outer membrane.