BNIP3L: BNIP3L Protein | BNIP3L Antibody

BNIP3L Background

The deletion of BNIP3L results in retention of mitochondria during lens fiber cell remodeling, and that deletion of BNIP3L also results in the retention of endoplasmic reticulum and Golgi apparatus. BNIP3L localizes to the endoplasmic reticulum and Golgi apparatus of wild-type newborn mouse lenses and is contained within mitochondria, endoplasmic reticulum and Golgi apparatus isolated from adult mouse liver. As the cells become packed with keratin bundles, Bnip3L expression triggers mitophagy to rid the cells of the last remaining 'living' characteristic, thus completing the march from 'living' to 'dead' within the hair follicle. during retinal development tissue hypoxia triggers HIF1A/HIF-1 stabilization, resulting in increased expression of the mitophagy receptor BNIP3L/NIX. BNIP3L-dependent mitophagy results in a metabolic shift toward glycolysis essential for RGC neurogenesis. BNIP3L could be a potential therapeutic target for ischemic stroke

Reference for BNIP3L

  • Brennan LA, et al. (2018) Bnip3l/nix is required for elimination of mitochondria, endoplasmic reticulum and golgi apparatus during eye lens organelle-free zone formation. Exp Eye Res 174(173-184.
  • Jones LA, et al. (2018) The walking dead: Sequential nuclear and organelle destruction during hair development. Br J Dermatol 178(6), 1341-1352.
  • Esteban-Martinez L, et al. (2018) Bnip3l/nix-dependent mitophagy regulates cell differentiation via metabolic reprogramming. Autophagy 14(5), 915-917.
  • Yuan Y, et al. (2017) Bnip3l/nix-mediated mitophagy protects against ischemic brain injury independent of park2. Autophagy 13(10), 1754-1766.
  • Imazu T, et al. (1999) Bcl-2 / E1B 19 kDa-interacting protein 3-like protein (Bnip3L) interacts with bcl-2 / Bcl-xL and induces apoptosis by altering mitochondrial membrane permeability. Oncogene. 18(32): 4523-9.
  • Sun JL, et al. (2004) Expression and structure of BNIP3L in lung cancer. Ai Zheng. 23(1): 8-14.

BNIP3L Protein

BNIP3L protein function

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 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. May function as a tumor suppressor. {ECO:0000269|PubMed:10381623, ECO:0000269|PubMed:21264228}.

BNIP3L protein sequence

This sequence information is just for reference only.From Uniport

  • Length
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BNIP3L Antibody

There are 2 BNIP3L antibodies which are validated in multiple tissues with various applications, including ELISA, WB, IHC-P, IP. There are 2 BNIP3L antibody for ELISA, 1 BNIP3L antibody for WB, 1 BNIP3L antibody for IHC-P, 1 BNIP3L antibody for IP. Among all these BNIP3L antibodies, there are 2 anti-BNIP3L rabbit polyclonal antibodies . All the BNIP3L anbodies are produced in house and all are in stock. BNIP3L antibody customerized service is available.


BNIP3L gene / cDNA is a protein-coding gene which located on 8p21.2. The BNIP3L gene is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, and frog.195 organisms have orthologs with human gene BNIP3L.