BNIP3
Description
The BNIP3 (BCL2 interacting protein 3) is a protein-coding gene located on chromosome 10.
BNIP3 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3) is a protein involved in both cell death and survival. It belongs to the apoptotic Bcl-2 protein family and regulates mitochondrial permeability by forming oligomers within the mitochondrial membrane. Increased BNIP3 levels lead to decreased mitochondrial potential, increased reactive oxygen species, mitochondrial swelling and fission, and increased mitochondrial turnover via autophagy. While no sequence similarity to Bcl-2 family members has been found, BNIP3 shares a structural similarity with them. The transmembrane domain of BNIP3 can act as an ion channel, suggesting a link between its activity and necrosis-like cell death. Humans and other organisms have multiple BNIP3 paralogues, including human NIP3L, which induces apoptosis through interaction with viral and cellular anti-apoptosis proteins.
BNIP3 is an apoptosis-inducing protein that can overcome the suppression of BCL2. It may play a role in repartitioning calcium between the two major intracellular calcium stores in conjunction with BCL2. BNIP3 interacts with SPATA18/MIEAP, contributing to mitochondrial quality control. In response to mitochondrial damage, BNIP3 participates in the mitochondrial protein catabolic process (MALM), leading to the degradation of damaged proteins within the mitochondria. The interaction between SPATA18/MIEAP, BNIP3, and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane, facilitating the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix. BNIP3 is also involved in the calprotectin (S100A8/A9)-induced cell death pathway.
BNIP3 is also known as HABON, NIP3.
