BNIP3L
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.
Post-translational modifications
Undergoes progressive proteolysis to an 11 kDa C-terminal fragment, which is blocked by the proteasome inhibitor lactacystin.
Sequence Similarities
Belongs to the NIP3 family.
Cellular localization
- Nucleus envelope
- Endoplasmic reticulum
- Mitochondrion outer membrane
- Membrane
- Single-pass membrane protein
- Colocalizes with SPATA18 at the mitochondrion outer membrane.
Alternative names
BNIP3A, BNIP3H, NIX, BNIP3L, 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