BNIP3 — BCL2 interacting protein 3
BNIP3 belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
BNIP3's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | Hypoxia metabolic stress Stress | ARG2, ARL4D, AXIN2, CITED4, CNKSR2, GCA, GSTM3, ID3 +13 more | View in SCUBA |
| Endothelial | Lipid Droplet Hypoxia Stress | CEMIP2, CNN3, FCGRT, FGD6, PLIN2, SNTB2, TSPAN4 | View in SCUBA |
| Lymphatic endothelial | Hypoxia HIF Response Stress | AKR1C1, AKR1C2, AKR1C3, ATP1A1, CARHSP1, CSRP2, CTSS, EGLN3 +4 more | View in SCUBA |
| Macrophages | Hypoxia Stress Response Stress | ACE, AMPD3, APP, ASPH, BCAT1, BEX3, BHLHE41, CAPN2 +34 more | View in SCUBA |
About the gene
| Synonyms | HABON, Nip3 |
|---|---|
| Chromosome | 10: 131967684-131981967 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | Cancer-related genes, Predicted membrane proteins, Transporters |
| Biological process | Apoptosis, Host-virus interaction |
Function
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
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.