BNIP3 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3; NIP3) is an atypical BH3-only member of the BCL-2 family and the paralog of BNIP3L/NIX. It is a tail-anchored membrane protein with a C-terminal transmembrane helix that inserts it into the mitochondrial outer membrane and also the endoplasmic reticulum; the same helix drives stable homodimerization. Its N-terminal cytosolic region contains an LC3-interacting region (LIR), through which BNIP3 binds Atg8-family proteins and acts as a selective autophagy receptor that delivers mitochondria (mitophagy) and ER (ER-phagy) to autophagosomes. BNIP3 is strongly induced by hypoxia through HIF-1. Together with NIX it is required for hypoxia-induced autophagy, partly because its atypical BH3 domain releases Beclin 1 from BCL-2. BNIP3 also takes part in Mieap/SPATA18-dependent intramitochondrial quality control (MALM) and inhibits OPA1-mediated fusion. When overexpressed or under some stresses it promotes cell death, typically necrosis-like death through opening of the permeability transition pore and loss of membrane potential rather than classical cytochrome c/caspase apoptosis. Basal BNIP3 levels are kept low by SCF(FBXL4)/PPTC7-dependent ubiquitination and proteasomal turnover.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000422 autophagy of mitochondrion | NAS PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 is an LC3-binding autophagy receptor that targets mitochondria (and ER) for autophagic removal; LIR mutation reduces mitophagy. Reason: Core function; well supported by PMID:22505714. Supporting Evidence: PMID:22505714 Our data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0000423 mitophagy | IBA GO_REF:0000033 | ACCEPT | Summary: BNIP3 mediates selective autophagy of mitochondria as an LC3-binding receptor. Reason: Core process. Supporting Evidence: PMID:22505714 Our data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0000423 mitophagy | IMP PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 mediates selective autophagy of mitochondria as an LC3-binding receptor. Reason: Core process. Supporting Evidence: PMID:22505714 Our data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0001666 response to hypoxia | IEA GO_REF:0000107 | ACCEPT | Summary: BNIP3 is induced by HIF under hypoxia and mediates hypoxia-induced autophagy. Reason: Well-supported effector role in the hypoxia response. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy |
| GO:0001666 response to hypoxia | ISS GO_REF:0000024 | ACCEPT | Summary: BNIP3 is induced by HIF under hypoxia and mediates hypoxia-induced autophagy. Reason: Well-supported effector role in the hypoxia response. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy |
| GO:0005515 protein binding | IPI PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:15868100 Membrane translocation and oligomerization of hBok are trigg... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:16189514 Towards a proteome-scale map of the human protein-protein in... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:16189514 Towards a proteome-scale map of the human protein-protein in... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:17360363 Legionella pneumophila inhibits macrophage apoptosis by targ... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:18371312 Acetyl-Coenzyme A acyltransferase 2 attenuates the apoptotic... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:19060904 An empirical framework for binary interactome mapping. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:21516116 Next-generation sequencing to generate interactome datasets. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:22292033 BNIP3 and NIX mediate Mieap-induced accumulation of lysosoma... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:24981860 Human-chromatin-related protein interactions identify a deme... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:27107012 Pooled-matrix protein interaction screens using Barcode Fusi... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:27107012 Pooled-matrix protein interaction screens using Barcode Fusi... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:27499296 Mitochondrial Protein Interaction Mapping Identifies Regulat... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:28514442 Architecture of the human interactome defines protein commun... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:28514442 Architecture of the human interactome defines protein commun... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:28514442 Architecture of the human interactome defines protein commun... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:39526800 A comprehensive two-hybrid analysis to explore the Legionell... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:7954800 Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a com... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005515 protein binding | IPI PMID:7954800 Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a com... | REMOVE | Summary: Protein-protein interaction (e.g. with BNIP3L, BCL2/E1B-19K, OPA1, SPATA18, ACAA2, BOK, PPTC7, TMEM11, or high-throughput yeast two-hybrid partners). Reason: Generic protein binding is uninformative. The functionally informative activities of BNIP3 are captured by GO:0140580, GO:0140506 and GO:0042803. Removal does not imply the interactions are false. |
| GO:0005634 nucleus | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: A nuclear pool of BNIP3 has been reported in some cell types. Reason: Minor, cell-type-specific location; not the site of the core function. |
| GO:0005634 nucleus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: A nuclear pool of BNIP3 has been reported in some cell types. Reason: Minor, cell-type-specific location; not the site of the core function. |
| GO:0005634 nucleus | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: A nuclear pool of BNIP3 has been reported in some cell types. Reason: Minor, cell-type-specific location; not the site of the core function. |
| GO:0005635 nuclear envelope | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Nuclear-envelope localization has been reported for BNIP3 (contiguous with ER). Reason: Minor location, consistent with ER/nuclear envelope continuity. |
| GO:0005635 nuclear envelope | IDA PMID:7954800 Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a com... | KEEP AS NON CORE | Summary: Nuclear-envelope localization has been reported for BNIP3 (contiguous with ER). Reason: Minor location, consistent with ER/nuclear envelope continuity. |
| GO:0005654 nucleoplasm | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: A nuclear pool of BNIP3 has been reported in some cell types (e.g. glioma), transferred by orthology. Reason: Minor, cell-type-specific location; not the site of the core function. |
| GO:0005654 nucleoplasm | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: A nuclear pool of BNIP3 has been reported in some cell types (e.g. glioma), transferred by orthology. Reason: Minor, cell-type-specific location; not the site of the core function. |
| GO:0005737 cytoplasm | IEA GO_REF:0000107 | ACCEPT | Summary: BNIP3 is a cytoplasmic organelle-membrane protein (mitochondria and ER). The term is broad but correct. Reason: Correct, broad location. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). |
| GO:0005737 cytoplasm | ISS GO_REF:0000024 | ACCEPT | Summary: BNIP3 is a cytoplasmic organelle-membrane protein (mitochondria and ER). The term is broad but correct. Reason: Correct, broad location. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). |
| GO:0005739 mitochondrion | HTP PMID:34800366 Quantitative high-confidence human mitochondrial proteome an... | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005739 mitochondrion | IDA PMID:18371312 Acetyl-Coenzyme A acyltransferase 2 attenuates the apoptotic... | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005739 mitochondrion | IDA PMID:7954800 Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a com... | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005739 mitochondrion | IDA PMID:9396766 The E1B 19K/Bcl-2-binding protein Nip3 is a dimeric mitochon... | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005739 mitochondrion | IEA GO_REF:0000120 | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005739 mitochondrion | TAS PMID:9973195 BNIP3alpha: a human homolog of mitochondrial proapoptotic pr... | ACCEPT | Summary: BNIP3 is a mitochondrial protein. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:9396766 Nip3 is expressed in mitochondria and a mutant (Nip3(163)) lacking the putative transmembrane domain and COOH terminus does not dimerize or localize to mitochondria. |
| GO:0005740 mitochondrial envelope | IEA GO_REF:0000002 | ACCEPT | Summary: InterPro-based mitochondrial envelope location; correct but less specific than mitochondrial outer membrane. Reason: Correct, less specific. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005741 mitochondrial outer membrane | IBA GO_REF:0000033 | ACCEPT | Summary: BNIP3 is a tail-anchored mitochondrial outer-membrane protein with its N terminus (containing the LIR) facing the cytosol. Reason: Primary functional location. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005741 mitochondrial outer membrane | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | ACCEPT | Summary: BNIP3 is a tail-anchored mitochondrial outer-membrane protein with its N terminus (containing the LIR) facing the cytosol. Reason: Primary functional location. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005741 mitochondrial outer membrane | IDA PMID:22292033 BNIP3 and NIX mediate Mieap-induced accumulation of lysosoma... | ACCEPT | Summary: BNIP3 is a tail-anchored mitochondrial outer-membrane protein with its N terminus (containing the LIR) facing the cytosol. Reason: Primary functional location. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005741 mitochondrial outer membrane | IDA PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 is a tail-anchored mitochondrial outer-membrane protein with its N terminus (containing the LIR) facing the cytosol. Reason: Primary functional location. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005741 mitochondrial outer membrane | IEA GO_REF:0000044 | ACCEPT | Summary: BNIP3 is a tail-anchored mitochondrial outer-membrane protein with its N terminus (containing the LIR) facing the cytosol. Reason: Primary functional location. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0005783 endoplasmic reticulum | IBA GO_REF:0000033 | ACCEPT | Summary: Endogenous BNIP3 localizes to the ER as well as mitochondria, and ER-targeted BNIP3 induces ER-phagy. Reason: Supported by direct evidence (PMID:22505714) and the IBA. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). |
| GO:0005783 endoplasmic reticulum | NAS PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: Endogenous BNIP3 localizes to the ER as well as mitochondria, and ER-targeted BNIP3 induces ER-phagy. Reason: Supported by direct evidence (PMID:22505714) and the IBA. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). |
| GO:0005789 endoplasmic reticulum membrane | IBA GO_REF:0000033 | ACCEPT | Summary: BNIP3 is a tail-anchored protein that inserts into the ER membrane as well as the mitochondrial outer membrane. Reason: Supported by direct evidence (PMID:22505714) and the IBA. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). PMID:22505714 We also discovered that Bnip3 induced removal of both ER (ERphagy) and mitochondria (mitophagy) via autophagy. |
| GO:0005789 endoplasmic reticulum membrane | IDA PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 is a tail-anchored protein that inserts into the ER membrane as well as the mitochondrial outer membrane. Reason: Supported by direct evidence (PMID:22505714) and the IBA. Supporting Evidence: PMID:22505714 In addition, we discovered that endogenous Bnip3 is localized to both mitochondria and the endoplasmic reticulum (ER). PMID:22505714 We also discovered that Bnip3 induced removal of both ER (ERphagy) and mitochondria (mitophagy) via autophagy. |
| GO:0010508 positive regulation of autophagy | TAS PMID:18309324 No death without life: vital functions of apoptotic effector... | ACCEPT | Summary: BNIP3 promotes autophagy (via its atypical BH3 domain releasing Beclin1 from Bcl-2, and as an autophagy receptor). Reason: Well supported by PMID:19273585 and PMID:22505714. Supporting Evidence: PMID:19273585 Herein, we propose a model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death. PMID:18309324 These results corroborate the conjecture that any kind of protein that has previously been specifically implicated in apoptosis might have a phylogenetically conserved apoptosis-unrelated function, most likely as part of an adaptive response to cellular stress. |
| GO:0010637 negative regulation of mitochondrial fusion | IDA PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: BNIP3 binding to OPA1 inhibits OPA1-mediated mitochondrial fusion. Reason: Experimental and mechanistically specific, but secondary to the receptor role. Supporting Evidence: PMID:20436456 Fission is due to inhibition of Opa1-mediated fusion and is counteracted by Opa1 in an Mfn1-dependent manner. |
| GO:0010659 cardiac muscle cell apoptotic process | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: BNIP3 is a hypoxia-induced pro-death factor in cardiomyocytes (ortholog transfer from rodent data). Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0010666 positive regulation of cardiac muscle cell apoptotic process | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Ortholog-transferred pro-death role in cardiomyocytes. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. |
| GO:0010917 negative regulation of mitochondrial membrane potential | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: BNIP3 suppresses mitochondrial membrane potential via PT pore opening. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:10891486 These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. |
| GO:0014069 postsynaptic density | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred postsynaptic density localization. Reason: BNIP3 is a mitochondrial/ER membrane protein; there is no evidence that it is a PSD component. |
| GO:0016020 membrane | IEA GO_REF:0000002 | ACCEPT | Summary: BNIP3 is an integral membrane protein (C-terminal TM). Reason: Correct, broad location. |
| GO:0016239 positive regulation of macroautophagy | IGI PMID:19273585 Hypoxia-induced autophagy is mediated through hypoxia-induci... | ACCEPT | Summary: Ectopic BNIP3/BNIP3L activates autophagy in normoxia, and their combined loss suppresses hypoxic autophagy. Reason: Directly supported. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy PMID:19273585 Herein, we propose a model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death. |
| GO:0021987 cerebral cortex development | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred developmental process. Reason: Ortholog-transferred developmental process. BNIP3 has no established direct role in this developmental program; any phenotype is most plausibly secondary to its effects on mitochondrial turnover and cell death. |
| GO:0030425 dendrite | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Ortholog-transferred dendrite localization (rodent neurons), probably reflecting mitochondria and ER in dendrites. Reason: Plausible cell-type-specific location, not informative about the core function. |
| GO:0030425 dendrite | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Ortholog-transferred dendrite localization (rodent neurons), probably reflecting mitochondria and ER in dendrites. Reason: Plausible cell-type-specific location, not informative about the core function. |
| GO:0031966 mitochondrial membrane | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | ACCEPT | Summary: BNIP3 integrates into mitochondrial membranes; more specifically the outer membrane. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0031966 mitochondrial membrane | IEA GO_REF:0000107 | ACCEPT | Summary: BNIP3 integrates into mitochondrial membranes; more specifically the outer membrane. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0031966 mitochondrial membrane | IMP PMID:9396766 The E1B 19K/Bcl-2-binding protein Nip3 is a dimeric mitochon... | ACCEPT | Summary: BNIP3 integrates into mitochondrial membranes; more specifically the outer membrane. Reason: Correct; GO:0005741 is more specific. Supporting Evidence: PMID:10891486 We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. |
| GO:0035694 mitochondrial protein catabolic process | IMP PMID:22292033 BNIP3 and NIX mediate Mieap-induced accumulation of lysosoma... | KEEP AS NON CORE | Summary: BNIP3, with NIX and Mieap/SPATA18, mediates MALM (accumulation of lysosomal proteins within mitochondria to eliminate oxidized proteins); knockdown inhibits MALM. Reason: Genuine, distinct mitochondrial quality-control function, but less established than receptor-mediated mitophagy. Supporting Evidence: PMID:22292033 BNIP3 interacts with Mieap in a reactive oxygen species (ROS)-dependent manner via the BH3 domain of BNIP3 and the coiled-coil domains of Mieap. The knockdown of endogenous BNIP3 expression severely inhibited MALM. PMID:22292033 These results suggest that two mitochondrial outer membrane proteins, BNIP3 and NIX, mediate MALM in order to maintain mitochondrial integrity. |
| GO:0042802 identical protein binding | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042802 identical protein binding | IPI PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042802 identical protein binding | IPI PMID:16189514 Towards a proteome-scale map of the human protein-protein in... | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042802 identical protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042802 identical protein binding | IPI PMID:27107012 Pooled-matrix protein interaction screens using Barcode Fusi... | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042802 identical protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Summary: BNIP3 forms stable homodimers through its C-terminal transmembrane helix (GxxxG-type packing). Homodimerization is required for both its pro-death and its autophagy-inducing activities. Reason: Self-association is real and functionally important, but it is a structural property, not the core activity. The more specific protein homodimerization activity is also annotated. Supporting Evidence: PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. |
| GO:0042803 protein homodimerization activity | IDA PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | ACCEPT | Summary: BNIP3 homodimerizes through its transmembrane domain; dimerization is required for mitochondrial targeting, pro-death activity and induction of autophagy. Reason: Directly shown and functionally required. Supporting Evidence: PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. |
| GO:0042803 protein homodimerization activity | IDA PMID:9396766 The E1B 19K/Bcl-2-binding protein Nip3 is a dimeric mitochon... | ACCEPT | Summary: BNIP3 homodimerizes through its transmembrane domain; dimerization is required for mitochondrial targeting, pro-death activity and induction of autophagy. Reason: Directly shown and functionally required. Supporting Evidence: PMID:9396766 Nip3 is detected as both a 60- and 30-kD protein in vivo and in vitro and exhibits strong homologous interaction in a yeast two-hybrid system indicating that it can homodimerize. PMID:22505714 Bnip3 contains a C-terminal transmembrane domain that is essential for homodimerization and proapoptotic function. In this study, we show that homodimerization of Bnip3 is also a requirement for induction of autophagy. |
| GO:0043065 positive regulation of apoptotic process | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: BNIP3 overexpression induces cell death, and BNIP3 was identified as a pro-apoptotic BCL-2-family protein. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:9396766 In conclusion, Nip3 is an apoptosis-inducing dimeric mitochondrial protein that can overcome Bcl-2 suppression. PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0043065 positive regulation of apoptotic process | IDA PMID:10381623 A novel adenovirus E1B19K-binding protein B5 inhibits apopto... | KEEP AS NON CORE | Summary: BNIP3 overexpression induces cell death, and BNIP3 was identified as a pro-apoptotic BCL-2-family protein. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:9396766 In conclusion, Nip3 is an apoptosis-inducing dimeric mitochondrial protein that can overcome Bcl-2 suppression. PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0043065 positive regulation of apoptotic process | IDA PMID:9973195 BNIP3alpha: a human homolog of mitochondrial proapoptotic pr... | KEEP AS NON CORE | Summary: BNIP3 overexpression induces cell death, and BNIP3 was identified as a pro-apoptotic BCL-2-family protein. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:9396766 In conclusion, Nip3 is an apoptosis-inducing dimeric mitochondrial protein that can overcome Bcl-2 suppression. PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0043065 positive regulation of apoptotic process | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: BNIP3 overexpression induces cell death, and BNIP3 was identified as a pro-apoptotic BCL-2-family protein. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:9396766 In conclusion, Nip3 is an apoptosis-inducing dimeric mitochondrial protein that can overcome Bcl-2 suppression. PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0043066 negative regulation of apoptotic process | TAS PMID:7954800 Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a com... | MARK AS OVER ANNOTATED | Summary: The cited 1994 paper identified Nip3 as a protein that interacts with E1B 19K and Bcl-2. The anti-apoptotic activity is that of E1B 19K/Bcl-2, not BNIP3. Reason: BNIP3 is itself pro-death (PMID:9396766). Its pro-survival effect under hypoxia goes through autophagy and is captured by GO:0043069 (IGI). The cited reference does not support BNIP3 as a negative regulator of apoptosis. Supporting Evidence: PMID:7954800 Our results suggest that two diverse proteins, the E1B 19 kDa and the Bcl-2 proteins, promote cell survival through interaction with a common set of cellular proteins. PMID:9396766 In conclusion, Nip3 is an apoptosis-inducing dimeric mitochondrial protein that can overcome Bcl-2 suppression. |
| GO:0043068 positive regulation of programmed cell death | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | KEEP AS NON CORE | Summary: BNIP3 mediates necrosis-like cell death via PT pore opening. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. |
| GO:0043069 negative regulation of programmed cell death | IGI PMID:19273585 Hypoxia-induced autophagy is mediated through hypoxia-induci... | KEEP AS NON CORE | Summary: Under hypoxia, BNIP3/BNIP3L-induced autophagy is pro-survival, and ablating them triggers cell death. Reason: Supported by genetic evidence; cell-fate roles are context-dependent and secondary. Supporting Evidence: PMID:19273585 In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. |
| GO:0043243 positive regulation of protein-containing complex disassembly | IDA PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: BNIP3-OPA1 interaction triggers disruption of OPA1 complexes. Reason: Experimentally supported mechanistic detail; secondary. Supporting Evidence: PMID:20436456 Bnip3-Opa1 interaction is necessary to trigger Opa1 complex disruption in a Bax- and/or Bak-dependent manner, ultimately leading to apoptosis. |
| GO:0043653 mitochondrial fragmentation involved in apoptotic process | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: BNIP3 promotes mitochondrial fragmentation by inhibiting OPA1-mediated fusion, associated with apoptosis. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:20436456 We show that Bnip3 interacts with Opa1, leading to mitochondrial fragmentation and apoptosis. PMID:20436456 Fission is due to inhibition of Opa1-mediated fusion and is counteracted by Opa1 in an Mfn1-dependent manner. |
| GO:0043653 mitochondrial fragmentation involved in apoptotic process | IDA PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: BNIP3 promotes mitochondrial fragmentation by inhibiting OPA1-mediated fusion, associated with apoptosis. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:20436456 We show that Bnip3 interacts with Opa1, leading to mitochondrial fragmentation and apoptosis. PMID:20436456 Fission is due to inhibition of Opa1-mediated fusion and is counteracted by Opa1 in an Mfn1-dependent manner. |
| GO:0045837 negative regulation of membrane potential | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | MODIFY | Summary: BNIP3 expression causes suppression of the mitochondrial inner-membrane potential through PT-pore opening. Reason: The effect is specifically on mitochondrial membrane potential, so the mitochondrial term is more precise. It is a secondary, death-associated effect. Proposed replacements: negative regulation of mitochondrial membrane potential Supporting Evidence: PMID:10891486 These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. |
| GO:0046902 regulation of mitochondrial membrane permeability | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | KEEP AS NON CORE | Summary: BNIP3 promotes opening of the mitochondrial permeability transition pore. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:10891486 These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. |
| GO:0048102 autophagic cell death | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: BNIP3 has historically been linked to "autophagic cell death", but direct human-cell studies show BNIP3-induced death is necrosis-like (PT pore opening), and BNIP3-driven hypoxic autophagy is protective. Reason: Electronic ortholog transfer of a contested process concept. The evidence supports BNIP3 promoting autophagy and, separately, necrosis-like death. It does not show that autophagy is the means by which cells die. Supporting Evidence: PMID:10891486 We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. PMID:19273585 Herein, we propose a model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death. |
| GO:0048678 response to axon injury | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred response to axon injury. Reason: This is an ortholog transfer (Ensembl Compara) of a rodent annotation that most likely rests on altered BNIP3 expression or phenotype under this stimulus. BNIP3 is a hypoxia/HIF-responsive gene, and a stress-induced change in its level does not show that it performs part of a dedicated response to this stimulus. |
| GO:0048709 oligodendrocyte differentiation | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred developmental process. Reason: Ortholog-transferred developmental process. BNIP3 has no established direct role in this developmental program; any phenotype is most plausibly secondary to its effects on mitochondrial turnover and cell death. |
| GO:0051020 GTPase binding | IPI PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: BNIP3 binds the inner-membrane dynamin-like GTPase OPA1, which leads to OPA1 complex disruption, mitochondrial fragmentation and apoptosis. Reason: Experimentally supported interaction with a GTPase (OPA1), informative about the fragmentation/apoptosis mechanism but secondary to the receptor function. Supporting Evidence: PMID:20436456 We show that Bnip3 interacts with Opa1, leading to mitochondrial fragmentation and apoptosis. |
| GO:0051402 neuron apoptotic process | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: BNIP3 contributes to hypoxic/ischemic neuronal death (ortholog transfer). Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. |
| GO:0051402 neuron apoptotic process | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: BNIP3 contributes to hypoxic/ischemic neuronal death (ortholog transfer). Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. |
| GO:0051561 positive regulation of mitochondrial calcium ion concentration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: BNIP3 has been linked to ER-to-mitochondria Ca2+ repartitioning (ortholog transfer). Reason: Plausible secondary role; not core. |
| GO:0051607 defense response to virus | IDA PMID:9973195 BNIP3alpha: a human homolog of mitochondrial proapoptotic pr... | UNDECIDED | Summary: The cited paper characterizes BNIP3alpha (BNIP3L) and describes BNIP3 as a pro-apoptotic protein targeted by viral anti-apoptotic proteins (E1B-19K, BHRF1). Reason: Binding by viral anti-apoptotic proteins makes BNIP3 a viral target, not a defence effector, and the abstract shows no antiviral activity. Only the abstract is available, so I cannot see what the curator relied on. Supporting Evidence: PMID:9973195 Cellular protein BNIP3 is a BCL-2 family proapoptotic protein that interacts with viral antiapoptosis proteins such as adenoviruses E1B-19K and EBV-BHRF1 and cellular antiapoptosis proteins such as BCL-2 and BCL-xL. |
| GO:0055093 response to hyperoxia | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred response to hyperoxia. Reason: This is an ortholog transfer (Ensembl Compara) of a rodent annotation that most likely rests on altered BNIP3 expression or phenotype under this stimulus. BNIP3 is a hypoxia/HIF-responsive gene, and a stress-induced change in its level does not show that it performs part of a dedicated response to this stimulus. |
| GO:0061709 reticulophagy | IBA GO_REF:0000033 | ACCEPT | Summary: BNIP3 mediates selective autophagy of the ER (ER-phagy) as an LC3-binding receptor; LIR mutation reduces ER-phagy. Reason: Directly supported by PMID:22505714 and the IBA. Supporting Evidence: PMID:22505714 We also discovered that Bnip3 induced removal of both ER (ERphagy) and mitochondria (mitophagy) via autophagy. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0061709 reticulophagy | IMP PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 mediates selective autophagy of the ER (ER-phagy) as an LC3-binding receptor; LIR mutation reduces ER-phagy. Reason: Directly supported by PMID:22505714 and the IBA. Supporting Evidence: PMID:22505714 We also discovered that Bnip3 induced removal of both ER (ERphagy) and mitochondria (mitophagy) via autophagy. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0061753 obsolete substrate localization to autophagosome | IEA GO_REF:0000108 | REMOVE | Summary: Logical-inference IEA to a term that GOA labels obsolete ("obsolete substrate localization to autophagosome"). Reason: GOA marks the term obsolete. The underlying biology (BNIP3 delivering mitochondria and ER to autophagosomes) is captured by GO:0140580, GO:0140506, GO:0000423 and GO:0061709. |
| GO:0070301 cellular response to hydrogen peroxide | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred response to hydrogen peroxide. Reason: This is an ortholog transfer (Ensembl Compara) of a rodent annotation that most likely rests on altered BNIP3 expression or phenotype under this stimulus. BNIP3 is a hypoxia/HIF-responsive gene, and a stress-induced change in its level does not show that it performs part of a dedicated response to this stimulus. |
| GO:0071260 cellular response to mechanical stimulus | IEP PMID:19593445 Expression of the Bcl-2 protein BAD promotes prostate cancer... | UNDECIDED | Summary: The cited paper is about BAD in prostate cancer growth; BNIP3 is not mentioned in the cached text. Reason: I could not find the evidence for a BNIP3 response to a mechanical stimulus in the cached text. It may be in supplementary data, so I do not overrule the curator, but the annotation cannot be verified. |
| GO:0071279 cellular response to cobalt ion | IMP PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | MARK AS OVER ANNOTATED | Summary: Cobalt chloride was used as a chemical hypoxia mimetic to induce BNIP3 expression in the OPA1 study. Reason: Cobalt here is a stand-in for hypoxia (HIF stabilization). The relevant biology is captured by cellular response to hypoxia, and BNIP3 has no cobalt-specific role. Supporting Evidence: PMID:20436456 We show that Bnip3 interacts with Opa1, leading to mitochondrial fragmentation and apoptosis. |
| GO:0071456 cellular response to hypoxia | IEA GO_REF:0000107 | ACCEPT | Summary: BNIP3 is a HIF target, and together with BNIP3L it is required for hypoxia-induced autophagy; it also mediates hypoxia-associated mitochondrial fragmentation. Reason: BNIP3 is a key effector of the cellular response to hypoxia (induction by HIF; required, with NIX, for hypoxic autophagy), so this is a well-supported process annotation. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy PMID:19273585 In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. |
| GO:0071456 cellular response to hypoxia | IGI PMID:19273585 Hypoxia-induced autophagy is mediated through hypoxia-induci... | ACCEPT | Summary: BNIP3 is a HIF target, and together with BNIP3L it is required for hypoxia-induced autophagy; it also mediates hypoxia-associated mitochondrial fragmentation. Reason: BNIP3 is a key effector of the cellular response to hypoxia (induction by HIF; required, with NIX, for hypoxic autophagy), so this is a well-supported process annotation. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy PMID:19273585 In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. |
| GO:0071456 cellular response to hypoxia | IMP PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | ACCEPT | Summary: BNIP3 is a HIF target, and together with BNIP3L it is required for hypoxia-induced autophagy; it also mediates hypoxia-associated mitochondrial fragmentation. Reason: BNIP3 is a key effector of the cellular response to hypoxia (induction by HIF; required, with NIX, for hypoxic autophagy), so this is a well-supported process annotation. Supporting Evidence: PMID:19273585 the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy PMID:19273585 In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. |
| GO:0072593 reactive oxygen species metabolic process | IDA PMID:10891486 BNIP3 and genetic control of necrosis-like cell death throug... | MARK AS OVER ANNOTATED | Summary: BNIP3 expression increases ROS production as part of the mitochondrial dysfunction it induces. Reason: Increased ROS is a downstream consequence of mitochondrial damage, not participation in ROS metabolism. Supporting Evidence: PMID:10891486 These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. |
| GO:0090141 positive regulation of mitochondrial fission | IDA PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | MARK AS OVER ANNOTATED | Summary: BNIP3 causes mitochondrial fragmentation, but the cited study attributes it to inhibition of OPA1-mediated fusion rather than to promotion of fission. Reason: The mechanism reported is anti-fusion (captured by GO:0010637), so a positive-regulation-of-fission annotation misdescribes it. Supporting Evidence: PMID:20436456 Fission is due to inhibition of Opa1-mediated fusion and is counteracted by Opa1 in an Mfn1-dependent manner. |
| GO:0090200 positive regulation of release of cytochrome c from mitochondria | IDA PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: In the OPA1 study, BNIP3 promoted cytochrome c release and apoptosis. Reason: Experimental but context-dependent. Other studies find BNIP3-induced death independent of cytochrome c release. Supporting Evidence: PMID:20436456 Bnip3-Opa1 interaction is necessary to trigger Opa1 complex disruption in a Bax- and/or Bak-dependent manner, ultimately leading to apoptosis. PMID:10891486 Surprisingly, BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. |
| GO:0090649 response to oxygen-glucose deprivation | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred response to oxygen-glucose deprivation. Reason: This is an ortholog transfer (Ensembl Compara) of a rodent annotation that most likely rests on altered BNIP3 expression or phenotype under this stimulus. BNIP3 is a hypoxia/HIF-responsive gene, and a stress-induced change in its level does not show that it performs part of a dedicated response to this stimulus. |
| GO:0097345 mitochondrial outer membrane permeabilization | IDA PMID:18371312 Acetyl-Coenzyme A acyltransferase 2 attenuates the apoptotic... | KEEP AS NON CORE | Summary: BNIP3 can promote mitochondrial outer membrane permeabilization and apoptosis, which ACAA2 attenuates. Reason: Experimental, but cell-death roles are secondary and context-dependent, and other studies find BNIP3-induced death independent of cytochrome c release. Supporting Evidence: PMID:18371312 Furthermore, the apoptosis induced by over-expressed BNIP3 via transfection or hypoxia treatment was abolished by ACAA2 in human hepatocellular carcinoma HepG2 cells and osteosarcoma U-2 OS cells. PMID:10891486 Surprisingly, BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. |
| GO:0140506 endoplasmic reticulum-autophagosome adaptor activity | IDA PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: ER-localized BNIP3 binds LC3 to induce ER-phagy; LIR mutation reduces ER-phagy. Reason: Specific receptor activity supported directly by PMID:22505714. Supporting Evidence: PMID:22505714 We also discovered that Bnip3 induced removal of both ER (ERphagy) and mitochondria (mitophagy) via autophagy. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0140507 granzyme-mediated programmed cell death signaling pathway | IDA PMID:9396766 The E1B 19K/Bcl-2-binding protein Nip3 is a dimeric mitochon... | MARK AS OVER ANNOTATED | Summary: Overexpressed Nip3 increased sensitivity to granzyme B-induced apoptosis. Reason: A sensitization effect of overexpression does not show that BNIP3 is a component of the granzyme signalling pathway. Supporting Evidence: PMID:9396766 Nip3 overexpression increases the sensitivity to apoptosis induced by granzyme B and topoisomerase I and II inhibitors. |
| GO:0140580 mitochondrion autophagosome adaptor activity | IBA GO_REF:0000033 | ACCEPT | Summary: BNIP3 in the mitochondrial outer membrane binds LC3 through its N-terminal LIR, linking mitochondria to autophagosomes; LIR mutation reduces mitophagy. Reason: Core molecular function, consistent with the IBA and directly supported by PMID:22505714. Supporting Evidence: PMID:22505714 The clearance of these organelles was mediated in part via binding of Bnip3 to LC3 on the autophagosome. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:0140580 mitochondrion autophagosome adaptor activity | IDA PMID:22505714 Microtubule-associated protein 1 light chain 3 (LC3) interac... | ACCEPT | Summary: BNIP3 in the mitochondrial outer membrane binds LC3 through its N-terminal LIR, linking mitochondria to autophagosomes; LIR mutation reduces mitophagy. Reason: Core molecular function, consistent with the IBA and directly supported by PMID:22505714. Supporting Evidence: PMID:22505714 The clearance of these organelles was mediated in part via binding of Bnip3 to LC3 on the autophagosome. PMID:22505714 Although ablation of the Bnip3-LC3 interaction by mutating the LC3 binding site did not impair the prodeath activity of Bnip3, it significantly reduced both mitophagy and ERphagy. |
| GO:1902109 negative regulation of mitochondrial membrane permeability involved in apoptotic process | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Ortholog-transferred negative regulation of mitochondrial membrane permeability in apoptosis. Reason: The direction conflicts with direct human-cell evidence that BNIP3 promotes PT-pore opening and loss of membrane potential (PMID:10891486). The rodent source may reflect a context-specific finding, but it is not a representative function of BNIP3. Supporting Evidence: PMID:10891486 These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. |
| GO:1903599 positive regulation of autophagy of mitochondrion | IEA GO_REF:0000107 | ACCEPT | Summary: BNIP3 promotes autophagy of mitochondria as a receptor and by promoting PINK1/Parkin-dependent mitophagy. Reason: Consistent with the core function. Supporting Evidence: PMID:22505714 Our data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER. |
| GO:1990144 intrinsic apoptotic signaling pathway in response to hypoxia | IMP PMID:20436456 The BH3-only Bnip3 binds to the dynamin Opa1 to promote mito... | KEEP AS NON CORE | Summary: Hypoxia-induced BNIP3 binds OPA1 and contributes to apoptosis under hypoxia. Reason: BNIP3 regulates cell death in a context-dependent way (often necrosis-like death through the permeability transition pore rather than classical caspase-dependent apoptosis, and sometimes pro-survival through autophagy). This is a genuine but secondary aspect of its biology relative to the conserved Atg8-binding organelle-receptor function. Supporting Evidence: PMID:20436456 Bnip3-Opa1 interaction is necessary to trigger Opa1 complex disruption in a Bax- and/or Bak-dependent manner, ultimately leading to apoptosis. |
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Download this section (compressed HTML)Q: Which signals decide whether BNIP3 drives protective mitophagy/ER-phagy or necrosis-like death, and is the switch set by phosphorylation near the LIR or by its abundance (FBXL4/PPTC7 turnover)?
Q: Is BNIP3-mediated ER-phagy physiologically significant in vivo, or mainly a result of overexpression/ER-targeted constructs?
Experiment: In BNIP3/BNIP3L double-knockout cells, express LIR-mutant, BH3-mutant and TM-dimerization-mutant BNIP3 at endogenous-like levels under hypoxia, and quantify mitophagy (mt-Keima), ER-phagy (ER-Keima) and cell death (PI uptake, PTP opening).
Hypothesis: BNIP3 LIR-dependent mitophagy and its pro-death activity are separable.
Type: structure-function rescue
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