MAP1LC3B (LC3B) is a ubiquitin-like protein of the Atg8 family (LC3 subfamily) and the most widely used marker of autophagic membranes. Newly made pro-LC3B is cleaved by ATG4 proteases after Gly120 to give cytosolic LC3B-I, which the E1-like ATG7, the E2-like ATG3 and the ATG12-ATG5-ATG16L1 E3-like complex conjugate to phosphatidylethanolamine on the phagophore, forming membrane-anchored LC3B-II; ATG4 also removes it again. On the phagophore and autophagosome, LC3B promotes membrane expansion and serves as a docking platform: its hydrophobic LIR-docking site binds LC3-interacting region motifs of selective autophagy receptors (for example SQSTM1, PHB2, BNIP3, AMBRA1, TEX264), core autophagy proteins and regulators, coupling cargo capture to the autophagic membrane and supporting mitophagy and ER-phagy. Atg8-family proteins are collectively needed for efficient autophagosome formation and especially for autophagosome-lysosome fusion, where the GABARAP subfamily predominates. LC3B was originally identified as a light chain of microtubule-associated proteins MAP1A/MAP1B and binds microtubules; it also binds ceramide during ceramide-induced lethal mitophagy and stimulates JMY-mediated actin nucleation on autophagic membranes.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000045 autophagosome assembly | IBA GO_REF:0000033 | ACCEPT | Summary: PE-conjugated LC3B decorates the expanding phagophore and promotes its elongation and the efficiency of autophagosome formation. Reason: LC3-subfamily proteins act in phagophore elongation. Atg8 hexa-knockout cells still form autophagosomes, but they are smaller and form more slowly, so LC3B contributes to membrane expansion rather than being strictly required for initiation. Direct participation in assembly is therefore supported, at the expansion step. Supporting Evidence: PMID:20418806 our results indicate that LC3s are involved in elongation of the phagophore membrane whereas the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation PMID:27864321 loss of all Atg8s yields smaller autophagosomes and a slowed initial rate of autophagosome formation PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000045 autophagosome assembly | IDA PMID:21873635 Phylogenetic-based propagation of functional annotations wit... | ACCEPT | Summary: PE-conjugated LC3B decorates the expanding phagophore and promotes its elongation and the efficiency of autophagosome formation. Reason: LC3-subfamily proteins act in phagophore elongation. Atg8 hexa-knockout cells still form autophagosomes, but they are smaller and form more slowly, so LC3B contributes to membrane expansion rather than being strictly required for initiation. Direct participation in assembly is therefore supported, at the expansion step. Supporting Evidence: PMID:20418806 our results indicate that LC3s are involved in elongation of the phagophore membrane whereas the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation PMID:27864321 loss of all Atg8s yields smaller autophagosomes and a slowed initial rate of autophagosome formation PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000045 autophagosome assembly | IDA PMID:37943659 ATM-CHK2-TRIM32 axis regulates ATG7 ubiquitination to initia... | ACCEPT | Summary: PE-conjugated LC3B decorates the expanding phagophore and promotes its elongation and the efficiency of autophagosome formation. Reason: LC3-subfamily proteins act in phagophore elongation. Atg8 hexa-knockout cells still form autophagosomes, but they are smaller and form more slowly, so LC3B contributes to membrane expansion rather than being strictly required for initiation. Direct participation in assembly is therefore supported, at the expansion step. Supporting Evidence: PMID:20418806 our results indicate that LC3s are involved in elongation of the phagophore membrane whereas the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation PMID:27864321 loss of all Atg8s yields smaller autophagosomes and a slowed initial rate of autophagosome formation PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000045 autophagosome assembly | IEA GO_REF:0000117 | ACCEPT | Summary: PE-conjugated LC3B decorates the expanding phagophore and promotes its elongation and the efficiency of autophagosome formation. Reason: LC3-subfamily proteins act in phagophore elongation. Atg8 hexa-knockout cells still form autophagosomes, but they are smaller and form more slowly, so LC3B contributes to membrane expansion rather than being strictly required for initiation. Direct participation in assembly is therefore supported, at the expansion step. Supporting Evidence: PMID:20418806 our results indicate that LC3s are involved in elongation of the phagophore membrane whereas the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation |
| GO:0000421 autophagosome membrane | IBA GO_REF:0000033 | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0000421 autophagosome membrane | IDA PMID:21873635 Phylogenetic-based propagation of functional annotations wit... | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0000421 autophagosome membrane | IDA PMID:33499712 Mammalian BCAS3 and C16orf70 associate with the phagophore a... | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0000421 autophagosome membrane | IEA GO_REF:0000044 | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000421 autophagosome membrane | TAS Reactome:R-HSA-5682388 | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000421 autophagosome membrane | TAS Reactome:R-HSA-8854588 | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000421 autophagosome membrane | TAS Reactome:R-HSA-9687435 | ACCEPT | Summary: LC3B-II is lipid-anchored on both faces of the phagophore and autophagosome membrane. Reason: Canonical location of the PE-conjugated form, shown by many studies and used as the standard autophagosome marker. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0000422 autophagy of mitochondrion | IEA GO_REF:0000117 | ACCEPT | Summary: LC3B on the phagophore binds LIR-containing mitophagy receptors (for example PHB2, AMBRA1, BNIP3, NIX) to engulf mitochondria. Reason: Receptor engagement by LC3 on the forming autophagosome is a direct contribution of LC3B to mitophagy, although GABARAP-subfamily proteins dominate in PINK1/Parkin mitophagy in HeLa cells. Supporting Evidence: PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PMID:25215947 upon mitophagy induction, AMBRA1 binds the autophagosome adapter LC3 through a LIR (LC3 interacting region) motif |
| GO:0000423 mitophagy | IBA GO_REF:0000033 | ACCEPT | Summary: LC3B on the phagophore binds LIR-containing mitophagy receptors (for example PHB2, AMBRA1, BNIP3, NIX) to engulf mitochondria. Reason: Receptor engagement by LC3 on the forming autophagosome is a direct contribution of LC3B to mitophagy, although GABARAP-subfamily proteins dominate in PINK1/Parkin mitophagy in HeLa cells. Supporting Evidence: PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PMID:25215947 upon mitophagy induction, AMBRA1 binds the autophagosome adapter LC3 through a LIR (LC3 interacting region) motif |
| GO:0000423 mitophagy | IDA PMID:28017329 Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Re... | ACCEPT | Summary: LC3B on the phagophore binds LIR-containing mitophagy receptors (for example PHB2, AMBRA1, BNIP3, NIX) to engulf mitochondria. Reason: Receptor engagement by LC3 on the forming autophagosome is a direct contribution of LC3B to mitophagy, although GABARAP-subfamily proteins dominate in PINK1/Parkin mitophagy in HeLa cells. Supporting Evidence: PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PMID:25215947 upon mitophagy induction, AMBRA1 binds the autophagosome adapter LC3 through a LIR (LC3 interacting region) motif |
| GO:0000423 mitophagy | IGI PMID:19279012 Loss of PINK1 function promotes mitophagy through effects on... | ACCEPT | Summary: LC3 knockdown reduced mitophagy-associated mitochondrial fragmentation in PINK1-deficient SH-SY5Y cells. Reason: Genetic interaction data consistent with LC3B acting in mitophagy; the mechanistic basis (LIR-receptor binding on the phagophore) is established by other work. Supporting Evidence: PMID:19279012 RNAi knockdown of autophagy proteins Atg7 and LC3/Atg8 also decreased mitochondrial fragmentation without affecting oxidative stress PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. |
| GO:0005515 protein binding | IPI PMID:15187094 HsAtg4B/HsApg4B/autophagin-1 cleaves the carboxyl termini of... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:15355958 Human light chain 3/MAP1LC3B is cleaved at its carboxyl-term... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16169070 A human protein-protein interaction network: a resource for ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16169070 A human protein-protein interaction network: a resource for ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16169070 A human protein-protein interaction network: a resource for ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16169070 A human protein-protein interaction network: a resource for ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16189514 Towards a proteome-scale map of the human protein-protein in... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16303767 Phosphatidylserine in addition to phosphatidylethanolamine i... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:16303767 Phosphatidylserine in addition to phosphatidylethanolamine i... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:17580304 p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18083104 Homeostatic levels of p62 control cytoplasmic inclusion body... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:18296641 A role for the NAD-dependent deacetylase Sirt1 in the regula... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:19250911 A role for NBR1 in autophagosomal degradation of ubiquitinat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:19250911 A role for NBR1 in autophagosomal degradation of ubiquitinat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:19250911 A role for NBR1 in autophagosomal degradation of ubiquitinat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:19250911 A role for NBR1 in autophagosomal degradation of ubiquitinat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:19322194 The structure of Atg4B-LC3 complex reveals the mechanism of ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20010802 Nix is a selective autophagy receptor for mitochondrial clea... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20010802 Nix is a selective autophagy receptor for mitochondrial clea... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20010802 Nix is a selective autophagy receptor for mitochondrial clea... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20100911 FYCO1 is a Rab7 effector that binds to LC3 and PI3P to media... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20153330 PINK1 is recruited to mitochondria with parkin and associate... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20200478 Nix, a receptor protein for mitophagy in mammals. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20200478 Nix, a receptor protein for mitophagy in mammals. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20417604 The selective macroautophagic degradation of aggregated prot... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20562859 Network organization of the human autophagy system. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:20956295 Autophagy protein microtubule-associated protein 1 light cha... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21617041 Phosphorylation of the autophagy receptor optineurin restric... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:21900206 A directed protein interaction network for investigating int... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22056771 Insights into noncanonical E1 enzyme activation from the str... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22056771 Insights into noncanonical E1 enzyme activation from the str... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22267086 Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22354992 Rab GTPase-activating proteins in autophagy: regulation of e... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22470510 DOR/Tp53inp2 and Tp53inp1 constitute a metazoan gene family ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22470510 DOR/Tp53inp2 and Tp53inp1 constitute a metazoan gene family ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:22948227 MAPK15/ERK8 stimulates autophagy by interacting with LC3 and... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:23459205 Ubiquilin4 is an adaptor protein that recruits Ubiquilin1 to... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:23459205 Ubiquilin4 is an adaptor protein that recruits Ubiquilin1 to... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:23736261 Autolysosomal Ξ²-catenin degradation regulates Wnt-autophagy-... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24089205 Autophagy promotes primary ciliogenesis by removing OFD1 fro... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24290141 Structural basis of the autophagy-related LC3/Atg13 LIR comp... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24290141 Structural basis of the autophagy-related LC3/Atg13 LIR comp... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24668264 Structural determinants in GABARAP required for the selectiv... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24668264 Structural determinants in GABARAP required for the selectiv... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24671035 ULK1 translocates to mitochondria and phosphorylates FUNDC1 ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:24879152 Phosphorylation of NBR1 by GSK3 modulates protein aggregatio... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25215947 AMBRA1 is able to induce mitophagy via LC3 binding, regardle... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25684205 CUL3-KBTBD6/KBTBD7 ubiquitin ligase cooperates with GABARAP ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:25684205 CUL3-KBTBD6/KBTBD7 ubiquitin ligase cooperates with GABARAP ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:26040720 Regulation of endoplasmic reticulum turnover by selective au... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:26040720 Regulation of endoplasmic reticulum turnover by selective au... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:26524528 Autophagy mediates degradation of nuclear lamina. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:26524528 Autophagy mediates degradation of nuclear lamina. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:28017329 Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Re... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:30420355 LC3 and STRAP regulate actin filament assembly by JMY during... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:31006538 Intrinsically Disordered Protein TEX264 Mediates ER-phagy. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:31006538 Intrinsically Disordered Protein TEX264 Mediates ER-phagy. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:31515488 Extensive disruption of protein interactions by genetic vari... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32315611 A DNM2 Centronuclear Myopathy Mutation Reveals a Link betwee... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:33368531 Regulation of autophagosome biogenesis by OFD1-mediated sele... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:33436498 Cytoplasmic short linear motifs in ACE2 and integrin Ξ²(3) li... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:34524948 Global Proximity Interactome of the Human Macroautophagy Pat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:34524948 Global Proximity Interactome of the Human Macroautophagy Pat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:34524948 Global Proximity Interactome of the Human Macroautophagy Pat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:34524948 Global Proximity Interactome of the Human Macroautophagy Pat... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35044719 Proteome-scale mapping of binding sites in the unstructured ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35044719 Proteome-scale mapping of binding sites in the unstructured ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35044719 Proteome-scale mapping of binding sites in the unstructured ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:35932293 Neuronal-specific septin-3 binds Atg8/LC3B, accumulates and ... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:36935496 CLDN6 inhibits breast cancer metastasis through WIP-dependen... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:37219487 Large-scale phosphomimetic screening identifies phospho-modu... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:37219487 Large-scale phosphomimetic screening identifies phospho-modu... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:39009827 Proteome-scale characterisation of motif-based interactome r... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:39009827 Proteome-scale characterisation of motif-based interactome r... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:39009827 Proteome-scale characterisation of motif-based interactome r... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005515 protein binding | IPI PMID:39284914 ER-phagy restrains inflammatory responses through its recept... | REMOVE | Summary: The reported interaction is retained as evidence, but generic protein binding is uninformative. Reason: The cited interaction evidence can inform complex membership, LIR-mediated recruitment or a demonstrated regulatory/adaptor mechanism. Generic protein binding does not identify that function; removing this annotation does not reject the measured interaction or assign an untested mechanism to every interactor. |
| GO:0005543 phospholipid binding | IEA GO_REF:0000117 | ACCEPT | Summary: LC3B is covalently conjugated to phosphatidylethanolamine (and can be conjugated to phosphatidylserine) through its C-terminal glycine. Reason: Broad parent of the phosphatidylethanolamine binding term used for Atg8-family lipidation; correct though less specific. Supporting Evidence: PMID:15355958 Human light chain 3/MAP1LC3B, an autophagosomal ortholog of yeast Atg8, is conjugated to phospholipid (PL) via ubiquitylation-like reactions mediated by human Atg7 and Atg3. |
| GO:0005739 mitochondrion | IDA PMID:25215947 AMBRA1 is able to induce mitophagy via LC3 binding, regardle... | KEEP AS NON CORE | Summary: LC3B is recruited to mitochondria during mitophagy via receptors and ceramide. Reason: Recruitment occurs on the forming autophagosome wrapping mitochondria; mitochondria are not a resident location of LC3B. Supporting Evidence: PMID:25215947 upon mitophagy induction, AMBRA1 binds the autophagosome adapter LC3 through a LIR (LC3 interacting region) motif |
| GO:0005739 mitochondrion | IDA PMID:25244949 Hepatitis C virus core protein suppresses mitophagy by inter... | KEEP AS NON CORE | Summary: LC3B is recruited to mitochondria during mitophagy via receptors and ceramide. Reason: Recruitment occurs on the forming autophagosome wrapping mitochondria; mitochondria are not a resident location of LC3B. Supporting Evidence: PMID:25244949 decreased the number of mitochondria sequestered in isolation membranes |
| GO:0005776 autophagosome | IDA PMID:22948227 MAPK15/ERK8 stimulates autophagy by interacting with LC3 and... | ACCEPT | Summary: LC3B-II is a defining component of autophagosomes. Reason: Well established; LC3B puncta are the standard readout of autophagosomes. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0005776 autophagosome | IDA PMID:28223137 Human CLEC16A regulates autophagy through modulating mTOR ac... | ACCEPT | Summary: LC3B-II is a defining component of autophagosomes. Reason: Well established; LC3B puncta are the standard readout of autophagosomes. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0005776 autophagosome | IEA GO_REF:0000117 | ACCEPT | Summary: LC3B-II is a defining component of autophagosomes. Reason: Well established; LC3B puncta are the standard readout of autophagosomes. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0005776 autophagosome | ISS PMID:12740394 Post-translational modifications of three members of the hum... | ACCEPT | Summary: LC3B-II is a defining component of autophagosomes. Reason: Well established; LC3B puncta are the standard readout of autophagosomes. Supporting Evidence: PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5205649 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5205663 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5678490 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5681987 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5682011 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5682377 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-5682388 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-8959571 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-8959573 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9664855 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9664867 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9664880 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9687109 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9687121 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9687435 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9754775 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9766656 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9766677 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9824892 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005829 cytosol | TAS Reactome:R-HSA-9947387 | ACCEPT | Summary: Unconjugated LC3B-I is cytosolic, where it is processed by ATG4 and conjugated by ATG7 and ATG3. Reason: Correct; the cytosolic LC3-I pool is the substrate of the conjugation cascade represented in Reactome. |
| GO:0005856 cytoskeleton | IEA GO_REF:0000044 | KEEP AS NON CORE | Summary: LC3B was first identified as a light chain associated with microtubule-associated proteins MAP1A/MAP1B and binds microtubules. Reason: Cytoskeletal association is real but peripheral to the autophagy function. |
| GO:0005930 axoneme | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: LC3B is reported in discrete puncta along the ciliary axoneme. Reason: Transferred from mouse and also recorded in UniProt; likely reflects LC3-positive structures linked to ciliogenesis-related autophagy. Not a core location. Supporting Evidence: file:human/MAP1LC3B/MAP1LC3B-uniprot.txt Also localizes to discrete punctae along the ciliary axoneme |
| GO:0006914 autophagy | IDA PMID:23629966 Deacetylation of p53 induces autophagy by suppressing Bmf ex... | ACCEPT | Summary: LC3B is an Atg8-family protein required for autophagy. Reason: Correct general process; the cited study used LC3 conversion as an autophagy readout, which is consistent with LC3B being an autophagy component. Supporting Evidence: PMID:20418806 we dissect the activity of each subfamily and show that both are indispensable for the autophagic process in mammalian cells |
| GO:0006995 cellular response to nitrogen starvation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Atg8-family proteins participate in starvation-induced autophagy. Reason: Nitrogen starvation is the yeast paradigm; in human cells the comparable trigger is amino-acid or serum starvation. The process is a context for autophagy rather than a distinct LC3B function. |
| GO:0008017 microtubule binding | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: LC3 binds microtubules, consistent with its identification as a MAP1 light chain. Reason: Microtubule binding is supported in the LC3 subfamily (rat) and may assist autophagosome transport, but it is not the core activity of LC3B. |
| GO:0008429 phosphatidylethanolamine binding | IBA GO_REF:0000033 | ACCEPT | Summary: LC3B is processed by ATG4B at Gly120 and covalently conjugated to phosphatidylethanolamine by ATG7 and ATG3, forming membrane-anchored LC3B-II. Reason: Core molecular property; GO represents Atg8-family lipidation with this binding term. Earlier claims that LC3B is not C-terminally cleaved were corrected by later work showing Gly120-dependent cleavage and conjugation. Supporting Evidence: PMID:15355958 Human light chain 3/MAP1LC3B, an autophagosomal ortholog of yeast Atg8, is conjugated to phospholipid (PL) via ubiquitylation-like reactions mediated by human Atg7 and Atg3. PMID:15355958 These results indicate that the carboxyl terminus of MAP1LC3B is cleaved to expose Gly(120) for further ubiquitylation-like reactions. |
| GO:0008429 phosphatidylethanolamine binding | IDA PMID:15355958 Human light chain 3/MAP1LC3B is cleaved at its carboxyl-term... | ACCEPT | Summary: LC3B is processed by ATG4B at Gly120 and covalently conjugated to phosphatidylethanolamine by ATG7 and ATG3, forming membrane-anchored LC3B-II. Reason: Core molecular property; GO represents Atg8-family lipidation with this binding term. Earlier claims that LC3B is not C-terminally cleaved were corrected by later work showing Gly120-dependent cleavage and conjugation. Supporting Evidence: PMID:15355958 Human light chain 3/MAP1LC3B, an autophagosomal ortholog of yeast Atg8, is conjugated to phospholipid (PL) via ubiquitylation-like reactions mediated by human Atg7 and Atg3. PMID:15355958 These results indicate that the carboxyl terminus of MAP1LC3B is cleaved to expose Gly(120) for further ubiquitylation-like reactions. |
| GO:0008429 phosphatidylethanolamine binding | IDA PMID:37943659 ATM-CHK2-TRIM32 axis regulates ATG7 ubiquitination to initia... | ACCEPT | Summary: LC3B is processed by ATG4B at Gly120 and covalently conjugated to phosphatidylethanolamine by ATG7 and ATG3, forming membrane-anchored LC3B-II. Reason: Core molecular property; GO represents Atg8-family lipidation with this binding term. Earlier claims that LC3B is not C-terminally cleaved were corrected by later work showing Gly120-dependent cleavage and conjugation. Supporting Evidence: PMID:15355958 Human light chain 3/MAP1LC3B, an autophagosomal ortholog of yeast Atg8, is conjugated to phospholipid (PL) via ubiquitylation-like reactions mediated by human Atg7 and Atg3. PMID:15355958 These results indicate that the carboxyl terminus of MAP1LC3B is cleaved to expose Gly(120) for further ubiquitylation-like reactions. |
| GO:0009267 cellular response to starvation | IDA PMID:28223137 Human CLEC16A regulates autophagy through modulating mTOR ac... | KEEP AS NON CORE | Summary: LC3B lipidation and puncta increase during starvation-induced autophagy. Reason: In these studies LC3B was a readout of starvation-induced autophagy. LC3B does act in this autophagy, but the response-to-starvation term is a context rather than its function. Supporting Evidence: PMID:28223137 which in turn diminished LC3 autophagic activity following nutrient deprivation |
| GO:0009267 cellular response to starvation | IDA PMID:30420355 LC3 and STRAP regulate actin filament assembly by JMY during... | KEEP AS NON CORE | Summary: LC3B lipidation and puncta increase during starvation-induced autophagy. Reason: In these studies LC3B was a readout of starvation-induced autophagy. LC3B does act in this autophagy, but the response-to-starvation term is a context rather than its function. Supporting Evidence: PMID:30420355 Upon starvation, JMY shifts to motile, LC3-containing membranes that move on actin comet tails. |
| GO:0012505 endomembrane system | EXP PMID:12740394 Post-translational modifications of three members of the hum... | ACCEPT | Summary: LC3B-II is a lipid-anchored peripheral membrane protein of autophagic membranes. Reason: Correct general membrane location of the lipidated form. Supporting Evidence: PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0012505 endomembrane system | IEA GO_REF:0000120 | ACCEPT | Summary: LC3B-II is a lipid-anchored peripheral membrane protein of autophagic membranes. Reason: Correct general membrane location of the lipidated form. Supporting Evidence: PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0016020 membrane | IEA GO_REF:0000117 | ACCEPT | Summary: LC3B-II is a lipid-anchored peripheral membrane protein of autophagic membranes. Reason: Correct general membrane location of the lipidated form. Supporting Evidence: PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0016236 macroautophagy | IDA PMID:28223137 Human CLEC16A regulates autophagy through modulating mTOR ac... | ACCEPT | Summary: LC3B functions in macroautophagy. Reason: Core process; supported by its role on phagophore and autophagosome membranes. Supporting Evidence: PMID:28223137 which in turn diminished LC3 autophagic activity following nutrient deprivation |
| GO:0031090 organelle membrane | ISS PMID:12740394 Post-translational modifications of three members of the hum... | ACCEPT | Summary: LC3B-II is a lipid-anchored peripheral membrane protein of autophagic membranes. Reason: Correct general membrane location of the lipidated form. Supporting Evidence: PMID:12740394 Subcellular localization by cell fractionation and immunofluorescence revealed that three human isoforms are associated with membranes involved in the autophagic pathway. |
| GO:0031410 cytoplasmic vesicle | IDA PMID:30420355 LC3 and STRAP regulate actin filament assembly by JMY during... | ACCEPT | Summary: LC3B-II marks autophagosomes and other LC3-positive vesicles, including motile JMY-positive membranes. Reason: Correct, if general; autophagosome membrane is the more specific location. Supporting Evidence: PMID:30420355 Upon starvation, JMY shifts to motile, LC3-containing membranes that move on actin comet tails. |
| GO:0031410 cytoplasmic vesicle | IEA GO_REF:0000044 | ACCEPT | Summary: LC3B-II marks autophagosomes and other LC3-positive vesicles, including motile JMY-positive membranes. Reason: Correct, if general; autophagosome membrane is the more specific location. Supporting Evidence: PMID:33499712 MAP1LC3B is known to associate with elongating phagophores as well as enclosed autophagosomal membranes. |
| GO:0031625 ubiquitin protein ligase binding | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: LC3B binds LIR-containing E3 ubiquitin ligases such as TRIM proteins. Reason: Atg8-family proteins recruit many LIR-containing partners, including E3 ligases; the binding is real but reflects one class of the many LIR partners rather than a specific LC3B function. |
| GO:0031625 ubiquitin protein ligase binding | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: LC3B binds LIR-containing E3 ubiquitin ligases such as TRIM proteins. Reason: Atg8-family proteins recruit many LIR-containing partners, including E3 ligases; the binding is real but reflects one class of the many LIR partners rather than a specific LC3B function. |
| GO:0031625 ubiquitin protein ligase binding | IPI PMID:25127057 TRIM proteins regulate autophagy and can target autophagic s... | KEEP AS NON CORE | Summary: LC3B binds LIR-containing E3 ubiquitin ligases such as TRIM proteins. Reason: Atg8-family proteins recruit many LIR-containing partners, including E3 ligases; the binding is real but reflects one class of the many LIR partners rather than a specific LC3B function. Supporting Evidence: PMID:25127057 TRIMs associate with autophagy factors and act as platforms assembling ULK1 and Beclin 1 in their activated states |
| GO:0031966 mitochondrial membrane | EXP PMID:25215947 AMBRA1 is able to induce mitophagy via LC3 binding, regardle... | KEEP AS NON CORE | Summary: During mitophagy LC3B associates with mitochondrial membranes, including inner membrane PHB2 after outer membrane rupture. Reason: Stimulus-dependent association with mitophagy receptors on mitochondrial membranes; not a resident location. Supporting Evidence: PMID:25215947 upon mitophagy induction, AMBRA1 binds the autophagosome adapter LC3 through a LIR (LC3 interacting region) motif |
| GO:0031966 mitochondrial membrane | EXP PMID:28017329 Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Re... | KEEP AS NON CORE | Summary: During mitophagy LC3B associates with mitochondrial membranes, including inner membrane PHB2 after outer membrane rupture. Reason: Stimulus-dependent association with mitophagy receptors on mitochondrial membranes; not a resident location. Supporting Evidence: PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. |
| GO:0031966 mitochondrial membrane | IEA GO_REF:0000044 | KEEP AS NON CORE | Summary: During mitophagy LC3B associates with mitochondrial membranes, including inner membrane PHB2 after outer membrane rupture. Reason: Stimulus-dependent association with mitophagy receptors on mitochondrial membranes; not a resident location. Supporting Evidence: PMID:28017329 PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. |
| GO:0070062 extracellular exosome | TAS Reactome:R-HSA-9947387 | KEEP AS NON CORE | Summary: Reactome places LC3B in extracellular exosome/vesicle cargo-loading events. Reason: LC3-dependent loading of cargo into extracellular vesicles is a secondary, non-canonical role; LC3B is not a characteristic exosome protein. |
| GO:0097001 ceramide binding | IDA PMID:22922758 Ceramide targets autophagosomes to mitochondria and induces ... | KEEP AS NON CORE | Summary: LC3B-II binds C18-ceramide on mitochondrial membranes, anchoring autophagolysosomes during ceramide-induced lethal mitophagy. Reason: Direct binding evidence with a ceramide-binding mutant; a specialized, context-specific mitophagy route rather than a general LC3B function. Supporting Evidence: PMID:22922758 Thus, these data suggest a new receptor function of ceramide for anchoring LC3B-II autophagolysosomes to mitochondrial membranes, defining a key mechanism for the induction of lethal mitophagy. file:human/MAP1LC3B/MAP1LC3B-uniprot.txt binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria |
| GO:0097352 autophagosome maturation | IBA GO_REF:0000033 | ACCEPT | Summary: Atg8-family proteins, including LC3B, are needed for autophagosome maturation and fusion with lysosomes. Reason: Atg8 knockout cells have a severe block in autophagosome-lysosome fusion. The GABARAP subfamily contributes most, but LC3B on the outer membrane binds fusion-related LIR proteins. Supporting Evidence: PMID:27864321 We show that Atg8s are dispensable for autophagosome formation and selective engulfment of mitochondria, but essential for autophagosome-lysosome fusion. |
| GO:0097352 autophagosome maturation | IDA PMID:28223137 Human CLEC16A regulates autophagy through modulating mTOR ac... | ACCEPT | Summary: Atg8-family proteins, including LC3B, are needed for autophagosome maturation and fusion with lysosomes. Reason: Atg8 knockout cells have a severe block in autophagosome-lysosome fusion. The GABARAP subfamily contributes most, but LC3B on the outer membrane binds fusion-related LIR proteins. Supporting Evidence: PMID:27864321 We show that Atg8s are dispensable for autophagosome formation and selective engulfment of mitochondria, but essential for autophagosome-lysosome fusion. |
| GO:0097352 autophagosome maturation | IEA GO_REF:0000117 | ACCEPT | Summary: Atg8-family proteins, including LC3B, are needed for autophagosome maturation and fusion with lysosomes. Reason: Atg8 knockout cells have a severe block in autophagosome-lysosome fusion. The GABARAP subfamily contributes most, but LC3B on the outer membrane binds fusion-related LIR proteins. Supporting Evidence: PMID:27864321 We show that Atg8s are dispensable for autophagosome formation and selective engulfment of mitochondria, but essential for autophagosome-lysosome fusion. |
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Download this section (compressed HTML)Q: Is there a GO molecular function term suitable for Atg8-family LIR-docking (the shared activity behind most of the protein binding rows), and should GO adopt one?
Q: Which LC3B functions are not shared with LC3A, LC3C and the GABARAP subfamily in cells that express all six Atg8 proteins?
Experiment: Re-express LC3B alone in Atg8 hexa-knockout cells, with wild-type or LIR-docking-site mutants, and measure autophagosome size, formation rate and fusion.
Hypothesis: LC3B alone restores phagophore expansion but only partly restores autophagosome-lysosome fusion.
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