Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Electronic Gene Ontology annotations created by ARBA machine learning models
Structure of the human ATG12~ATG5 conjugate required for LC3 lipidation in autophagy.
Atg16L2, a novel isoform of mammalian Atg16L that is not essential for canonical autophagy despite forming an Atg12–5-16L2 complex.
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Atg16L2 forms an ~800-kDa Atg12-5-16L2 complex.
"Biochemical analysis revealed that Atg16L2 interacts with Atg5 and self-oligomerizes to form an ~800-kDa complex, the same as Atg16L1 does."
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Membrane-targeted Atg12-5-16L2-N has E3-like LC3-lipidation activity.
"S5 ), indicating that the Atg12–5-16L2-N complex has the ability to function as an E3-like enzyme, the same as the Atg12–5-16L1-N complex does."
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Atg16L2 is cytosolic and not recruited to phagophores.
"A subcellular distribution analysis indicated that, despite forming the Atg12–5-16L2 complex, Atg16L2 is not recruited to phagophores and is mostly present in the cytosol."
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Atg16L2 is not required for canonical autophagy.
"Based on these results, we concluded that Atg16L2 is not required for canonical autophagy, despite forming an ~800-kDa complex with Atg12–5 and having E3-like activity."
Distinct Tissue-Specific Roles for the Disease-Associated Autophagy Genes ATG16L2 and ATG16L1.
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ATG16L2 knockout has lineage-specific effects distinct from ATG16L1.
"Our results show that ATG16L1 and ATG16L2 contribute very distinctly to autophagy and cellular ontogeny in myeloid, lymphoid, and epithelial lineages."
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ATG16L2 is implicated in Crohn disease and SLE.
"Interestingly, ATG16L1 has a single homolog, ATG16L2, which is independently implicated in diseases, including Crohn disease and systemic lupus erythematosus."
ATG16L2 inhibits NLRP3 inflammasome activation through promoting ATG5-12-16L1 complex assembly and autophagy.
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ATG16L2 loss reduces LPS-induced autophagy flux in macrophages.
"Here we report that ATG16L2 deficiency attenuates LPS-induced autophagy flux in macrophages through mediating ATG5-12-16L1 complex assembly."
Atg16l2 augments Nlrc4 inflammasome activation by facilitating NAIPs-NLRC4 association.
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ATG16L2 binds NAIPs and promotes NAIP-NLRC4 association.
"Furthermore, ATG16L2 enhanced the association between NAIPs and NLRC4 by binding to NAIPs."
Reactome R-HSA-9936620: ATG5:ATG12 binds ATG16L2
UniProt entry Q8NAA4 (A16L2_HUMAN)
Affinage mechanistic annotation for ATG16L2 (human)