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From Proteopedia
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== Disease == | == Disease == | ||
| - | + | [https://www.uniprot.org/uniprot/WIPI2_HUMAN WIPI2_HUMAN] The disease is caused by variants affecting the gene represented in this entry. | |
== Function == | == Function == | ||
| - | + | [https://www.uniprot.org/uniprot/WIPI2_HUMAN WIPI2_HUMAN] Component of the autophagy machinery that controls the major intracellular degradation process by which cytoplasmic materials are packaged into autophagosomes and delivered to lysosomes for degradation (PubMed:20505359, PubMed:28561066). Involved in an early step of the formation of preautophagosomal structures (PubMed:20505359, PubMed:28561066). Binds and is activated by phosphatidylinositol 3-phosphate (PtdIns3P) forming on membranes of the endoplasmic reticulum upon activation of the upstream ULK1 and PI3 kinases (PubMed:28561066). Mediates ER-isolation membranes contacts by interacting with the ULK1:RB1CC1 complex and PtdIns3P (PubMed:28890335). Once activated, WIPI2 recruits at phagophore assembly sites the ATG12-ATG5-ATG16L1 complex that directly controls the elongation of the nascent autophagosomal membrane (PubMed:20505359, PubMed:28561066).<ref>PMID:20505359</ref> <ref>PMID:28561066</ref> <ref>PMID:28890335</ref> <ref>PMID:30968111</ref> Recruits the ATG12-ATG5-ATG16L1 complex to omegasomes and preautophagosomal structures, resulting in ATG8 family proteins lipidation and starvation-induced autophagy. Isoform 4 is also required for autophagic clearance of pathogenic bacteria. Isoform 4 binds the membrane surrounding Salmonella and recruits the ATG12-5-16L1 complex, initiating LC3 conjugation, autophagosomal membrane formation, and engulfment of Salmonella.<ref>PMID:24954904</ref> | |
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 07:40, 18 January 2023
Crystal structure of WIPI2b in complex with ATG16L1
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