{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["45(4)"],"submitter":["Zhu YF"],"pubmed_abstract":["Autophagy plays a pivotal role in diverse biological processes, including the maintenance and differentiation of neural stem cells (NSCs). Interestingly, while complete deletion of <i>Fip200</i> severely impairs NSC maintenance and differentiation, inhibiting canonical autophagy via deletion of core genes, such as <i>Atg5</i>, <i>Atg16l1</i>, and <i>Atg7</i>, or blockade of canonical interactions between FIP200 and ATG13 (designated as FIP200-4A mutant or FIP200 KI) does not produce comparable detrimental effects. This highlights the likely critical involvement of the non-canonical functions of FIP200, the mechanisms of which have remained elusive. Here, utilizing genetic mouse models, we demonstrated that FIP200 mediates non-canonical autophagic degradation of p62/sequestome1, primarily v"],"journal":["Zoological research"],"pagination":["937-950"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11298671"],"repository":["biostudies-literature"],"pubmed_title":["TAX1BP1 and FIP200 orchestrate non-canonical autophagy of p62 aggregates for mouse neural stem cell maintenance."],"pmcid":["PMC11298671"],"pubmed_authors":["Yu RH","Thorne RF","Wu M","Zhang JL","Zhu YF","Zhou S","Xu R","Zhang YW","Zhang R","Shi XJ","Tang PP","Zhang XD","Liu GZ","Wang YY","Chen S","Wei JM","Wu YX","Li MK"],"additional_accession":[]},"is_claimable":false,"name":"TAX1BP1 and FIP200 orchestrate non-canonical autophagy of p62 aggregates for mouse neural stem cell maintenance.","description":"Autophagy plays a pivotal role in diverse biological processes, including the maintenance and differentiation of neural stem cells (NSCs). Interestingly, while complete deletion of <i>Fip200</i> severely impairs NSC maintenance and differentiation, inhibiting canonical autophagy via deletion of core genes, such as <i>Atg5</i>, <i>Atg16l1</i>, and <i>Atg7</i>, or blockade of canonical interactions between FIP200 and ATG13 (designated as FIP200-4A mutant or FIP200 KI) does not produce comparable detrimental effects. This highlights the likely critical involvement of the non-canonical functions of FIP200, the mechanisms of which have remained elusive. Here, utilizing genetic mouse models, we demonstrated that FIP200 mediates non-canonical autophagic degradation of p62/sequestome1, primarily v","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2025-04-05T15:03:20.575Z","creation":"2025-02-19T04:40:34.299Z"},"accession":"S-EPMC11298671","cross_references":{"pubmed":["39021082"],"doi":["10.24272/j.issn.2095-8137.2024.021"]}}