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Non-canonical roles of autophagy proteins in endocytosis and exocytosis


Münz, Christian (2021). Non-canonical roles of autophagy proteins in endocytosis and exocytosis. Biochemical Society Transactions, 49(6):2841-2851.

Abstract

Autophagy, the pathways that degrade cytoplasmic constituents in lysosomes, contribute to most biological processes from aging and neurodegeneration to pathogen restriction and immunity. In recent years, it was realized that the autophagy machinery serves additional functions, primarily in endo- and exocytosis. In this review, I summarize recent advances in our understanding on how these non-canonical functions differ from canonical macroautophagy, and contribute to immune activation and viral replication. Understanding these pathways will allow us to harness them for the treatment of human diseases, as well as appreciate how cells use modules of membrane remodeling and trafficking for multiple biological functions.

Abstract

Autophagy, the pathways that degrade cytoplasmic constituents in lysosomes, contribute to most biological processes from aging and neurodegeneration to pathogen restriction and immunity. In recent years, it was realized that the autophagy machinery serves additional functions, primarily in endo- and exocytosis. In this review, I summarize recent advances in our understanding on how these non-canonical functions differ from canonical macroautophagy, and contribute to immune activation and viral replication. Understanding these pathways will allow us to harness them for the treatment of human diseases, as well as appreciate how cells use modules of membrane remodeling and trafficking for multiple biological functions.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > Biochemistry
Language:English
Date:17 December 2021
Deposited On:28 Jan 2022 14:22
Last Modified:28 Jan 2024 02:41
Publisher:Portland Press
ISSN:0300-5127
OA Status:Closed
Publisher DOI:https://doi.org/10.1042/BST20210811
PubMed ID:34783341