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The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions

Autophagy is an intracellular degradation and recycling process that can also remove pathogenic intracellular bacteria and viruses from within cells (referred to as xenophagy) and activate the adaptive immune responses. But autophagy—especially Atg proteins including Atg8 family members—can also hav...

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Detalles Bibliográficos
Autores principales: Tóth, Dávid, Horváth, Gábor V., Juhász, Gábor
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8634866/
https://www.ncbi.nlm.nih.gov/pubmed/34670023
http://dx.doi.org/10.1002/2211-5463.13318
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author Tóth, Dávid
Horváth, Gábor V.
Juhász, Gábor
author_facet Tóth, Dávid
Horváth, Gábor V.
Juhász, Gábor
author_sort Tóth, Dávid
collection PubMed
description Autophagy is an intracellular degradation and recycling process that can also remove pathogenic intracellular bacteria and viruses from within cells (referred to as xenophagy) and activate the adaptive immune responses. But autophagy—especially Atg proteins including Atg8 family members—can also have proviral and probacterial effects. In this review, we summarize known interactions of bacterial, parasitic, and viral proteins with Atg8 family proteins and the outcome of these interactions on pathogen replication, autophagy, or mitophagy. We discuss the value of prediction software and the research methodology in the study of pathogen protein‐Atg8 family protein interactions, with selected examples of potential LC3‐interacting region motif‐containing SARS‐CoV‐2 proteins.
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spelling pubmed-86348662021-12-08 The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions Tóth, Dávid Horváth, Gábor V. Juhász, Gábor FEBS Open Bio Reviews Autophagy is an intracellular degradation and recycling process that can also remove pathogenic intracellular bacteria and viruses from within cells (referred to as xenophagy) and activate the adaptive immune responses. But autophagy—especially Atg proteins including Atg8 family members—can also have proviral and probacterial effects. In this review, we summarize known interactions of bacterial, parasitic, and viral proteins with Atg8 family proteins and the outcome of these interactions on pathogen replication, autophagy, or mitophagy. We discuss the value of prediction software and the research methodology in the study of pathogen protein‐Atg8 family protein interactions, with selected examples of potential LC3‐interacting region motif‐containing SARS‐CoV‐2 proteins. John Wiley and Sons Inc. 2021-11-17 /pmc/articles/PMC8634866/ /pubmed/34670023 http://dx.doi.org/10.1002/2211-5463.13318 Text en © 2021 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Tóth, Dávid
Horváth, Gábor V.
Juhász, Gábor
The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title_full The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title_fullStr The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title_full_unstemmed The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title_short The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
title_sort interplay between pathogens and atg8 family proteins: thousand‐faced interactions
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8634866/
https://www.ncbi.nlm.nih.gov/pubmed/34670023
http://dx.doi.org/10.1002/2211-5463.13318
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