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p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control

Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve as platforms for autophagosome formation and nuclear factor erythroid 2-related factor 2 (NRF2) activa...

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Detalles Bibliográficos
Autores principales: Eskelinen, Eeva-Liisa, Kageyama, Shun, Komatsu, Masaaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018406/
https://www.ncbi.nlm.nih.gov/pubmed/33855170
http://dx.doi.org/10.1080/23723556.2021.1890990
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author Eskelinen, Eeva-Liisa
Kageyama, Shun
Komatsu, Masaaki
author_facet Eskelinen, Eeva-Liisa
Kageyama, Shun
Komatsu, Masaaki
author_sort Eskelinen, Eeva-Liisa
collection PubMed
description Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve as platforms for autophagosome formation and nuclear factor erythroid 2-related factor 2 (NRF2) activation. Further, p62-mediated NRF2 activation is not cytotoxic, but combination of NRF2 activation with impaired bulk and selective autophagy causes liver injury.
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spelling pubmed-80184062021-04-13 p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control Eskelinen, Eeva-Liisa Kageyama, Shun Komatsu, Masaaki Mol Cell Oncol Author’s Views Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve as platforms for autophagosome formation and nuclear factor erythroid 2-related factor 2 (NRF2) activation. Further, p62-mediated NRF2 activation is not cytotoxic, but combination of NRF2 activation with impaired bulk and selective autophagy causes liver injury. Taylor & Francis 2021-03-09 /pmc/articles/PMC8018406/ /pubmed/33855170 http://dx.doi.org/10.1080/23723556.2021.1890990 Text en © 2021 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Author’s Views
Eskelinen, Eeva-Liisa
Kageyama, Shun
Komatsu, Masaaki
p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title_full p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title_fullStr p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title_full_unstemmed p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title_short p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control
title_sort p62/sqstm1 droplets initiate autophagosome biogenesis and oxidative stress control
topic Author’s Views
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018406/
https://www.ncbi.nlm.nih.gov/pubmed/33855170
http://dx.doi.org/10.1080/23723556.2021.1890990
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