Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition

The mitochondrial Unfolded Protein Response (UPR(mt)) pathway confers protection from misfolded and aggregated proteins by activating factors that promote protein folding and degradation. Our recent work on Lon protease, a member of the mitochondrial ATPase Associated with diverse cellular Activitie...

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Autores principales: Pareek, Gautam, Pallanck, Leo J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Comment
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6281655/
https://www.ncbi.nlm.nih.gov/pubmed/30518747
http://dx.doi.org/10.1038/s41419-018-1213-6
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author Pareek, Gautam
Pallanck, Leo J.
author_facet Pareek, Gautam
Pallanck, Leo J.
author_sort Pareek, Gautam
collection PubMed
description The mitochondrial Unfolded Protein Response (UPR(mt)) pathway confers protection from misfolded and aggregated proteins by activating factors that promote protein folding and degradation. Our recent work on Lon protease, a member of the mitochondrial ATPase Associated with diverse cellular Activities (AAA(+)) family of mitochondrial resident proteases, suggests that mitochondrial translational inhibition may also be a feature of the UPR(mt) pathway.
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spelling pubmed-62816552018-12-06 Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition Pareek, Gautam Pallanck, Leo J. Cell Death Dis Comment The mitochondrial Unfolded Protein Response (UPR(mt)) pathway confers protection from misfolded and aggregated proteins by activating factors that promote protein folding and degradation. Our recent work on Lon protease, a member of the mitochondrial ATPase Associated with diverse cellular Activities (AAA(+)) family of mitochondrial resident proteases, suggests that mitochondrial translational inhibition may also be a feature of the UPR(mt) pathway. Nature Publishing Group UK 2018-12-05 /pmc/articles/PMC6281655/ /pubmed/30518747 http://dx.doi.org/10.1038/s41419-018-1213-6 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Comment
Pareek, Gautam
Pallanck, Leo J.
Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title_full Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title_fullStr Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title_full_unstemmed Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title_short Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
title_sort inactivation of lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition
topic Comment
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6281655/
https://www.ncbi.nlm.nih.gov/pubmed/30518747
http://dx.doi.org/10.1038/s41419-018-1213-6
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