Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation

Heteroplasmic mtDNA mutations cause disease in humans. Here, Chung et al find the PI3K-Akt-mTORC1 pathway constitutively activated in cells with the heteroplasmic m.3243 A > G mutation, and inhibition of the pathway cell autonomously reduces mutant mtDNA load and rescues mitochondrial bioenergeti...

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Autores principales:	Chih-Yao Chung, Kritarth Singh, Vassilios N. Kotiadis, Gabriel E. Valdebenito, Jee Hwan Ahn, Emilie Topley, Joycelyn Tan, William D. Andrews, Benoit Bilanges, Robert D. S. Pitceathly, Gyorgy Szabadkai, Mariia Yuneva, Michael R. Duchen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/b9f6630675044451be3ddb118624adeb
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spelling	oai:doaj.org-article:b9f6630675044451be3ddb118624adeb2021-11-08T11:08:14ZConstitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation10.1038/s41467-021-26746-22041-1723https://doaj.org/article/b9f6630675044451be3ddb118624adeb2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-26746-2https://doaj.org/toc/2041-1723Heteroplasmic mtDNA mutations cause disease in humans. Here, Chung et al find the PI3K-Akt-mTORC1 pathway constitutively activated in cells with the heteroplasmic m.3243 A > G mutation, and inhibition of the pathway cell autonomously reduces mutant mtDNA load and rescues mitochondrial bioenergetics.Chih-Yao ChungKritarth SinghVassilios N. KotiadisGabriel E. ValdebenitoJee Hwan AhnEmilie TopleyJoycelyn TanWilliam D. AndrewsBenoit BilangesRobert D. S. PitceathlyGyorgy SzabadkaiMariia YunevaMichael R. DuchenNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Chih-Yao Chung Kritarth Singh Vassilios N. Kotiadis Gabriel E. Valdebenito Jee Hwan Ahn Emilie Topley Joycelyn Tan William D. Andrews Benoit Bilanges Robert D. S. Pitceathly Gyorgy Szabadkai Mariia Yuneva Michael R. Duchen Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
description	Heteroplasmic mtDNA mutations cause disease in humans. Here, Chung et al find the PI3K-Akt-mTORC1 pathway constitutively activated in cells with the heteroplasmic m.3243 A > G mutation, and inhibition of the pathway cell autonomously reduces mutant mtDNA load and rescues mitochondrial bioenergetics.
format	article
author	Chih-Yao Chung Kritarth Singh Vassilios N. Kotiadis Gabriel E. Valdebenito Jee Hwan Ahn Emilie Topley Joycelyn Tan William D. Andrews Benoit Bilanges Robert D. S. Pitceathly Gyorgy Szabadkai Mariia Yuneva Michael R. Duchen
author_facet	Chih-Yao Chung Kritarth Singh Vassilios N. Kotiadis Gabriel E. Valdebenito Jee Hwan Ahn Emilie Topley Joycelyn Tan William D. Andrews Benoit Bilanges Robert D. S. Pitceathly Gyorgy Szabadkai Mariia Yuneva Michael R. Duchen
author_sort	Chih-Yao Chung
title	Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
title_short	Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
title_full	Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
title_fullStr	Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
title_full_unstemmed	Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation
title_sort	constitutive activation of the pi3k-akt-mtorc1 pathway sustains the m.3243 a > g mtdna mutation
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/b9f6630675044451be3ddb118624adeb
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Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation

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