Structural basis for a complex I mutation that blocks pathological ROS production

Reactive oxygen species (ROS) production by reverse electron transfer (RET) through complex I is thought to cause tissue damage from heart attacks. Here, the authors combine in vivo work with biochemical and cryo-EM analyses to characterize the effects of a P25L mutation in the ND6 subunit of mitoch...

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Autores principales:	Zhan Yin, Nils Burger, Duvaraka Kula-Alwar, Dunja Aksentijević, Hannah R. Bridges, Hiran A. Prag, Daniel N. Grba, Carlo Viscomi, Andrew M. James, Amin Mottahedin, Thomas Krieg, Michael P. Murphy, Judy Hirst
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/1317dd8d29fd49259db11814845c32ea
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spelling	oai:doaj.org-article:1317dd8d29fd49259db11814845c32ea2021-12-02T13:57:53ZStructural basis for a complex I mutation that blocks pathological ROS production10.1038/s41467-021-20942-w2041-1723https://doaj.org/article/1317dd8d29fd49259db11814845c32ea2021-01-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-20942-whttps://doaj.org/toc/2041-1723Reactive oxygen species (ROS) production by reverse electron transfer (RET) through complex I is thought to cause tissue damage from heart attacks. Here, the authors combine in vivo work with biochemical and cryo-EM analyses to characterize the effects of a P25L mutation in the ND6 subunit of mitochondrial complex I. They observe that this mutation does not affect oxidative phosphorylation but renders complex I unable to generate ROS by RET: ND6-P25L mice are protected against cardiac ischaemia–reperfusion injury, thus providing evidence for the proposed role of ROS production in myocardial infarction.Zhan YinNils BurgerDuvaraka Kula-AlwarDunja AksentijevićHannah R. BridgesHiran A. PragDaniel N. GrbaCarlo ViscomiAndrew M. JamesAmin MottahedinThomas KriegMichael P. MurphyJudy HirstNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Zhan Yin Nils Burger Duvaraka Kula-Alwar Dunja Aksentijević Hannah R. Bridges Hiran A. Prag Daniel N. Grba Carlo Viscomi Andrew M. James Amin Mottahedin Thomas Krieg Michael P. Murphy Judy Hirst Structural basis for a complex I mutation that blocks pathological ROS production
description	Reactive oxygen species (ROS) production by reverse electron transfer (RET) through complex I is thought to cause tissue damage from heart attacks. Here, the authors combine in vivo work with biochemical and cryo-EM analyses to characterize the effects of a P25L mutation in the ND6 subunit of mitochondrial complex I. They observe that this mutation does not affect oxidative phosphorylation but renders complex I unable to generate ROS by RET: ND6-P25L mice are protected against cardiac ischaemia–reperfusion injury, thus providing evidence for the proposed role of ROS production in myocardial infarction.
format	article
author	Zhan Yin Nils Burger Duvaraka Kula-Alwar Dunja Aksentijević Hannah R. Bridges Hiran A. Prag Daniel N. Grba Carlo Viscomi Andrew M. James Amin Mottahedin Thomas Krieg Michael P. Murphy Judy Hirst
author_facet	Zhan Yin Nils Burger Duvaraka Kula-Alwar Dunja Aksentijević Hannah R. Bridges Hiran A. Prag Daniel N. Grba Carlo Viscomi Andrew M. James Amin Mottahedin Thomas Krieg Michael P. Murphy Judy Hirst
author_sort	Zhan Yin
title	Structural basis for a complex I mutation that blocks pathological ROS production
title_short	Structural basis for a complex I mutation that blocks pathological ROS production
title_full	Structural basis for a complex I mutation that blocks pathological ROS production
title_fullStr	Structural basis for a complex I mutation that blocks pathological ROS production
title_full_unstemmed	Structural basis for a complex I mutation that blocks pathological ROS production
title_sort	structural basis for a complex i mutation that blocks pathological ros production
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/1317dd8d29fd49259db11814845c32ea
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Structural basis for a complex I mutation that blocks pathological ROS production

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