MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy.

MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy.

Recently, mutations in the mitochondrial translation optimization factor 1 gene (MTO1) were identified as causative in children with hypertrophic cardiomyopathy, lactic acidosis and respiratory chain defect. Here, we describe an MTO1-deficient mouse model generated by gene trap mutagenesis that mirr...

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Bibliographic Details
Main Authors: Lore Becker, Eva Kling, Evelyn Schiller, Ramona Zeh, Anja Schrewe, Sabine M Hölter, Ilona Mossbrugger, Julia Calzada-Wack, Valentina Strecker, Ilka Wittig, Iulia Dumitru, Tina Wenz, Andreas Bender, Michaela Aichler, Dirk Janik, Frauke Neff, Axel Walch, Leticia Quintanilla-Fend, Thomas Floss, Raffi Bekeredjian, Valérie Gailus-Durner, Helmut Fuchs, Wolfgang Wurst, Thomas Meitinger, Holger Prokisch, Martin Hrabě de Angelis, Thomas Klopstock
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0114918

Internet

https://doi.org/10.1371/journal.pone.0114918

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