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. 2018 Oct 10;11:368. doi: 10.3389/fnmol.2018.00368

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Copyright © 2018 Harmuth, Prell-Schicker, Weber, Gellerich, Funke, Drießen, Magg, Krebiehl, Wolburg, Hayer, Hauser, Krüger, Schöls, Riess and Hübener-Schmid.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Abnormalities in mitochondrial morphology are not mainly caused by differential expression of fission and fusion proteins. (A,C) Western blot analyses in whole brain lysates of 12 months old mice (3 animals per genotype; A,B) or MEF lysates (one sample per genotype; C,D) represent an equal expression of fission (Dnm1l and Fis1) and fusion proteins (Mfn-1, Mfn-2 and Opa1). β-actin is shown as loading control. (B,D) Densitometric quantification revealed significantly increased Dnm1l protein levels in mice homozygous for truncated Atx3_1-259 compared to wildtype (p = 0.028).