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. 2021 Aug 3;22(4):297–312. doi: 10.1007/s10048-021-00657-2

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Cell fractionation in MEFs, comparing mitochondrial with nuclear (a) and cytosolic (b) compartments. Immunoblotting was used to control the purity of the fractionation with the mitochondrial marker PORIN, the nuclear marker LAMIN A/C, and the cytosolic marker GAPDH, comparing littermate WT and ClpP^−/− cells of matched sex. The detection of DNAJA3 revealed ClpP deficiency to cause accumulation of DNAJA3 short isoform (S) in the mitochondria and nucleus, while STAT1 (87 kDa) accumulation occurred in the mitochondria and cytosol