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. 2020 Sep 24;11:4837. doi: 10.1038/s41467-020-18607-1

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© The Author(s) 2020

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

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Fig. 6 — a, b Proposed models of MFSD7C regulation of mitochondrial respiration in response to heme, with MFSD7C residing in the inner (a) or the outer (b) mitochondrial membrane. When heme level is low, MFSD7C interacts with ETC components and SERCA2b, leading to SERCA2b ubiquitination and degradation and coupled mitochondrial respiration: increased ATP synthesis and reduced thermogenesis. When heme level is high, heme binding to the NTD of MFSD7C disrupts its interactions with ETC components and SERCA2b, leading to SERCA2b stabilization and uncoupled mitochondrial respiration: increased thermogenesis and reduced ATP synthesis.