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. 2022 Dec 1;17:37. doi: 10.1186/s13062-022-00344-8

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Synj2bp silencing in the mouse liver upregulates mitochondria fatty acid respiration capacity. A–D Comparative quantitative proteomic analysis of WAM-enriched fractions prepared from livers of mice injected with control AAV8-shScrambled and AAV8-shSynj2bp (livers collected at 3 h postprandial). A The graph shows that silencing Synj2bp, which reduces the amount of wrapper associated with mitochondria (Fig. 2E), reduces the percentage of ER proteins but proportionally increases only the amount of mitochondrial proteins, not that of other subcellular compartments. B, C Reactome biological process analysis of the pathways up-regulated in Synj2bp-silenced mouse livers. D Estimation statistics analysis [24, 25] of the WAM proteomics data related to the indicated proteins. Pdk4 and Hmgcs2 up-regulation in Synj2bp-silenced livers indicates activation of mitochondrial FA respiration