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. 2021 Oct 20;4:1200. doi: 10.1038/s42003-021-02730-w

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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 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. 5 — a Heat maps of relative protein abundance from kidneys isolated from both PKD1 mouse models, RC/RC and RC/null, vs. WT controls in the middle columns and the mCAT treatment effect next to the corresponding group. The middle columns showed that most proteins were in blue, indicating a decreased abundance of several proteins in PKD1 mutation. The mCAT effects were mostly in red, suggesting various degrees of reversal of the PKD1 mutation effect. The asterisks highlight the proteins that show significant suppression by PKD1, with significant gene dosage effect and significant reversal by mCAT. (9 RC/RC, 7RC/RC treated with mCAT, 4 RC/null, 3 RC/null treated with mCAT, and 4 WT mice were used) b Table showing the average magnitude of the effects of PKD1 mutation, mCAT treatment, and the percentage restored by mCAT treatment on proteins involved in mitochondrial and metabolic pathways, as identified in A. Only highlighted numbers are significant.