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. 2021 Dec 20;19:521. doi: 10.1186/s12967-021-03178-6

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© The Author(s) 2021

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. 4 — SIRT5 regulates PDHA1 activity and remodels metabolic pathways. A Succinyl-CoA was added to the PDHA1 system, and the levels of succinylated PDHA1 and PDHA1 enzyme activity were determined. The levels of succinylated PDHA1 and PDHA1 enzyme activity were determined following the overexpression (B) or knock down of PDHA1 (C). D OCRs were detected for untransfected and SIRT5-transfected KMRC-20 cells that were treated with DMHG. OCRs were recorded from cells treated with oligomycin, carbonyl cyanide-m-chlorophenylhydrazone (FCCP), and antimycin A/rotenone at the indicated time points. E SIRT5 was knocked down in Caki-1 cells, and the OCR was detected and quantified. F The levels of key metabolites produced by glycolysis and the TCA cycle were determined following SIRT5 overexpression or knockdown