Fig. 1: Quantitative acetylome profiling identifies CLYBL as a physiological substrate of SIRT2. | Cell Death & Disease

Fig. 1: Quantitative acetylome profiling identifies CLYBL as a physiological substrate of SIRT2.

From: Positive feedback loop involving AMPK and CLYBL acetylation links metabolic rewiring and inflammatory responses

Fig. 1

A Proteomics and modification analyses among cardiac tissues of SIRT2-KO, SIRT2-WT, and SIRT2-Flag-TG mice treated with Ang II. B Heatmap of different acetylated proteins among SIRT2-KO, SIRT2-WT, and SIRT2-Flag-TG mouse heart samples. C Volcano plot showing differential acetylation sites in SIRT2-KO versus SIRT2-WT (p < 0.05, fold change>1.5). D Volcano plot showing differential acetylation sites in SIRT2-Flag-TG versus SIRT2-WT (p < 0.05, fold change>1.5). E Venn diagram showing the shared and specific acetylation-modified proteins among SIRT2-KO versus SIRT2-WT and SIRT2-Flag-TG versus SIRT2-WT. F Venn diagram showing the shared and specific acetylated sites among SIRT2-KO versus SIRT2-WT and SIRT2-Flag-TG versus SIRT2-WT. G Histogram showing enrichment of biological process pathways of differential proteins, whose acetylation levels were downregulated in SIRT2-Flag-TG and upregulated in SIRT2-KO. H Histogram showing the KEGG pathways enrichment of distinct proteins, whose acetylation levels were downregulated in SIRT2-Flag-TG and upregulated in SIRT2-KO. I Lysine residues, highlighted in red text, demonstrating possible sites modified by SIRT2 in amino acid sequences of CLYBL.

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