Fig. 4: SETD2 deficiency leads to metabolic reprogramming and upregulated sphingomyelin biosynthesis.
From: SETD2 deficiency accelerates sphingomyelin accumulation and promotes the development of renal cancer
a GSEA of KEGG metabolic pathways enriched in KMS mice compared to KM mice. Upregulated and downregulated pathways are shown in red and blue, respectively. b Heat map and quantitative analysis of altered proteins (FDR < 0.05) in upregulated and downregulated pathways between KMS and KM mice. c, d Reprogrammed metabolic pathways in KMS mice compared to KM mice. e Schema of de novo sphingomyelin biosynthesis with upregulated proteins and metabolites in KMS mice compared to KM mice. The most critical representative proteins and metabolites were highlighted in green and yellow, respectively (FDR < 0.05 and fold change >1.5). f KMS mice showed increased TECR (P < 0.0001), KDSR (P = 0.0049), LPCAT3 (P < 0.0001), Palmitic acid (P = 0.0235), and Sphingomyelin d18:1/18:0 (P = 0.0374), d40:1 (P = 0.0299) and d41:1 (P = 0.0198) compared to KM mice. Statistical comparisons were made using a 2-tailed Student’s t test. Data are represented as mean ± SEM. Source data are provided as a Source Data file.
