Additional file 1 of PANX1-mediated ATP release confers FAM3A’s suppression effects on hepatic gluconeogenesis and lipogenesis

Additional file 1: Fig. S1 Overexpression of pannexin 1 (PANX1) inhibited glucose production and lipid accumulation in HepG2 cells. Fig. S2 Verifying the efficiency of AAV-shPANX1 in mouse hepatocytes. Fig. S3 Hepatic PANX1 inhibition aggravated HFD-induced dysregulated glucolipid metabolism in HFD-fed mice. Fig. S4 PANX1-deficient mice exhibited impaired glucose tolerance fed on a normal diet. Fig. S5 Treatment with PBN or suramin blunted PANX1-mediated regulatory effects on glucolipid metabolism in HepG2 cells. Fig. S6 Free fatty acids upregulated PANX1 expression by inhibiting MafK in HepG2 cells. Fig. S7 FAM3A overexpression induced PANX1 expression in HepG2 cells. Fig. S8 HSF1 activated the expression of PANX1 in HepG2 cells. Fig. S9 PBN treatment blocked FAM3A-promoted ATP release in HepG2 cells. Fig. S10 Liver FAM3A overexpression failed to improve the impaired glucose tolerance in PANX1-deficient mice. Table S1 Clinical parameters of individuals with or without NAFLD. Table S2 siRNA sequence against mouse MafK mRNAs. Table S3 List of oligonucleotide primer pairs used in Real-time PCR analysis. Table S4 MS data of CaM co-immunoprecipitation. Table S5 MS data of DNA pull-down.