Fig. 5.

Kinases activation mediates Angptl8-induced Per1 expression. a Western blot analyses of ERK1/2, P38, NF-κB, AKT, and GSK-3β phosphorylation in Hepa1c1c-7 cells stimulated with 40 nM Angptl8 for indicated times. b Reporter gene assays in Hepa1c1c-7 cells transfected with plasmids expressing Per1-Luc for 36 h and then treated with 40 nM Angptl8 alone or in combinations of various signaling pathway inhibitors for 2 h. n = 6, **P < 0.01 Angptl8 vs. Vehicle group, ^##P < 0.01 Angptl8 + inhibitor vs. Angptl8 alone group, one-way ANOVA followed by Bonferroni’s post hoc test. c, d qPCR and Western blot analyses of Per1 expression in Hepa1c1c-7 cells treated with 40 nM Angptl8 alone or in combinations of various signaling pathway inhibitors for 2 h. n = 3, **P < 0.01 Angptl8 vs. Vehicle group, ^#P < 0.05 and ^##P < 0.01 Angptl8 + inhibitor vs. Angptl8 alone group, one-way ANOVA followed by Bonferroni’s post hoc test. e Quantitative analysis of Per1 protein levels in d. n = 3, **P < 0.01 Angptl8 vs. Vehicle group, ^##P < 0.01 Angptl8 + inhibitor vs. Angptl8 alone group, one-way ANOVA followed by Bonferroni’s posthoc test. All data are presented as the means ± SD. Concentrations: U0126, 10 μM; SB203580, 10 μM; Bay11-7082, 40 μM; Wortmannin 10 μM. Source data are provided as a Source Data file