Fig. 2: TGF-β inhibits the phosphorylation of ULK1 and promotes autophagy in activated PSCs. | Cell Death & Disease

Fig. 2: TGF-β inhibits the phosphorylation of ULK1 and promotes autophagy in activated PSCs.

From: RB1CC1-enhanced autophagy facilitates PSCs activation and pancreatic fibrogenesis in chronic pancreatitis

Fig. 2

a, b The expressions of ATG5, ATG7, ULK1, p-ULK1 (Se555), and Beclin1 were tested in quiescent and activated PSCs. The relative expression represents the ratio of target to GAPDH. c, d The autophagic related indicators P62 and LC3 were examined via western blot assays. The relative expression represents the ratio of target to GAPDH. e, g The effects of autophagic inhibitor CQ (10μmol/L) was used to determine the RB1CC1 expression, autophagic levels (P62 and LC3), ULK1 expression and its kinase activity, and PSC activation (α-SMA and Collagen I) in quiescent, TGF-β-treated, CQ and TGF-β-treated plus CQ groups. f, h Role of autophagic activator RAPA (5μmol/L) was used to investigate the RB1CC1 expression, autophagic activation (P62 and LC3), ULK1 expression and its kinase activity, α-SMA and Collagen II in quiescent, activated, RAPA and activated plus RAPA groups. Data are expressed as mean ± SD. The results are representative of three independent experiments (*p < 0.05, **p < 0.01, ***p < 0.001)

Back to article page