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. 2021 Apr 30;12(5):432. doi: 10.1038/s41419-021-03709-5

Fig. 5. GSK3β suppresses the activity of CREB, which competes with Smad proteins for binding to CBP and abolishes the TGF-β1 induced TEC profibrogenic plasticity.

Fig. 5

TKPT cells were pretreated with lithium, TDZD-8, or forskolin, or were subjected to liposome-mediated transient transfection with vectors encoding KD, or S9A, followed by TGF-β1 treatment for 6 h. A Cell lysates were subjected to immunoprecipitation with the anti-CBP antibody. Immunoprecipitates were processed for immunoblot analysis for p-CREB (ser 133), p-Smad2, and CBP. Representative immunoblots were shown. B Cell lysates prepared from TKPT cells with indicated treatments were processed for immunoblot analysis for E-cadherin, vimentin, FN, CTGF, PAI-1, pH3, and β-actin. Representative immunoblots were shown. C TKPT were fixed after indicated treatments and prepared for immunofluorescent staining for E-cadherin, vimentin, FN, and pH3 with nuclear counterstaining with PI. Representative fluorescent micrographs were shown. Scale Bar = 100 μm. CREB, cAMP response element-binding protein; CBP, CREB-binding protein; PI, propidium iodide.