Fig. 6: TGF-β induces PCAF degradation via the lysosomal pathway in PTCs.

a,b, Time-dependent changes in PCAF protein levels (a) and mRNA levels (b) in HK2 cells after TGF-β treatment (20 ng/ml for 24 h). c, Representative immunofluorescence images showing changes in ZO-1 and vimentin in HK2 cells after TGF-β treatment, with PCAF knockdown or overexpression. d, mRNA levels of fibrosis-related genes in HK2 cells upon TGF-β treatment with PCAF overexpression. e, Protein levels of PCAF in HK2 cells upon TGF-β treatment with lysosomal degradation inhibitors (CQ at 100 nM and BafA at 20 nM). f, Immunoprecipitation of PCAF and LC3 in HK2 cells upon TGF-β treatment. FLAG-PCAF and GFP-LC3 were transfected, and CQ was added 24 h later. The cells were collected 24 h after CQ treatment. g, Representative immunofluorescence images showing the co-localization of PCAF and LC3 puncta in HK2 cells after TGF-β treatment. The number of LC3 puncta per cell and the number of LC3 puncta co-localized with PCAF were quantified. Data are presented as mean ± s.e.m., *P < 0.05 **P < 0.01, ***P < 0.001, ****P < 0.0001 by t-test for two groups and ordinary one-way ANOVA for multiple groups.