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. 2021 Oct 1;14(9):dmm048249. doi: 10.1242/dmm.048249

Fig. 6.

Fig. 6.

Depletion of Tgfb3 leads to higher phosphorylation of TIR–TIIR-mediated pathways. (A–C) Representative western blots and densitometry of the ERK1/2 pathway (n=8–9) (A), SMAD2/3 pathway (n=8-9) (B) and JNK pathway (n=4-7) (C) in whole kidney. (D,E) Relative mRNA expression of SMAD7 (n=5) (D) and TIR and TIIR (n=4–6) (E) in whole kidney. (F) Relative mRNA expression of TIR and TIIR in siTGFβ3 podocytes. (G,H) Representative western blots and densitometry of the ERK1/2 pathway (G) and SMAD2/3 pathway (H) in siTGFβ3 podocytes. All in vivo experiments were done in whole kidney of 4-month-old male mice. Data are shown as mean±s.e.m.; unpaired Student's t-test with Welch's correction was performed. *P<0.05 versus the control. C−, negative control; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; p, phospho; siTGFβ3, siRNA-silenced Tgfb3; SMAD, mothers against decapentaplegic homolog; t, total; TIR, TGFβ type I receptor; TIIR, TGFβ type II receptor; WT, wild type.