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. Author manuscript; available in PMC: 2023 Oct 12.
Published in final edited form as: Cell Rep. 2018 Nov 13;25(7):1841–1855.e5. doi: 10.1016/j.celrep.2018.10.056

Figure 2. Knockdown of ESCRT Components Leads to a Persistence in SMAD2 Phosphorylation upon TGF-β Treatment.

Figure 2

(A–D) HaCaT cells were transfected with non-targeting (NT) control siRNAs or siRNAs targeting VPS28 (A), UBAP1 (B), PTPN23 (C), or VPS4B (D)and stimulated with TGF-β for the times indicated. Levels of PSMAD2, SMAD2/3, TGFBR1, TGFBR2, and tubulin as a loading control were assayed by western blot. Quantifications are the normalized average ± SD of three independent experiments. *p < 0.05. The extent of knockdown was assessed by qPCR, and the normalized average ± SD from the same three independent experiments is shown bottom right.