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. 2014 Mar;28(3):1248–1267. doi: 10.1096/fj.13-239178

Figure 2.

Figure 2.

BMP2-induced Smad2/3 phosphorylation is differentially regulated by type II TGF-β superfamily receptors. A) MDA-MB-231 cells were transfected with a DN TβRII or an empty vector (EV) control. TβRII expression was silenced by transfection of a shRNA to TβRII (shTβRII) and a nontargeting control (NTC) shRNA was used as the control. shRNA-mediated silencing of TβRII was rescued by transfecting in shRNA-resistant TβRII (shTβRII+TβRII). Transfected cells were UT, stimulated with 100 pM TGF-β or 10 nM BMP2 for 40 min, lysed, and analyzed by Western blot with the indicated antibodies. B, C) TβRII wild-type (WT) mammary epithelial cells (B) or fibroblast cells (C) and TβRII-null (KO) mammary epithelial cells (B) or fibroblast cells (C) were UT or treated and analyzed as in A. D) Mv1Lu and DR mink lung cells were UT or treated and analyzed as in A. E) MDA-MB-231 cells were transfected with an EV, a DN mutant of BMPRII (DN BMPRII), nontargeting control (NTC), or shRNA against BMPRII (shBMPRII). Silencing of BMPRII was rescued by transfection of shRNA-resistant BMPRII (shBMPRII+BMPRII). Transfected cells were UT or treated and analyzed as in A. F) Wild-type pulmonary artery smooth muscle cells (WT) and BMPRII null PASMCs (KO) were UT or treated and analyzed as in A. Data are representative of 2 independent experiments.