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. 2019 Apr 4;294(21):8490–8504. doi: 10.1074/jbc.RA118.005763

Figure 5.

Figure 5.

Enhanced TGF-β receptor availability at the cell surface confers increased TβRI–TβRII receptor association and Smad activation. A, coimmunoprecipitation of TβRI and TβRII in HaCaT cells treated with TGF-β1 for 30 min in the presence of AktVIII inhibitor or control solution. Inhibition of Akt with AktVIII decreased the ligand-induced interaction of TβRI and TβRII. B, cell-surface analysis of HaCaT cells treated with TGF-β1 in the presence or absence of AktVIII. TGF-β1 promoted association of Smad3 with cell-surface proteins, which was inhibited by AktVIII. C and D, immunoblot (IB) analysis of Smad2 and Smad3 activation. HaCaT cells were stimulated with TGF-β1 for the times indicated in the presence of AktVIII or control solution (C) or for 30 min with TGF-β1 in the presence of MK2206 or control (D). Smad2 and Smad3 activation in response to TGF-β1, assessed by anti–phospho-Smad2 or -Smad3 immunoblotting, was attenuated by AktVIII or MK2206, whereas total Smad2 and Smad3 protein levels were unaffected by TGF-β1 or AktVIII or MK2206. Note that in this figure, B presents data from the same experiment shown in Fig. 2C, and D presents data obtained from the same experiment as shown in the right panel of Fig. 2A.