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. Author manuscript; available in PMC: 2015 Mar 3.
Published in final edited form as: J Pharm Sci Pharmacol. 2014 Sep 1;1(3):175–181. doi: 10.1166/jpsp.2014.1022

Figure 4.

Figure 4

ERG relieves the effect of SB431542, small molecule inhibitor of TGF-β receptor I on TGF-β/Smad3 signaling pathway. (a) PNT1A cells were transiently co-transfected with p3TP reporter gene, pCMVβ and the expression plasmids for ERG and Smad3 or parental empty expression vector. The cells were treated with or without SB431542 at 10 μM for 24 hours as shown and with TGF-β1 for 6 hours before harvesting the cells. Reporter activity was measured at 48 hours after transfection. All reporter activity was shown as mean ± S. E. from 3 samples. *, p < 0 05; **, p < 0 01. (b) Possible mechanism of action by ERG on SB431542. Smad3 is phosphorylated by TGF-β binding to its receptor. SB431542 inhibits the activity of TGF-β receptor I and decrease the amount of phosphorylated Smad3. ERG activates TGF-β receptor I activity through direct or indirect interaction with TGF-β receptor I. (P: Phosphorylated group).

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