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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Cytokine. 2013 Sep 24;64(3):652–659. doi: 10.1016/j.cyto.2013.09.004

Figure 1. TGFβ1 induces NFκB-luciferase activity in a NFκB and Smad3 dependent manner.

Figure 1

(A) pNFκB-luc reporter activity in primary mouse keratinocytes treated with or without TGFβ1 (1 ng/mL), TNFα (10 ng/mL), parthenolide (20 nM) or cotransfection with IκB super-repressor plasmid (IκBsr). (B) TGFβ1 induced pNFκB-luc activity in Nfκb1 +/+, +/− and−/− primary keratinocytes. (C) pNFκB-luc or pSBE-luc activity in keratinocytes treated with TGFβ1 in presence or absence of ALK5 inhibitor SB431542 (1 uM). (D) pNFκB-luc activity in Smad3 +/+, +/− and −/− primary keratinocytes. (E) TGFβ1 induced pNFκB-luc in keratinocytes cotransfected with the Smad3 expression vector pCMV-Smad3. All experiments were averaged from N=6 wells repeated 3 times. * indicates significant difference between indicated groups p<.05. For 1A *, # indicate significantly different from control, **, ## significantly different from TGFβ1 or TNFα alone, p<.05. c= no treatment; v=vehicle (DMSO)