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A hypothetical model of DNA-independent inhibition of NKX2.1 and FOXA1 by SMAD3. (A) In the absence of TGF-beta treatment, NKX2.1 and FOXA1 can readily bind to their cognate sites and activate transcription of the SpB promoter. (B) Treatment with TGF-beta activates SMAD3, which in turn binds through its MH domains to NKX2.1 and FOXA1 and prevents their binding to the SpB promoter. Factors I and II represent other transcription, or co-factors participating in SpB gene activation.
