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. Author manuscript; available in PMC: 2013 Aug 5.
Published in final edited form as: Curr Opin Gastroenterol. 2001 Sep;17(5):434–440. doi: 10.1097/00001574-200109000-00006

Figure 3. Crosstalk between the epidermal growth factor (EGF)-Ras- extracellular regulated kinase (Erk)-mitogen-activated protein (MAP) kinase pathway and both the transforming growth factor-β-inducible early response gene TIEG and Smad signaling pathway in cancer.

Figure 3

Hypersensitive Ras and its downstream mediator kinase Erk block transforming growth factor-β (TGFβ) signaling through phosphorylation of the receptor Smads S2/S3 and thereby inhibit the complex formation with Smad4. In addition, EGF-activated Erk MAPkinase phosphorylates TIEG2 and thereby antagonizes its transcriptional repression activity through interfering with the binding of the Sin3A corepressor complex.