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Extra info for Cancer Risk Coeffs for Environmental Exposure to Radionuclides (EPA 402-r-99-001)
Upon binding to TGF-~ , TGF-~RII autophosphorylates itself and phosphorylates TGF-~RI, activating its serine/threonine kinase activity (12) . This activated receptor complex then transduces TGF-~ signals to the intracellular milieu ( 13) . Numerous intracellular mediators downstream of the TGF-~ receptor complex have been identified. Members of the Smad family are major intracellular mediators of TGF-~ signaling (14) . To date , eight Smad isoforms have been found in mammals and these are divided into three groups .
Controlling TGF-beta signaling. Genes Dev 2000;14(6):627-644. 8. Derynck R, Zhang YEo Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature 2003;425(6958):577-584. 9. Akhurst RJ, Derynck R. TGF-beta signaling in cancer-a double-edged sword. Trends Cell Biol 2001;11(11):S44-S51. 10. Derynck R, Akhurst RJ, Balmain A. TGF-beta signaling in tumor suppression and cancer progression. Nat Genet 2001 ;29(2): 117-129. 11. Derynck R, Gelbart WM, Harland RM, et al. Nomenclature: vertebrate mediators of TGFbeta family signals.
The key players in this pathway include the heteromeric TGF-~ transmembrane receptor complex that, following binding to TGF-~, phosphorylates and activates a family of intracellular signaling molecules known as the Smads. Several molecules, including c-Ski and SnoN, negatively regulate TGF-~ signaling. Given the key role that transforming growth factor-f (TGF-~) plays in cell growth and survival, it is not unexpected that alterations in this pathway at different levels can result in a loss of regulated cell growth, facilitating the accumulation of further genetic insults, which can result in malignant transformation.