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Fig. 9. SMAD4^100T may cause tumors via an `APC-like' mechanism not previously associated with defective TGFß signaling. Model for the mechanism of tumorigenesis used by SMAD4^100T based upon its ability to activate WG target genes in flies. (Left) In the model, SMAD4^100T functions in a way that mimics the repression of the ARM-destruction complex (ZW3, APC and Axin) in the WG pathway. In this illustration, we show SMAD4^100T actively inhibiting the destruction complex, but SMAD4^100T may interact with the WG pathway at other points, such as target promoters. SMAD4^100T and proteins potentially affected by its activity are shown in red. (Right) The mechanism of tumorigenesis associated with loss-of-function mutations in APC. Loss of APC activity inhibits the ß-catenin destruction complex (GSK3ß, APC and Axin) leading to the overexpression of WNT target genes and Familial Adenomatous Polyposis. APC and proteins affected by the loss of APC function are shown in red.

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