| Degradation of the tumor suppressor Smad4 by WW and HECT domain ubiquitin ligases. | None |
| These data define the expression control of an essential BM component as a novel function for the tumor suppressor Smad4. | None |
| A targeted constitutive mutation in the APC tumor suppressor gene underlies mammary but not intestinal tumorigenesis. | None |
| A restricted spectrum of mutations in the SMAD4 tumor-suppressor gene underlies Myhre syndrome. | None |
| In vitro induction of TIAF1 self-association upregulated the expression of tumor suppressors Smad4 and WW domain-containing oxidoreductase (WOX1 or WWOX), and WOX1 in turn increased the TIAF1 expression. | None |
| These results indicate that Smad4 acts as a tumor suppressor by activating FOXH1, and then suppressing the expression of estrogen receptor, in addition to tumor migration and invasion. | None |
| Point mutations in the tumor suppressor Smad4/DPC4 enhance its phosphorylation by GSK3 and reversibly inactivate TGF-? signaling | None |
| The tumor suppressor gene SMAD4 (DPC4) may help predict which surgical patients are at higher risk for failure after definitive management and may benefit from intensified adjuvant therapy. | None |
| DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. | None |
| Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-inducible transcriptional complexes. | None |
| The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo. | None |
| The tumor suppressor SMAD4/DPC4 is essential for epiblast proliferation and mesoderm induction in mice. | None |