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- W1983324713 abstract "Both canonical Wnt/β-catenin and TGFβ/Smad signaling pathways coordinately regulate pattern formation during embryogenesis as well as tumor progression. Evidence of cross-talk between these two pathways has been reported. Here we demonstrated that the Activin-like kinase 4 (Alk4)/Smad2 pathway facilitates the transcriptional activity of the oncogenic Wnt/β-catenin/Tcf4 pathway through a novel Smad4-independent mechanism. Upon activation, Smad2 physically interacted with Tcf4, β-catenin and the co-activator p300 to enhance transcriptional activity of β-catenin/Tcf4 through the histone acetyltransferase activity of p300. Transactivation by Smad2 was independent of a Smad-binding element (SBE) and Smad4. Indeed, the enhancement of β-catenin/Tcf4 transcriptional activity by activated Smad2 was negatively regulated by the presence of Smad4. Moreover, a tumor-derived missense mutant of Smad2, lacking the ability to bind to Smad4 was still able to enhance the Tcf4 transcriptional reporter in the presence of β-catenin and Tcf4. Our findings suggest that Smad2 may function as an activator of canonical Wnt/β-catenin/Tcf4 signaling through a SBE/Smad4-independent pathway." @default.
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- W1983324713 date "2008-09-01" @default.
- W1983324713 modified "2023-10-13" @default.
- W1983324713 title "Smad2 functions as a co-activator of canonical Wnt/β-catenin signaling pathway independent of Smad4 through histone acetyltransferase activity of p300" @default.
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- W1983324713 doi "https://doi.org/10.1016/j.cellsig.2008.05.003" @default.
- W1983324713 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2578836" @default.
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