{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["25(4)"],"submitter":["Edlund S"],"pubmed_abstract":["Members of the transforming growth factor beta (TGF-beta) and Wnt/wingless superfamilies regulate cell fate during development and tissue maintenance. Here we report that Smad7 interacts with beta-catenin and lymphoid enhancer binding factor 1/T-cell-specific factor (LEF1/TCF), transcriptional regulators in Wnt signaling, in a TGF-beta-dependent manner. Smad7 was found to be required for TGF-beta1-induced accumulation of beta-catenin and LEF1 in human prostate cancer (PC-3U) cells as well as in human keratinocytes (HaCaT cells). Moreover, when the endogenous Smad7 was repressed by specific small interfering RNA, TGF-beta-induced increase of activated p38, Akt phosphorylated on Ser473, glycogen synthase kinase 3beta phosphorylated on Ser9 was prevented, as well as the TGF-beta-induced association between beta-catenin and LEF1. Notably, the observed physical association of Smad7 and beta-catenin was found to be important for TGF-beta-induced apoptosis, since suppression of beta-catenin expression by small interfering RNA decreased the apoptotic response to TGF-beta."],"journal":["Molecular and cellular biology"],"pagination":["1475-88"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC548008"],"repository":["biostudies-literature"],"pubmed_title":["Interaction between Smad7 and beta-catenin: importance for transforming growth factor beta-induced apoptosis."],"pmcid":["PMC548008"],"pubmed_authors":["Lee SY","Aspenstrom P","Grimsby S","Zhang S","Edlund S","Heldin CH","Landstrom M"],"additional_accession":[]},"is_claimable":false,"name":"Interaction between Smad7 and beta-catenin: importance for transforming growth factor beta-induced apoptosis.","description":"Members of the transforming growth factor beta (TGF-beta) and Wnt/wingless superfamilies regulate cell fate during development and tissue maintenance. Here we report that Smad7 interacts with beta-catenin and lymphoid enhancer binding factor 1/T-cell-specific factor (LEF1/TCF), transcriptional regulators in Wnt signaling, in a TGF-beta-dependent manner. Smad7 was found to be required for TGF-beta1-induced accumulation of beta-catenin and LEF1 in human prostate cancer (PC-3U) cells as well as in human keratinocytes (HaCaT cells). Moreover, when the endogenous Smad7 was repressed by specific small interfering RNA, TGF-beta-induced increase of activated p38, Akt phosphorylated on Ser473, glycogen synthase kinase 3beta phosphorylated on Ser9 was prevented, as well as the TGF-beta-induced association between beta-catenin and LEF1. Notably, the observed physical association of Smad7 and beta-catenin was found to be important for TGF-beta-induced apoptosis, since suppression of beta-catenin expression by small interfering RNA decreased the apoptotic response to TGF-beta.","dates":{"release":"2005-01-01T00:00:00Z","publication":"2005 Feb","modification":"2025-04-20T01:36:45.16Z","creation":"2019-03-27T01:08:34Z"},"accession":"S-EPMC548008","cross_references":{"pubmed":["15684397"],"doi":["10.1128/MCB.25.4.1475-1488.2005","10.1128/mcb.25.4.1475-1488.2005"]}}