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- W1969201427 abstract "The beta-catenin-lymphoid enhancer factor (LEF) protein complex is the key mediator of canonical Wnt signaling and initiates target gene transcription upon ligand stimulation. In addition to beta-catenin and LEF themselves, many other proteins have been identified as necessary cofactors. Here we report that the evolutionally conserved splicing factor and transcriptional co-regulator, SKIP/SNW/NcoA62, forms a ternary complex with LEF1 and HDAC1 and mediates the repression of target genes. Loss-of-function studies showed that SKIP is obligatory for Wnt signaling-induced target gene transactivation, suggesting an important role of SKIP in the canonical Wnt signaling. Consistent with its involvement in beta-catenin signaling, the C-terminally truncated forms of SKIP are able to stabilize beta-catenin and enhance Wnt signaling. In Xenopus embryos, both overexpression and knockdown of Skip lead to reduced neural crest induction, consistent with down-regulated Wnt signaling in both cases. Our results indicate that SKIP is a novel component of the beta-catenin transcriptional complex." @default.
- W1969201427 created "2016-06-24" @default.
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- W1969201427 date "2010-04-01" @default.
- W1969201427 modified "2023-10-13" @default.
- W1969201427 title "Xenopus Skip Modulates Wnt/β-Catenin Signaling and Functions in Neural Crest Induction" @default.
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- W1969201427 doi "https://doi.org/10.1074/jbc.m109.058347" @default.
- W1969201427 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2856295" @default.
- W1969201427 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20103590" @default.
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