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XB-ART-41051
J Biol Chem April 2, 2010; 285 (14): 10890-901.

Xenopus skip modulates Wnt/beta-catenin signaling and functions in neural crest induction.

Wang Y , Fu Y , Gao L , Zhu G , Liang J , Gao C , Huang B , Fenger U , Niehrs C , Chen YG , Wu W .


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.

PubMed ID: 20103590
PMC ID: PMC2856295
Article link: J Biol Chem

Genes referenced: actl6a axin2 en2 h4c4 hdac1 inpp5k lef1 myc ncam1 nog otx2 pin1 snai2 snw1 sox3 tbx2 tbxt uts2r wnt1 wnt3a wnt8a
GO keywords: beta-catenin binding [+]
Morpholinos: snw1 MO1 snw1 MO2


Article Images: [+] show captions
References [+] :
Abu-Elmagd, Frizzled7 mediates canonical Wnt signaling in neural crest induction. 2006, Pubmed, Xenbase


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