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http://purl.uniprot.org/citations/16724116http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16724116http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16724116http://www.w3.org/2000/01/rdf-schema#comment"The hypermethylated in cancer 1 (HIC1) gene is epigenetically inactivated in cancer, and in addition, the haploinsufficiency of HIC1 is linked to the development of human Miller-Dieker syndrome. HIC1 encodes a zinc-finger transcription factor that acts as a transcriptional repressor. Additionally, the HIC1 protein oligomerizes via the N-terminal BTB/POZ domain and forms discrete nuclear structures known as HIC1 bodies. Here, we provide evidence that HIC1 antagonizes the TCF/beta-catenin-mediated transcription in Wnt-stimulated cells. This appears to be due to the ability of HIC1 to associate with TCF-4 and to recruit TCF-4 and beta-catenin to the HIC1 bodies. As a result of the recruitment, both proteins are prevented from association with the TCF-binding elements of the Wnt-responsive genes. These data indicate that the intracellular amounts of HIC1 protein can modulate the level of the transcriptional stimulation of the genes regulated by canonical Wnt/beta-catenin signaling."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.org/dc/terms/identifier"doi:10.1038/sj.emboj.7601147"xsd:string
http://purl.uniprot.org/citations/16724116http://purl.org/dc/terms/identifier"doi:10.1038/sj.emboj.7601147"xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Lukas J."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Lukas J."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Korinek V."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Korinek V."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Doubravska L."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Doubravska L."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Fafilek B."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Fafilek B."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Valenta T."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/author"Valenta T."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/name"EMBO J."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/name"EMBO J."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/pages"2326-2337"xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/pages"2326-2337"xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/title"HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/title"HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies."xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/volume"25"xsd:string
http://purl.uniprot.org/citations/16724116http://purl.uniprot.org/core/volume"25"xsd:string