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HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies
Valenta T, Lukas J, Doubravska L, Fafilek B, Korinek V.
Jazyk angličtina Země Velká Británie
E-zdroje NLK Online
Free Medical Journals od 1982 do Před 1 rokemPubMed Central od 1982
Europe PubMed Central od 1982 do Před 1 rokem
ProQuest Central od 2000-01-04 do 2013-12-11
Open Access Digital Library od 1997-01-01
Open Access Digital Library od 1997-01-01
Medline Complete (EBSCOhost) od 1997-01-02 do Před 1 rokem
Health & Medicine (ProQuest) od 2000-01-04 do 2013-12-11
Public Health Database (ProQuest) od 2000-01-04 do 2013-12-11
Wiley Free Content od 1997 do Před 1 rokem
- MeSH
- beta-katenin genetika metabolismus MeSH
- buněčné jádro metabolismus MeSH
- cytoskeletální proteiny genetika metabolismus MeSH
- DNA vazebné proteiny genetika metabolismus MeSH
- financování organizované MeSH
- genetická transkripce MeSH
- kultivační média speciální MeSH
- lidé MeSH
- myši MeSH
- promotorové oblasti (genetika) MeSH
- proteiny Wnt genetika metabolismus MeSH
- regulace genové exprese MeSH
- RNA interference MeSH
- signální transdukce fyziologie MeSH
- transkripční faktory Krüppel-like MeSH
- transkripční faktory TCF genetika metabolismus MeSH
- transkripční faktory genetika metabolismus MeSH
- vazba proteinů MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
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.
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- $a 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.
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