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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.
Language English Country Great Britain
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- MeSH
- beta Catenin genetics metabolism MeSH
- Cell Nucleus metabolism MeSH
- Cytoskeletal Proteins genetics metabolism MeSH
- DNA-Binding Proteins genetics metabolism MeSH
- Financing, Organized MeSH
- Transcription, Genetic MeSH
- Culture Media, Conditioned MeSH
- Humans MeSH
- Mice MeSH
- Promoter Regions, Genetic MeSH
- Wnt Proteins genetics metabolism MeSH
- Gene Expression Regulation MeSH
- RNA Interference MeSH
- Signal Transduction physiology MeSH
- Kruppel-Like Transcription Factors MeSH
- TCF Transcription Factors genetics metabolism MeSH
- Transcription Factors genetics metabolism MeSH
- Protein Binding MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals 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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