Cited by 208Chromatin Remodeling and CancerWnt/β-catenin signaling in development and cancerGenomics and Chromatin Dynamics

CHD8 Is an ATP-Dependent Chromatin Remodeling Factor That Regulates β-Catenin Target Genes

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Thompson, Brandi A., Tremblay, Véronique, Lin, Grace, Bochar, Daniel A.·2008·Molecular and Cellular Biology

Abstract

ATP-dependent chromatin remodeling by the CHD family of proteins plays an important role in the regulation of gene transcription. Here we report that full-length CHD8 interacts directly with beta-catenin and that CHD8 is also recruited specifically to the promoter regions of several beta-catenin-responsive genes. Our results indicate that CHD8 negatively regulates beta-catenin-targeted gene expression, since short hairpin RNA against CHD8 results in the activation of several beta-catenin target genes. This regulation is also conserved through evolution; RNA interference against kismet, the apparent Drosophila ortholog of CHD8, results in a similar activation of beta-catenin target genes. We also report the first demonstration of chromatin remodeling activity for a member of the CHD6-9 family of proteins, suggesting that CHD8 functions in transcription through the ATP-dependent modulation of chromatin structure.

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Crossref · 10.1128/mcb.00322-08

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  • Evidence from fly and human work indicates that CHD8 negatively regulates β-catenin function, either by direct binding or by recruitment to promoters of β-catenin-responsive genes.

    “There is mounting evidence from work in both fly and humans that CHD8 negatively regulates β-catenin (CTNNB1) function, either through direct binding to β-catenin, or by recruitment to promoter regions of β-catenin-responsive genes (Thompson et al., 2008).”
  • CHD8 negatively regulates beta-catenin through direct binding and downregulates beta-catenin-responsive genes by recruiting to their promoters.

    “CHD8 negatively regulates beta-catenin via direct binding and, furthermore, downregulates beta-catenin-responsive genes by recruitment to their promoter regions [73].”

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Authors
Thompson, B. A., Tremblay, V., Lin, G., & Bochar, D. A.
Affiliations
University of Michigan (US)
Venue
Molecular and Cellular Biology
Published
2008-06-01
Volume
28
Issue
12
Pages
3894-3904
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2117456217
Cited by
208
References
84
Citations by year
2026: 9 · 2025: 8 · 2024: 9 · 2023: 11 · 2022: 12 · 2021: 15 · 2020: 11 · 2019: 17 · 2018: 14 · 2017: 11 · 2016: 8 · 2015: 14 · 2014: 12 · 2013: 10 · 2012: 12
FWCI
4.80
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Michigan (P30 CA46592, 5 P30 CA46592)
  • National Institutes of Health (CA46592)
  • National Cancer Institute (5P30 CA 46592, P30CA046592)
  • National Institute of General Medical Sciences (T32GM007315)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords
CHD8, chromatin remodeling, β-catenin, Wnt signaling, transcriptional regulation, protein-protein interaction, promoter recruitment, Kismet, gene expression inhibition, evolutionarily conserved function
MeSH terms
Adenosine Triphosphate, Animals, Cell Nucleus, Chromatin, DNA Helicases, DNA-Binding Proteins, Drosophila melanogaster, Gene Expression Regulation, HeLa Cells, Humans, Models, Biological, Histone-Lysine N-Methyltransferase, Transcription Factors, Transcription, Genetic, Homeodomain Proteins, Drosophila Proteins, RNA Interference, Intracellular Signaling Peptides and Proteins, beta Catenin

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