ArticleMolecular and cellular biology2012
Histone H1 recruitment by CHD8 is essential for suppression of the Wnt-β-catenin signaling pathway.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
83 citing papers in PubMed, 134 citations in OpenAlex.
- Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- A Novel Variant of theGenes · 2026Article
- Molecular interactions of Chd8 in mouse brain highlights a role in chromatin-associated RNA processing.bioRxiv : the preprint server for biology · 2025Article
- Cell-type-specific dysregulation of gene expression due to Chd8 haploinsufficiency during mouse cortical development.Cell genomics · 2025Article
- CHD8 adulthood microglial knockdown in C57BL6 mice induces behavioral, morphological, and transcriptional changes in a sex-dependent manner.Translational psychiatry · 2025Article
- Excess Wnt in neurological disease.The Biochemical journal · 2025Review
- SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Circadian activity and sleep architecture in autism spectrum disorder mouse model withFrontiers in sleep · 2025Article
- Mechanisms of brain overgrowth in autism spectrum disorder with macrocephaly.Frontiers in neuroscience · 2025Review
- Molecular characteristics and oncogenic role of CHD family genes: a pan-cancer analysis based on bioinformatic and biological analysis.Scientific reports · 2024Article
- The complex etiology of autism spectrum disorder due to missense mutations of CHD8.Molecular psychiatry · 2024Article
- Distinct regulatory networks control toxin gene expression in elapid and viperid snakes.BMC genomics · 2024Article
- Epigenetic Causes of Overgrowth Syndromes.The Journal of clinical endocrinology and metabolism · 2024Review
- Heterozygous deletion of the autism-associated gene CHD8 impairs synaptic function through widespread changes in gene expression and chromatin compaction.American journal of human genetics · 2023Article
- CHD8 regulates gut epithelial cell function and affects autism-related behaviors through the gut-brain axis.Translational psychiatry · 2023Article
- Integrated genomic analysis reveals aberrations in WNT signaling in germ cell tumors of childhood and adolescence.Nature communications · 2023Article
- Clinical and Pathologic Features of Congenital Myasthenic Syndromes Caused by 35 Genes-A Comprehensive Review.International journal of molecular sciences · 2023Review
- Review
- The enteric nervous system deficits in autism spectrum disorder.Frontiers in neuroscience · 2023Review
- CHD8 suppression impacts on histone H3 lysine 36 trimethylation and alters RNA alternative splicing.Nucleic acids research · 2022Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Members of the chromodomain helicase DNA-binding (CHD) family of proteins are thought to regulate gene expression. Among mammalian CHD proteins, CHD8 was originally isolated as a negative regulator of the Wnt-β-catenin signaling pathway that binds directly to β-catenin and suppresses its transactivation activity. The mechanism by which CHD8 inhibits β-catenin-dependent transcription has been unclear, however. Here we show that CHD8 promotes the association of β-catenin and histone H1, with formation of the trimeric complex on chromatin being required for inhibition of β-catenin-dependent transactivation. A CHD8 mutant that lacks the histone H1 binding domain did not show such inhibitory activity, indicating that histone H1 recruitment is essential for the inhibitory effect of CHD8. Furthermore, either depletion of histone H1 or expression of a dominant negative mutant of this protein resulted in enhancement of the response to Wnt signaling. These observations reveal a new mode of regulation of the Wnt signaling pathway by CHD8, which counteracts β-catenin function through recruitment of histone H1 to Wnt target genes. Given that CHD8 is expressed predominantly during embryogenesis, it may thus contribute to setting a threshold for responsiveness to Wnt signaling that operates in a development-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.