ArticleAmerican journal of human genetics2015
Chromatin-Remodeling-Factor ARID1B Represses Wnt/β-Catenin Signaling.
Article in American journal of human genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 82 citations in OpenAlex.
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.G3 (Bethesda, Md.) · 2026Article
- Cell fate specification during respiratory development requires ARID1A-containing canonical BAF complex activity.Nature communications · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.bioRxiv : the preprint server for biology · 2025Article
- A novel SWI/SNF complex promotes triple-negative breast cancer progression.Cellular & molecular biology letters · 2025Article
- The TRIP12 E3 ligase induces SWI/SNF component BRG1-β-catenin interaction to promote Wnt signaling.Nature communications · 2025Article
- Tracing genomic instability in induced mesenchymal stromal cell manufacture: an integration-free transfection approach.Experimental & molecular medicine · 2025Article
- GLTSCR1 deficiency promotes colorectal cancer development through regulating non-homologous end joining.Oncogene · 2024Article
- The missing link: ARID1B non-truncating variants causing Coffin-Siris syndrome due to protein aggregation.Human genetics · 2024Article
- Untying the Gordian knot of composite hemangioendothelioma: Discovery of novel fusions.Genes, chromosomes & cancer · 2024Article
- Targeting choroidal vasculopathy via up-regulation of tRNA-derived fragment tRF-22 expression for controlling progression of myopia.Journal of translational medicine · 2023Article
- Role of brahma-related gene 1/brahma-associated factor subunits in neural stem/progenitor cells and related neural developmental disorders.World journal of stem cells · 2023Review
- Genetic mouse models of autism spectrum disorder present subtle heterogenous cardiac abnormalities.Autism research : official journal of the International Society for Autism Research · 2022Article
- Reprogramming of the epigenome in neurodevelopmental disorders.Critical reviews in biochemistry and molecular biology · 2022Review
- Zebrafish Modeling of Autism Spectrum Disorders, Current Status and Future Prospective.Frontiers in psychiatry · 2022Review
- Neurobiology of ARID1B haploinsufficiency related to neurodevelopmental and psychiatric disorders.Molecular psychiatry · 2022Review
- Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders.Nature communications · 2021Article
- Revealing the Roles of Keratin 8/18-Associated Signaling Proteins Involved in the Development of Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
- The multilayer community structure of medulloblastoma.iScience · 2021Article
- Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors.Cell reports · 2021Article
- BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex.Genes & development · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The link of chromatin remodeling to both neurodevelopment and cancer has recently been highlighted by the identification of mutations affecting BAF chromatin-remodeling components, such as ARID1B, in individuals with intellectual disability and cancer. However, the underlying molecular mechanism(s) remains unknown. Here, we show that ARID1B is a repressor of Wnt/β-catenin signaling. Through whole-transcriptome analysis, we find that in individuals with intellectual disability and ARID1B loss-of-function mutations, Wnt/β-catenin target genes are upregulated. Using cellular models of low and high Wnt/β-catenin activity, we demonstrate that knockdown of ARID1B activates Wnt/β-catenin target genes and Wnt/β-catenin-dependent transcriptional reporters in a β-catenin-dependent manner. Reciprocally, forced expression of ARID1B inhibits Wnt/β-catenin signaling downstream of the β-catenin destruction complex. Both endogenous and exogenous ARID1B associate with β-catenin and repress Wnt/β-catenin-mediated transcription through the BAF core subunit BRG1. Accordingly, mutations in ARID1B leading to partial or complete deletion of its BRG1-binding domain, as is often observed in intellectual disability and cancers, compromise association with β-catenin, and the resultant ARID1B mutant proteins fail to suppress Wnt/β-catenin signaling. Finally, knockdown of ARID1B in mouse neuroblastoma cells leads to neurite outgrowth through β-catenin. The data suggest that aberrations in chromatin-remodeling factors, such as ARID1B, might contribute to neurodevelopmental abnormalities and cancer through deregulation of developmental and oncogenic pathways, such as the Wnt/β-catenin signaling pathway.
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