ArticleScientific reports2021
Differential roles of ARID1B in excitatory and inhibitory neural progenitors in the developing cortex.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Autism-like behavior Increases with age and is predated by molecular changes in Arid1b haploinsufficient mice.Neuroscience · 2026Article
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- De novo variants disrupt an LDB1-regulated transcriptional network in congenital ventriculomegaly.Brain : a journal of neurology · 2025Article
- FrozONE: quick cell nucleus enrichment for comprehensive proteomics analysis of frozen tissues.Life science alliance · 2025Article
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- Multiomic profiling of transcription factor binding and function in human brain.Nature neuroscience · 2024Article
- Autism Spectrum Disorder: Brain Areas Involved, Neurobiological Mechanisms, Diagnoses and Therapies.International journal of molecular sciences · 2024Review
- Dissecting the role of SWI/SNF component ARID1B in steady-state hematopoiesis.Blood advances · 2023Article
- CTNNB1 in neurodevelopmental disorders.Frontiers in psychiatry · 2023Review
- miScience · 2022Article
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Dendritic spine and synapse pathology in chromatin modifier-associated autism spectrum disorders and intellectual disability.Frontiers in molecular neuroscience · 2022Review
- Paving the way toward treatment solutions for CTNNB1 syndrome: a patient organization perspective.Therapeutic advances in rare diseaseReview
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Genetic evidence indicates that haploinsufficiency of ARID1B causes intellectual disability (ID) and autism spectrum disorder (ASD), but the neural function of ARID1B is largely unknown. Using both conditional and global Arid1b knockout mouse strains, we examined the role of ARID1B in neural progenitors. We detected an overall decrease in the proliferation of cortical and ventral neural progenitors following homozygous deletion of Arid1b, as well as altered cell cycle regulation and increased cell death. Each of these phenotypes was more pronounced in ventral neural progenitors. Furthermore, we observed decreased nuclear localization of β-catenin in Arid1b-deficient neurons. Conditional homozygous deletion of Arid1b in ventral neural progenitors led to pronounced ID- and ASD-like behaviors in mice, whereas the deletion in cortical neural progenitors resulted in minor cognitive deficits. This study suggests an essential role for ARID1B in forebrain neurogenesis and clarifies its more pronounced role in inhibitory neural progenitors. Our findings also provide insights into the pathogenesis of ID and ASD.
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