Evidence map›Paper›PMID 30149092›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2019

The role of ARID1B, a BAF chromatin remodeling complex subunit, in neural development and behavior.

Jeffrey J Moffat, Eui-Man Jung, Minhan Ka, Amanda L Smith, Byeong Tak Jeon, Gijs W E Santen, Woo-Yang Kim

Abstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Clonazepam repurposing inJournal of medical genetics · 2025
    Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. A nonsenseHeliyon · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Pleiotropic effects of a high confidence Autism Spectrum Disorder gene,Neurobiology of sleep and circadian rhythms · 2023
    Article
  13. miScience · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Jeffrey J MoffatUniversity of Nebraska Medical Center, Omaha, NE 68198, USA.
Eui-Man JungUniversity of Nebraska Medical Center, Omaha, NE 68198, USA.
Minhan KaResearch Center for Substance Abuse Pharmacology, Korea Institute of Toxicology, Daejeon, Republic of Korea.
Amanda L SmithUniversity of Nebraska Medical Center, Omaha, NE 68198, USA.
Byeong Tak JeonDepartment of Biological Sciences, Kent State University, Kent, OH 44242, USA.
Gijs W E SantenDepartment of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands.
Woo-Yang KimDepartment of Biological Sciences, Kent State University, Kent, OH 44242, USA. Electronic address: wkim2@kent.edu.
University of Nebraska Medical Center · USKent State University · USKorea Institute of Toxicology · KRLeiden University Medical Center · NL

Funding

Functional Characterization of a Causative Gene for Intellectual DisabilityR01NS091220 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KIM, WOO-YANG · 2015 to 2019
$1.7M
NINDS NIH HHS R01 NS091220
6 · The paper itself

Abstract

Haploinsufficiency of the chromatin remodeling factor ARID1B leads to autism spectrum disorder and intellectual disability. Several independent research groups, including our own, recently examined the effects of heterozygous deletion of Arid1b in mice and reported severe behavioral abnormalities reminiscent of autism spectrum disorders and intellectual disability as well as marked changes in gene expression and decreased body size. Arid1b heterozygous mice also display significant cortical excitatory/inhibitory imbalance due to altered GABAergic neuron numbers and impaired inhibitory synaptic transmission. Abnormal epigenetic modifications, including histone acetylation and methylation, are additionally associated with Arid1b haploinsufficiency in the brain. Treating adult Arid1b mutant mice with a positive GABA allosteric modulator, however, rescues multiple behavioral abnormalities, such as cognitive and social impairments, as well as elevated anxiety. While treating Arid1b haploinsufficient mice with recombinant mouse growth hormone successfully increases body size, it has no effect on aberrant behavior. Here we summarize the recent findings regarding the role of ARID1B in brain development and behavior and discuss the utility of the Arid1b heterozygous mouse model in neurodevelopmental and psychiatric research. We also discuss some of the opportunities and potential challenges in developing translational applications for humans and possible avenues for further research into the mechanisms of ARID1B pathology in the brain.

Indexed as

AnimalsBehaviorBrainDNA-Binding ProteinsHumansMental DisordersTranscription FactorsDNA-Binding ProteinsTranscription FactorsARID1BAutismBrain developmentGABA interventionIntellectual disabilityInterneuronNeural progenitor

Identifiers

PMID30149092
PMCPMC6249083
OpenAlexW2888126176

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.