Evidence map›Paper›PMID 35185468›Full record

ReviewFrontiers in molecular neuroscience2022

Insights Into the Emerging Role of Baf53b in Autism Spectrum Disorder.

Megan E Rowland, Jana M Jajarmi, Tess S M Osborne, Annie Vogel Ciernia

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Multi-omic analysis of the ciliogenic transcription factorbioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Review
  6. Decoding the genetic landscape of autism: A comprehensive review.World journal of clinical pediatrics · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. 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

4 authors at 1 institution in 1 country.

Megan E RowlandDepartment of Biochemistry and Molecular Biology, Djavad Mowafaghian Centre for Brain Health, The University of British Columbia, Vancouver, BC, Canada.
Jana M JajarmiDepartment of Biochemistry and Molecular Biology, Djavad Mowafaghian Centre for Brain Health, The University of British Columbia, Vancouver, BC, Canada.
Tess S M OsborneDepartment of Biochemistry and Molecular Biology, Djavad Mowafaghian Centre for Brain Health, The University of British Columbia, Vancouver, BC, Canada.
Annie Vogel CierniaDepartment of Biochemistry and Molecular Biology, Djavad Mowafaghian Centre for Brain Health, The University of British Columbia, Vancouver, BC, Canada.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accurate and precise regulation of gene expression is necessary to ensure proper brain development and plasticity across the lifespan. As an ATP-dependent chromatin-remodeling complex, the BAF (Brg1 Associated Factor) complex can alter histone-DNA interactions, facilitating dynamic changes in gene expression by controlling DNA accessibility to the transcriptional machinery. Mutations in 12 of the potential 29 subunit genes that compose the BAF nucleosome remodeling complex have been identified in several developmental disorders including Autism spectrum disorders (ASD) and intellectual disability. A novel, neuronal version of BAF (nBAF) has emerged as promising candidate in the development of ASD as its expression is tied to neuron differentiation and it's hypothesized to coordinate expression of synaptic genes across brain development. Recently, mutations in BAF53B, one of the neuron specific subunits of the nBAF complex, have been identified in patients with ASD and Developmental and epileptic encephalopathy-76 (DEE76), indicating BAF53B is essential for proper brain development. Recent work in cultured neurons derived from patients with BAF53B mutations suggests links between loss of nBAF function and neuronal dendritic spine formation. Deletion of one or both copies of mouse Baf53b disrupts dendritic spine development, alters actin dynamics and results in fewer synapses

Indexed as

BAF complexchromatin remodelinggene expressionlong-term memorysynaptic plasticity

Identifiers

PMID35185468
PMCPMC8852769
OpenAlexW4210447501

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.