Evidence map›Paper›PMID 25929186›Full record

ArticleNeuroscience letters2015

Camk2a-Cre-mediated conditional deletion of chromatin remodeler Brg1 causes perinatal hydrocephalus.

Mou Cao, Jiang I Wu

Abstract read
In one paragraph

Article in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A novel hypomorphic allele ofDisease models & mechanisms · 2020
    Article
  6. Article
  7. The Role of BRG1 in Antioxidant and Redox Signaling.Oxidative medicine and cellular longevity · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. 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

2 authors at 1 institution in 1 country.

Mou CaoDepartment of Physiology and Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Jiang I WuDepartment of Physiology and Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: jiang9.wu@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

Role of autism-associated chromatin remodeler Brg1 in neuronal developmentR21MH102820 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI WU, JIANG · 2014 to 2015
$437k
NIMH NIH HHS MH102820NIMH NIH HHS R21 MH102820
6 · The paper itself

Abstract

Mammalian SWI/SNF-like BAF chromatin remodeling complexes are essential for many aspects of neural development. Mutations in the genes encoding the core subunit Brg1/SmarcA4 or other complex components cause neurodevelopmental diseases and are associated with autism. Congenital hydrocephalus is a serious brain disorder often experienced by these patients. We report a role of Brg1 in the pathogenesis of hydrocephalus disorder. We discovered an unexpected early activity of mouse Camk2a-Cre transgene, which mediates Brg1 deletion in a subset of forebrain neurons beginning in the late embryonic stage. Brg1 deletion in these neurons led to severe congenital hydrocephalus with enlargement of the lateral ventricles and attenuation of the cerebral cortex. The Brg1-deficient mice had significantly smaller subcommissural organs and narrower Sylvian aqueducts than mice that express normal levels of Brg1. Effects were non-cell autonomous and may be responsible for the development of the congenital hydrocephalus phenotype. Our study provides evidence indicating that abnormalities in Brg1 function result in defects associated with neurodevelopmental disorders and autism.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cerebral AqueductConstriction, PathologicDNA HelicasesHydrocephalusIntegrasesMice, TransgenicNeuronsNuclear ProteinsProsencephalonSubcommissural OrganTranscription FactorsCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouseCre recombinaseDNA HelicasesIntegrasesNuclear ProteinsSmarca4 protein, mouseTranscription FactorsAqueductAutismBrg1/SmarcA4Camk2a-CreHydrocephalusSCO

Identifiers

PMID25929186
PMCPMC4444043
OpenAlexW2019080807

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.