ArticleNature communications2022
Rescue of deficits by Brwd1 copy number restoration in the Ts65Dn mouse model of Down syndrome.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Single-cell atlas of the developing Down syndrome brain cortex.Nature medicine · 2026Article
- Multi-omics reveals cross-tissue regulatory mechanisms of autism risk loci via gut microbiota-immunity-brain axis.AMB Express · 2025Article
- Chromatin accessibility provides a window into the genetic etiology of human brain disease.Trends in genetics : TIG · 2025Review
- CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly.Nature communications · 2025Article
- Elucidating neuroepigenetic mechanisms to inform targeted therapeutics for brain disorders.iScience · 2025Review
- DYRK1A Up-Regulation Specifically Impairs a Presynaptic Form of Long-Term Potentiation.Life (Basel, Switzerland) · 2025Article
- Prognostic assessment of early-stage liver cirrhosis induced by HCV using an integrated model of CX3CR1-associated immune infiltration genes.Scientific reports · 2025Article
- Article
- In and out: Benchmarking in vitro, in vivo, ex vivo, and xenografting approaches for an integrative brain disease modeling pipeline.Stem cell reports · 2024Review
- Context-specific functions of chromatin remodellers in development and disease.Nature reviews. Genetics · 2024Review
- Unraveling the shared genetics of common epilepsies and general cognitive ability.medRxiv : the preprint server for health sciences · 2024Article
- BRWD1 orchestrates small pre-B cell chromatin topology by converting static to dynamic cohesin.Nature immunology · 2024Article
- Molecular mechanisms insulating proliferation from genotoxic stress in B lymphocytes.Trends in immunology · 2023Review
- Basal forebrain cholinergic neurons are vulnerable in a mouse model of Down syndrome and their molecular fingerprint is rescued by maternal choline supplementation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
Corrections and comments
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Authors and funding
27 authors at 9 institutions in 1 country.
Funding
Abstract
With an incidence of ~1 in 800 births, Down syndrome (DS) is the most common chromosomal condition linked to intellectual disability worldwide. While the genetic basis of DS has been identified as a triplication of chromosome 21 (HSA21), the genes encoded from HSA21 that directly contribute to cognitive deficits remain incompletely understood. Here, we found that the HSA21-encoded chromatin effector, BRWD1, was upregulated in neurons derived from iPS cells from an individual with Down syndrome and brain of trisomic mice. We showed that selective copy number restoration of Brwd1 in trisomic animals rescued deficits in hippocampal LTP, cognition and gene expression. We demonstrated that Brwd1 tightly binds the BAF chromatin remodeling complex, and that increased Brwd1 expression promotes BAF genomic mistargeting. Importantly, Brwd1 renormalization rescued aberrant BAF localization, along with associated changes in chromatin accessibility and gene expression. These findings establish BRWD1 as a key epigenomic mediator of normal neurodevelopment and an important contributor to DS-related phenotypes.
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Registered trials
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.