ArticleNature neuroscience2013
Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor.
Article in Nature neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 papers, 2 of them syntheses that pooled it.
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Who cites it
254 citing papers in PubMed, 2 syntheses or guidelines pooled it, 403 citations in OpenAlex.
- Evidence Synthesis of Gene Therapy and Gene Editing from Different Disorders-Implications for Individuals with Rett Syndrome: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Autonomic dysfunction and sudden death in patients with Rett syndrome: a systematic reviewJournal of psychiatry & neuroscience : JPN · 2020Pooled it
- Drug Repurposing for Treating NCOR-Related Intellectual Disability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MeCP2 MBD-ID module: a unified DNA/RNA binding interface disrupted in Rett syndrome.Nucleic acids research · 2026Article
- Gene regulatory mechanisms downstream of DNA methylation.Nature reviews. Genetics · 2026Review
- Structures of MeCP2 bound to nucleosomes reveal distinct mechanisms of Rett syndrome mutations.bioRxiv : the preprint server for biology · 2026Article
- Metabolites with a message: impacts on epigenetics and implications for epimetabopathies.EMBO reports · 2026Review
- Translational reading frame predicts the pathogenicity of C-terminal frameshift deletions in MeCP2.eLife · 2026Article
- Programmable CRISPRtune dissects the transcriptional repressive activity of MeCP2.bioRxiv : the preprint server for biology · 2026Article
- miR126-mediated alteration of vascular integrity in Rett syndrome.Molecular psychiatry · 2026Article
- DNA methylation, nucleic acid structure, and rett mutations tune MeCP2 binding affinity and cooperativity.The Journal of biological chemistry · 2026Article
- Single-nucleus profiling reveals a core disease signature and cell type-specific vulnerabilities in early Rett syndrome.Science advances · 2026Article
- Early postnatal DNA methylation dynamics define neuronal subtypes and are disrupted by MECP2 loss.bioRxiv : the preprint server for biology · 2026Article
- Dysfunction of a SET3-like complex underlies a family of related neurological disorders.Nature communications · 2026Article
- MECP2 mutations rewire human ESC fate and bias cortical lineage commitment.Stem cell reports · 2026Article
- DNA Methylation Dynamics in Development and Disease: Insights from Zebrafish Models.Biomedicines · 2026Review
- MeCP2 gene dosage-dependent neurodevelopmentally restricted defects arise by aberrant activation of cell fate-determining bivalent genes.Nature communications · 2026Article
- MeCP2 requires interactions with nucleosome linker DNA to read chromatin DNA methylation.Nature communications · 2026Article
- MeCP2 NID interaction with RNA: implications for Rett syndrome-relevant protein regulation.Human molecular genetics · 2026Article
- Early differential impact of MeCP2 mutations on functional networks in Rett syndrome patient-derived human cortical organoids.Nature communications · 2026Article
194 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.
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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 OpenQuestion graph.