ArticleMolecular and cellular biology1996
DNA methylation specifies chromosomal localization of MeCP2.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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Who cites it
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 342 citations in OpenAlex.
- Genetic mechanisms underlying spermatic and testicular traits within and among cattle breeds: systematic review and prioritization of GWAS results.Journal of animal science · 2018Pooled it
- Release factor 3 degradation enhances aminoglycoside-mediated translational readthrough at MECP2 nonsense mutations.Journal of molecular medicine (Berlin, Germany) · 2026Article
- DNA methylation, nucleic acid structure, and rett mutations tune MeCP2 binding affinity and cooperativity.The Journal of biological chemistry · 2026Article
- Parental diet and offspring health: a role for the gut microbiome via epigenetics.Nature reviews. Gastroenterology & hepatology · 2025Review
- Human-Specific Organization of Proliferation and Stemness in Squamous Epithelia: A Comparative Study to Elucidate Differences in Stem Cell Organization.International journal of molecular sciences · 2025Article
- MeCP2 is a naturally supercharged protein with cell membrane transduction capabilities.Protein science : a publication of the Protein Society · 2024Article
- The Alpha-Synuclein Gene (SNCA) is a Genomic Target of Methyl-CpG Binding Protein 2 (MeCP2)-Implications for Parkinson's Disease and Rett Syndrome.Molecular neurobiology · 2024Article
- Magnetic Nanoparticle-Assisted Non-Viral CRISPR-Cas9 for Enhanced Genome Editing to Treat Rett Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MeCP2 binds to methylated DNA independently of phase separation and heterochromatin organisation.Nature communications · 2024Article
- Systematic and quantitative analysis of stop codon readthrough in Rett syndrome nonsense mutations.Journal of molecular medicine (Berlin, Germany) · 2024Article
- The role of prenatal choline and its impact on neurodevelopmental disorders.Frontiers in nutrition · 2024Review
- Epigenetics in rare neurological diseases.Frontiers in cell and developmental biology · 2024Review
- Non-canonical C-terminal variant of MeCP2 R344W exhibits enhanced degradation rate.IBRO neuroscience reports · 2023Article
- A novel pathogenic mutation of MeCP2 impairs chromatin association independent of protein levels.Genes & development · 2023Article
- The MECP2-TRD domain interacts with the DNMT3A-ADD domain at the H3-tail binding site.Protein science : a publication of the Protein Society · 2023Article
- MeCP2-induced heterochromatin organization is driven by oligomerization-based liquid-liquid phase separation and restricted by DNA methylation.Nucleus (Austin, Tex.) · 2022Article
- A brief history of MECP2 duplication syndrome: 20-years of clinical understanding.Orphanet journal of rare diseases · 2022Review
- Disruption of MeCP2-TCF20 complex underlies distinct neurodevelopmental disorders.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Comparative analysis of potential broad-spectrum neuronal Cre drivers.Wellcome open research · 2022Article
- Neuronal non-CG methylation is an essential target for MeCP2 function.Molecular cell · 2021Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MeCP2 is a chromosomal protein that is concentrated in the centromeric heterochromatin of mouse cells. In vitro, the protein binds preferentially to DNA containing a single symmetrically methylated CpG. To find out whether the heterochromatic localization of MeCP2 depended on DNA methylation, we transiently expressed MeCP2-LacZ fusion proteins in cultured cells. Intact protein was targeted to heterochromatin in wild-type cells but was inefficiently localized in mutant cells with low levels of genomic DNA methylation. Deletions within MeCP2 showed that localization to heterochromatin required the 85-amino-acid methyl-CpG binding domain but not the remainder of the protein. Thus MeCP2 is a methyl-CpG-binding protein in vivo and is likely to be a major mediator of downstream consequences of DNA methylation.
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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.