ArticleEuropean journal of human genetics : EJHG2012
Transgenic complementation of MeCP2 deficiency: phenotypic rescue of Mecp2-null mice by isoform-specific transgenes.
Article in European journal of human genetics : EJHG, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 56 citations in OpenAlex.
- Single-dose administration of therapeutic divalent siRNA targeting MECP2 prevents lethality in an MECP2 duplication mouse model.Nature communications · 2026Article
- The CaInternational journal of molecular sciences · 2025Review
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- Neuronal Plasticity-Dependent Paradigm and Young Plasma Treatment Prevent Synaptic and Motor Deficit in a Rett Syndrome Mouse Model.Biomolecules · 2025Article
- SRSF9-Mediated Exon Recognition Promotes Exon 2 Inclusion inInternational journal of molecular sciences · 2025Article
- Methyl-CpG-Binding Protein 2 Emerges as a Central Player in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders.Cellular and molecular neurobiology · 2023Review
- State-of-the-art therapies for Rett syndrome.Developmental medicine and child neurology · 2023Review
- RNA Transcript Diversity in Neuromuscular Research.Journal of neuromuscular diseases · 2023Review
- Rett Syndrome andNeuropsychiatric disease and treatment · 2022Review
- Transcriptomic and Epigenomic Landscape in Rett Syndrome.Biomolecules · 2021Review
- Role of DNA Methyl-CpG-Binding Protein MeCP2 in Rett Syndrome Pathobiology and Mechanism of Disease.Biomolecules · 2021Review
- MeCP2 and Major Satellite Forward RNA Cooperate for Pericentric Heterochromatin Organization.Stem cell reports · 2020Article
- Regulation, diversity and function of MECP2 exon and 3'UTR isoforms.Human molecular genetics · 2020Review
- Cell-Type-Specific Gene Inactivation andThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- MeCP2_e2 partially compensates for lack of MeCP2_e1: A male case of Rett syndrome.Molecular genetics & genomic medicine · 2020Article
- The MeCP2E1/E2-BDNF-Frontiers in cell and developmental biology · 2020Article
- MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with different protein and DNA interactions compared to MeCP2-E2.Epigenetics & chromatin · 2019Article
- High-fat diet accelerates extreme obesity with hyperphagia in female heterozygous Mecp2-null mice.PloS one · 2019Article
- Dendrimer-mediated delivery of N-acetyl cysteine to microglia in a mouse model of Rett syndrome.Journal of neuroinflammation · 2017Article
- MeCP2_E1 N-terminal modifications affect its degradation rate and are disrupted by the Ala2Val Rett mutation.Human molecular genetics · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rett syndrome (RTT) is a disorder that affects patients' ability to communicate, move and behave. RTT patients are characterized by impaired language, stereotypic behaviors, frequent seizures, ataxia and sleep disturbances, with the onset of symptoms occurring after a period of seemingly normal development. RTT is caused by mutations in methyl-CpG binding protein 2 (MECP2), an X-chromosome gene encoding for MeCP2, a protein that regulates gene expression. MECP2 generates two alternative splice variants encoding two protein isoforms that differ only in the N-terminus. Although no functional differences have been identified for these splice variants, it has been suggested that the RTT phenotype may occur in the presence of a functional MeCP2-e2 protein. This suggests that the two isoforms might be functionally distinct. Supporting this notion, the two variants show regional and age-related differences in transcript abundance. Here, we show that transgenic expression of either the MeCP2-e1 or MeCP2-e2 splice variant results in prevention of development of RTT-like phenotypic manifestations in a mouse model lacking Mecp2. Our results indicate that the two MeCP2 splice variants can substitute for each other and fulfill the basic functions of MeCP2 in the mouse brain.
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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.