ArticleProceedings of the National Academy of Sciences of the United States of America2007
Partial rescue of MeCP2 deficiency by postnatal activation of MeCP2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01777542 (Pharmacological Treatment of Rett Syndrome by Stimulation of Synaptic Maturation With Recombinant Human IGF-1), which is not on this map. Cited by 138 papers, 1 of them a synthesis that pooled it.
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.
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.
Pharmacological Treatment of Rett Syndrome by Stimulation of Synaptic Maturation With Recombinant Human IGF-1(Mecasermin [rDNA] Injection)
Who cites it
138 citing papers in PubMed, 1 synthesis or guideline pooled it, 270 citations in OpenAlex.
- Variable expression ofProceedings of the National Academy of Sciences of the United States of America · 2024Pooled it
- Single-dose administration of therapeutic divalent siRNA targeting MECP2 prevents lethality in an MECP2 duplication mouse model.Nature communications · 2026Article
- MeCP2 regulates telencephalic development in human cerebral organoids.Cell reports · 2025Article
- Restoration of NEXMIF expression rescues abnormalities in gene transcription, neuron maturation and autistic-like behaviors in Nexmif knockout mice.Translational psychiatry · 2025Article
- Ectopic transcription due to inherited histone methylation may interfere with the ongoing function of differentiated neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Evidence of neuronal DNA damage in the brains of patients with Rett syndrome.Disease models & mechanisms · 2025Article
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- AI-enabled drug prediction and gene network analysis reveal therapeutic use of vorinostat for Rett Syndrome in preclinical models.Communications medicine · 2025Article
- Neuronal Plasticity-Dependent Paradigm and Young Plasma Treatment Prevent Synaptic and Motor Deficit in a Rett Syndrome Mouse Model.Biomolecules · 2025Article
- Systematic and quantitative analysis of stop codon readthrough in Rett syndrome nonsense mutations.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Sex Differences in Brain Disorders.International journal of molecular sciences · 2023Review
- Multiplex epigenome editing ofScience translational medicine · 2023Article
- Differential Sensitivity of the Protein Translation Initiation Machinery and mTOR Signaling toCells · 2022Article
- Genetic and epigenetic determinants of reactivation of Mecp2 and the inactive X chromosome in neural stem cells.Stem cell reports · 2022Article
- Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.Frontiers in synaptic neuroscience · 2022Review
- Safety and efficacy of genetic MECP2 supplementation in the R294X mouse model of Rett syndrome.Genes, brain, and behavior · 2022Article
- Potential of Multiscale Astrocyte Imaging for Revealing Mechanisms Underlying Neurodevelopmental Disorders.International journal of molecular sciences · 2021Review
- Article
- Substantial acetylcholine reduction in multiple brain regions of Mecp2-deficient female rats and associated behavioral abnormalities.PloS one · 2021Article
- The Molecular Functions of MeCP2 in Rett Syndrome Pathology.Frontiers in genetics · 2021Review
78 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In humans, mutations in the X-linked MECP2 gene, are the cause of Rett syndrome (RTT), a neurodevelopmental disorder that affects mainly girls. MeCP2 binds to methylated CpGs and is thought to act as a transcriptional repressor. In male mice, deletion or targeted mutation of Mecp2 leads to lethality and causes a neuronal phenotype. Selective mutation of Mecp2 in postnatal neurons results in a similar, although delayed, phenotype, suggesting that the symptoms are caused by MeCP2 deficiency in postmitotic neurons. In agreement with this idea, expression of a Mecp2 transgene in postmitotic neurons of Mecp2-null mutant mice resulted in the phenotypical rescue of the symptoms. To assess whether postnatal activation of MeCP2 in mutant animals could also affect the progression of the disorder, we constructed a conditionally active Mecp2 "rescue transgene" that was activated between P0 and P30. The Mecp2 transgene was under the control of the CAGGS promoter and was activated by using brain specific Cre-mediated recombination. Our results indicate that postnatal, neuron-specific activation of MeCP2 as late as 2-4 weeks of age significantly prolonged the lifespan of mutant animals and delayed the onset of neurologic symptoms.
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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.