ArticleNature neuroscience2009
Non-cell autonomous influence of MeCP2-deficient glia on neuronal dendritic morphology.
Article in Nature neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
285 citing papers in PubMed, 1 synthesis or guideline pooled it, 461 citations in OpenAlex.
- Variable expression ofProceedings of the National Academy of Sciences of the United States of America · 2024Pooled it
- The Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability.Cells · 2026Review
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- Single-cell multiome profiling reveals neuronal bias of modulatory role of MeCP2 phosphorylation.Neurobiology of disease · 2026Article
- Astrocytes in Genetic Epilepsies: Supporting Actor or Key Player?Journal of neuroscience research · 2026Review
- The role of astrocytes in autism spectrum disorder and associated syndromes: Evidence, animal models, mechanisms, and therapeutic potential.Zoological research · 2026Review
- Neural peer pressure: intercellular dynamics and emergent phenotypes in the mosaic Rett syndrome brain.Cell communication and signaling : CCS · 2026Review
- Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Radial-glia-to-astrocyte trans-differentiation and astrocyte transcriptional convergence are coordinated by CEH-43/DLX inbioRxiv : the preprint server for biology · 2026Article
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- MeCP2-driven chromatin organization controls nuclear stiffness.Communications biology · 2025Article
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neuronal Plasticity-Dependent Paradigm and Young Plasma Treatment Prevent Synaptic and Motor Deficit in a Rett Syndrome Mouse Model.Biomolecules · 2025Article
- Neural precursor cells rescue symptoms of Rett syndrome by activation of the Interferon γ pathway.EMBO molecular medicine · 2024Article
- Rett syndrome.Nature reviews. Disease primers · 2024Review
- A genetically encoded actuator boosts L-type calcium channel function in diverse physiological settings.Science advances · 2024Article
- RettDb: the Rett syndrome omics database to navigate the Rett syndrome genomic landscape.Database : the journal of biological databases and curation · 2024Article
- Sex-specific single cell-level transcriptomic signatures of Rett syndrome disease progression.Communications biology · 2024Article
225 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
The neurodevelopmental disorder Rett syndrome (RTT) is caused by sporadic mutations in the transcriptional factor methyl-CpG-binding protein 2 (MeCP2). Although it is thought that the primary cause of RTT is cell autonomous, resulting from a lack of functional MeCP2 in neurons, whether non-cell autonomous factors contribute to the disease is unknown. We found that the loss of MeCP2 occurs not only in neurons but also in glial cells of RTT brains. Using an in vitro co-culture system, we found that mutant astrocytes from a RTT mouse model, and their conditioned medium, failed to support normal dendritic morphology of either wild-type or mutant hippocampal neurons. Our studies suggest that astrocytes in the RTT brain carrying MeCP2 mutations have a non-cell autonomous effect on neuronal properties, probably as a result of aberrant secretion of soluble factor(s).
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Identifiers
What OpenQuestion holds
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.