Evidence map›Paper›PMID 21453447›Full record

ReviewThe European journal of neuroscience2011

In sickness and in health: the role of methyl-CpG binding protein 2 in the central nervous system.

Sol Díaz de León-Guerrero, Gustavo Pedraza-Alva, Leonor Pérez-Martínez

Open access · bronzeAbstract readReview
In one paragraph

Review in The European journal of neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  10. Persistent Unresolved Inflammation in theMediators of inflammation · 2017
    Article
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  15. Epigenetic regulation of axon outgrowth and regeneration in CNS injury: the first steps forward.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013
    Review
  16. Folate and epigenetic mechanisms in neural tube development and defects.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2013
    Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sol Díaz de León-GuerreroLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, A.P. 510-3, Cuernavaca, Morelos 62271, México. leonor@ibt.unam.mx
Gustavo Pedraza-Alva
Leonor Pérez-Martínez
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The array of specialized neuronal and glial cell types that characterize the adult central nervous system originates from neuroepithelial proliferating precursor cells. The transition from proliferating neuroepithelial precursor cells to neuronal lineages is accompanied by rapid global changes in gene expression in coordination with epigenetic modifications at the level of the chromatin structure. A number of genetic studies have begun to reveal how epigenetic deregulation results in neurodevelopmental disorders such as mental retardation, autism, Rubinstein-Taybi syndrome and Rett syndrome. In this review we focus on the role of the methyl-CpG binding protein 2 (MeCP2) during development of the central nervous system and its involvement in Rett syndrome. First, we present recent findings that indicate a previously unconsidered role of glial cells in the development of Rett syndrome. Next, we discuss evidence of how MeCP2 deficiency or loss of function results in aberrant gene expression leading to Rett syndrome. We also discuss MeCP2's function as a repressor and activator of gene expression and the role of its different target genes, including microRNAs, during neuronal development. Finally, we address different signaling pathways that regulate MeCP2 expression at both the post-transcriptional and post-translational level, and discuss how mutations in MeCP2 may result in lack of responsiveness to environmental signals.

Indexed as

Brain-Derived Neurotrophic FactorCell DifferentiationCentral Nervous SystemDNA MethylationEpigenomicsGene ExpressionMethyl-CpG-Binding Protein 2MicroRNAsMutationNeurogliaNeuronsRett SyndromeRubinstein-Taybi SyndromeSignal TransductionBrain-Derived Neurotrophic FactorMethyl-CpG-Binding Protein 2MicroRNAs

Identifiers

PMID21453447
PMCPMC3110863
OpenAlexW1644008347

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.