Evidence map›Paper›PMID 24270455›Full record

ArticleRNA biology2013

Chromatin context and ncRNA highlight targets of MeCP2 in brain.

Scott S Maxwell, Gregory J Pelka, Patrick Pl Tam, Assam El-Osta

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  7. RNA Immunoprecipitation (RIP) from Purified Nuclei in Cells.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  8. mNature communications · 2024
    Article
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  19. Article
  20. Maternal Experience-Dependent Cortical Plasticity in Mice Is Circuit- and Stimulus-Specific and Requires MECP2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
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

4 authors at 4 institutions in 1 country.

Scott S MaxwellEpigenetics in Human Health and Disease Laboratory; Baker IDI Heart and Diabetes Institute; The Alfred Medical Research and Education Precinct; Melbourne, VIC, Australia.
Gregory J PelkaEmbryology Unit; Children's Medical Research Institute; Sydney, NSW, Australia.
Patrick Pl TamEmbryology Unit; Children's Medical Research Institute; Sydney, NSW, Australia; Sydney Medical School; University of Sydney; Sydney, NSW, Australia.
Assam El-OstaEpigenetics in Human Health and Disease Laboratory; Baker IDI Heart and Diabetes Institute; The Alfred Medical Research and Education Precinct; Melbourne, VIC, Australia; Epigenomic Profiling Facility; Baker IDI Heart and Diabetes Institute; The Alfred Medical Research and Education Precinct; Melbourne, VIC, Australia; Department of Pathology; The University of Melbourne; Parkville, VIC, Australia; Faculty of Medicine, Nursing and Health Sciences; Monash University; VIC, Australia.
Baker Heart and Diabetes Institute · AUChildren's Medical Research Institute · AUMigration Institute of Australia · AUThe Alfred Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery that Rett syndrome (RTT) is caused by mutation of the methyl-CpG-binding-protein MeCP2 provided a major breakthrough in understanding the neurodevelopmental disorder and accelerated MeCP2 research. However, gene regulation by MeCP2 is complicated. The current consensus for MeCP2 remains as a classical repressor complex, with major emphasis on its role in methylation-dependent binding and repression. However, recent evidence indicates additional regulatory roles, suggesting non-classical mechanisms in gene activation. This has opened the field of MeCP2 research and suggests that the gene targets may not be the usual suspects, that is, dependent only on DNA methylation. Here we examine how chromatin binding and sequence preference may confer MeCP2 functionality, and connect relevant pathways in an active genome. Finding both genomic and proteomic evidence to indicate MeCP2 spliceosome interaction, we consequently discovered broad MeCP2 enrichment of the transcriptome while our focus toward long non-coding RNA (lncRNA) revealed MeCP2 association with RNCR3. Our data may indicate an as-yet-unappreciated role between lncRNA and MeCP2. We hypothesize that ncRNA may mediate chromatin-remodeling events by interacting with MeCP2, thereby conferring changes in gene expression. We consider that these results may suggest new mechanisms of gene regulation conferred by MeCP2 and its interactions upon chromatin structure and gene function.

Indexed as

AnimalsBrainChromatinCpG IslandsDNA MethylationGene Expression RegulationGenomeMaleMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLProteomeRNA, Long NoncodingSpliceosomesChromatinMecp2 protein, mouseMethyl-CpG-Binding Protein 2ProteomeRNA, Long NoncodingchromatinDNA methylationgene expressionMeCP2ncRNAspliceosome

Identifiers

PMID24270455
PMCPMC3907483
OpenAlexW1967127643

What OpenQuestion holds

Textmetadata
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.