Evidence map›Paper›PMID 24954181›Full record

ReviewBiochimica et biophysica acta2014

Regulation of histone methylation by noncoding RNAs.

Richard I Joh, Christina M Palmieri, Ian T Hill, Mo Motamedi

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  8. The Role of microRNAs in Inflammation.International journal of molecular sciences · 2022
    Review
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  15. Role of Exosomal Non-Coding RNAs in Bone-Related Diseases.Frontiers in cell and developmental biology · 2021
    Review
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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

4 authors at 2 institutions in 1 country.

Richard I JohMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School,149 13th Street, Charlestown, MA 02129, USA.
Christina M PalmieriMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School,149 13th Street, Charlestown, MA 02129, USA.
Ian T HillMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School,149 13th Street, Charlestown, MA 02129, USA; PhD Program in Biological and Biomedical Sciences, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.
Mo MotamediMassachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School,149 13th Street, Charlestown, MA 02129, USA. Electronic address: mmotamedi@hms.harvard.edu.
Harvard University · USMassachusetts General Hospital · US

Funding

PROTON THERAPY RESEARCH AND TREATMENT CENTERC06CA059267 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI GOITEIN, MICHAEL · 1992 to 1995
–
NCI NIH HHS C06 CA059267
6 · The paper itself

Abstract

Cells can adapt to their environment and develop distinct identities by rewiring their transcriptional networks to regulate the output of key biological pathways without concomitant mutations to the underlying genes. These alterations, called epigenetic changes, persist stably through mitotic or, in some instances, meiotic cell divisions. In eukaryotes, heritable changes to chromatin structure are a prominent, but not exclusive, mechanism by which epigenetic changes are mediated. These changes are initiated by sequence-specific events, which trigger a cascade of molecular interactions resulting in feedback mechanisms, alterations in chromatin structure, histone posttranslational modifications (PTMs), and ultimately establishment of distinct transcriptional states. In recent years, advances in next generation sequencing have led to the discovery of several novel classes of noncoding RNAs (ncRNAs). In addition to their well-established cytoplasmic roles in posttranscriptional regulation of gene expression, ncRNAs have emerged as key regulators of epigenetic changes via chromatin-dependent mechanisms in organisms ranging from yeast to man. They function by affecting chromatin structure, histone PTMs, and the recruitment of transcriptional activating or repressing complexes. Among histone PTMs, lysine methylation serves as the binding substrate for the recruitment of key protein complexes involved in the regulation of genome architecture, stability, and gene expression. In this review, we will outline the known mechanisms by which ncRNAs of different origins regulate histone methylation, and in doing so contribute to a variety of genome regulatory functions in eukaryotes.

Indexed as

Epigenesis, GeneticAnimalsChromatinHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesHumansMethylationProtein Processing, Post-TranslationalRNA, UntranslatedChromatinHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesRNA, UntranslatedEpigeneticsHistone methylationlncRNANoncoding RNApiRNAsiRNA

Identifiers

PMID24954181
PMCPMC4258512
OpenAlexW1974491774

What OpenQuestion holds

Textmetadata
LicenceTDM
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.