Evidence map›Paper›PMID 31162605›Full record

ReviewNucleic acids research2019

Emerging roles of histone modifications and HDACs in RNA splicing.

Raneen Rahhal, Edward Seto

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 102 citations in OpenAlex.

  1. Splicing-driven post-translational dysregulation: a new frontier for precision cancer medicine and immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Article
  3. HDAC11 Regulates RNA Splicing via De-Fatty Acylation of SF3B2.bioRxiv : the preprint server for biology · 2026
    Article
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  7. Review
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  15. Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024
    Review
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  17. 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

2 authors at 1 institution in 1 country.

Raneen RahhalGeorge Washington Cancer Center, Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA.
Edward SetoGeorge Washington Cancer Center, Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA.
George Washington University · US

Funding

Targeting SIRT1 in Mantle Cell LymphomaR01CA187040 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI SETO, EDWARD · 2014 to 2018
$1.6M
The Basic and Translational Implication of SIRT1 and DNMT1 in CancerR01CA169210 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI SETO, EDWARD · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA169210NCI NIH HHS R01 CA187040
6 · The paper itself

Abstract

Histone modifications and RNA splicing, two seemingly unrelated gene regulatory processes, greatly increase proteome diversity and profoundly influence normal as well as pathological eukaryotic cellular functions. Like many histone modifying enzymes, histone deacetylases (HDACs) play critical roles in governing cellular behaviors and are indispensable in numerous biological processes. While the association between RNA splicing and histone modifications is beginning to be recognized, a lack of knowledge exists regarding the role of HDACs in splicing. Recent studies however, reveal that HDACs interact with spliceosomal and ribonucleoprotein complexes, actively control the acetylation states of splicing-associated histone marks and splicing factors, and thereby unexpectedly could modulate splicing. Here, we review the role of histone/protein modifications and HDACs in RNA splicing and discuss the convergence of two parallel fields, which supports the argument that HDACs, and perhaps most histone modifying enzymes, are much more versatile and far more complicated than their initially proposed functions. Analogously, an HDAC-RNA splicing connection suggests that splicing is regulated by additional upstream factors and pathways yet to be defined or not fully characterized. Some human diseases share common underlying causes of aberrant HDACs and dysregulated RNA splicing and, thus, further support the potential link between HDACs and RNA splicing.

Indexed as

Histone CodeProtein Processing, Post-TranslationalRNA SplicingHistone DeacetylasesHumansProtein BindingRibonucleoproteinsSpliceosomesTranscription, GeneticHistone DeacetylasesRibonucleoproteins

Identifiers

PMID31162605
PMCPMC6547430
OpenAlexW2940456023

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.