Evidence map›Paper›PMID 24910128›Full record

ArticleNature communications2014

An RNA polymerase II-coupled function for histone H3K36 methylation in checkpoint activation and DSB repair.

Deepak Kumar Jha, Brian D Strahl

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.0field-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

83 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
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  4. ACS omega · 2025
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  6. HumanResearch square · 2025
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23 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Deepak Kumar JhaDepartment of Biochemistry and Biophysics, School of Medicine, UNC-Chapel Hill, North Carolina, USA.
Brian D Strahl1] Department of Biochemistry and Biophysics, School of Medicine, UNC-Chapel Hill, North Carolina, USA [2] Lineberger Comprehensive Cancer Center, School of Medicine, UNC-Chapel Hill, North Carolina 27599, USA.
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Role of Set2 and H3 methylation in chromatin functionR01GM068088 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STRAHL, BRIAN D · 2003 to 2017
$3.4M
NCI NIH HHS P30 CA016086NIGMS NIH HHS GM068088NIGMS NIH HHS R01 GM068088
6 · The paper itself

Abstract

Histone modifications are major determinants of DNA double-strand break (DSB) response and repair. Here we elucidate a DSB repair function for transcription-coupled Set2 methylation at H3 lysine 36 (H3K36me). Cells devoid of Set2/H3K36me are hypersensitive to DNA-damaging agents and site-specific DSBs, fail to properly activate the DNA-damage checkpoint, and show genetic interactions with DSB-sensing and repair machinery. Set2/H3K36me3 is enriched at DSBs, and loss of Set2 results in altered chromatin architecture and inappropriate resection during G1 near break sites. Surprisingly, Set2 and RNA polymerase II are programmed for destruction after DSBs in a temporal manner--resulting in H3K36me3 to H3K36me2 transition that may be linked to DSB repair. Finally, we show a requirement of Set2 in DSB repair in transcription units--thus underscoring the importance of transcription-dependent H3K36me in DSB repair.

Indexed as

Cell Cycle CheckpointsDNA MethylationDNA RepairChromatinDNA DamageHistonesRNA Polymerase IITranscription, GeneticChromatinHistonesRNA Polymerase II

Identifiers

PMID24910128
PMCPMC4052371
OpenAlexW2086046991

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.