Evidence map›Paper›PMID 29610279›Full record

ArticleThe Journal of biological chemistry2018

H3K36me3-mediated mismatch repair preferentially protects actively transcribed genes from mutation.

Yaping Huang, Liya Gu, Guo-Min Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.8field-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

59 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  14. DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024
    Review
  15. Investigating low frequency somatic mutations inbioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  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

3 authors at 2 institutions in 2 countries.

Yaping HuangFrom the Department of Basic Medical Sciences, Tsinghua University School of Medicine, 100084 Beijing, China and.
Liya Guthe Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Guo-Min LiFrom the Department of Basic Medical Sciences, Tsinghua University School of Medicine, 100084 Beijing, China and guo-min.li@utsouthwestern.edu.
Tsinghua University · CNThe University of Texas Southwestern Medical Center · US

Funding

Novel Mechanism Ensuring Replication FidelityR01GM112702 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI LI, GUO-MIN · 2016 to 2019
$1.3M
Deciphering the pathogenesis of pediatric high-grade gliomasR21CA192003 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LI, GUO-MIN · 2015 to 2016
$405k
NCI NIH HHS R21 CA192003NIGMS NIH HHS R01 GM112702
6 · The paper itself

Abstract

Histone H3 trimethylation at lysine 36 (H3K36me3) is an important histone mark involved in both transcription elongation and DNA mismatch repair (MMR). It is known that H3K36me3 recruits the mismatch-recognition protein MutSα to replicating chromatin via its physical interaction with MutSα's PWWP domain, but the exact role of H3K36me3 in transcription is undefined. Using ChIP combined with whole-genome DNA sequencing analysis, we demonstrate here that H3K36me3, together with MutSα, is involved in protecting against mutation, preferentially in actively transcribed genomic regions. We found that H3K36me3 and MutSα are much more co-enriched in exons and actively transcribed regions than in introns and nontranscribed regions. The H3K36me3-MutSα co-enrichment correlated with a much lower mutation frequency in exons and actively transcribed regions than in introns and nontranscribed regions. Correspondingly, depleting H3K36me3 or disrupting the H3K36me3-MutSα interaction elevated the spontaneous mutation frequency in actively transcribed genes, but it had little influence on the mutation frequency in nontranscribed or transcriptionally inactive regions. Similarly, H

Indexed as

DNA Mismatch RepairMutationTranscription, GeneticCalreticulinCD79 AntigensCell ProliferationChromatinCRISPR-Cas SystemsDNA-Binding ProteinsG1 Phase Cell Cycle CheckpointsGATA1 Transcription FactorGene EditingGene Expression RegulationHeLa CellsHistone-Lysine N-MethyltransferaseHistonesCalreticulinCD79 AntigensCD79A protein, humanChromatinDNA-Binding ProteinsGATA1 protein, humanGATA1 Transcription FactorG-T mismatch-binding proteinHistone-Lysine N-MethyltransferaseHistonesMutS ProteinsMYC protein, humanProto-Oncogene Proteins c-mycSETD2 protein, humanTP53 protein, humanTumor Suppressor Protein p53chromatin structureDNA mismatch repairDNA-protein interactionDNA replicationDNA transcriptionH3K36me3histone methylationMSH6

Identifiers

PMID29610279
PMCPMC5961058
OpenAlexW2795600679

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.