Evidence map›Paper›PMID 31147750›Full record

ReviewCellular and molecular life sciences : CMLS2019

Understanding histone H3 lysine 36 methylation and its deregulation in disease.

Jie Li, Jeong Hyun Ahn, Gang Greg Wang

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
6.9field-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

97 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
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  5. Review
  6. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
  7. Article
  8. Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
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  19. Article
  20. Article

37 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jie LiLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Jeong Hyun AhnLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Gang Greg WangLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA. greg_wang@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Targeting Lysine Methyltransferases EZH2 and EZH1 for Treating MLL-rearranged LeukemiasR01CA218600 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI JIN, JIAN, WANG, G GREG · 2017 to 2021
$2.8M
Cancer Epigenetics: A novel PRC2 Dysregulation Mechanism in Multiple MyelomaR01CA211336 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, G GREG · 2017 to 2021
$2.0M
Determining the Role of DNA Methylation Deregulation in OncogenesisR01CA215284 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, G GREG · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA211336NCI NIH HHS R01 CA215284NCI NIH HHS R01 CA218600NIH HHS R01-CA211336NIH HHS R01-CA215284NIH HHS R01-CA218600
6 · The paper itself

Abstract

Methylation of histone H3 lysine 36 (H3K36) plays crucial roles in the partitioning of chromatin to distinctive domains and the regulation of a wide range of biological processes. Trimethylation of H3K36 (H3K36me3) demarcates body regions of the actively transcribed genes, providing signals for modulating transcription fidelity, mRNA splicing and DNA damage repair; and di-methylation of H3K36 (H3K36me2) spreads out within large intragenic regions, regulating distribution of histone H3 lysine 27 trimethylation (H3K27me3) and possibly DNA methylation. These H3K36 methylation-mediated events are biologically crucial and controlled by different classes of proteins responsible for either 'writing', 'reading' or 'erasing' of H3K36 methylation marks. Deregulation of H3K36 methylation and related regulatory factors leads to pathogenesis of disease such as developmental syndrome and cancer. Additionally, recurrent mutations of H3K36 and surrounding histone residues are detected in human tumors, further highlighting the importance of H3K36 in biology and medicine. This review will elaborate on current advances in understanding H3K36 methylation and related molecular players during various chromatin-templated cellular processes, their crosstalks with other chromatin factors, as well as their deregulations in the diseased contexts.

Indexed as

DNA Modification MethylasesDNA RepairHistone DemethylasesHistone-Lysine N-MethyltransferaseHistonesHumansMethylationNeoplasmsNeurodevelopmental DisordersRNA SplicingDNA Modification MethylasesHistone DemethylasesHistone-Lysine N-MethyltransferaseHistonesCancerChromatinDemethylaseDNA damage repairDNA methylationEpigeneticsGene transcriptionH3K27me3H3K36me2H3K36me3H3K36 methylationHistone modificationMethyltransferaseSplicing

Identifiers

PMID31147750
PMCPMC11105573
OpenAlexW2947216648

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.