Evidence map›Paper›PMID 30087349›Full record

ArticleNature communications2018

Inhibition of a K9/K36 demethylase by an H3.3 point mutation found in paediatric glioblastoma.

Hsiao P J Voon, Maheshi Udugama, Wendi Lin, Linda Hii, Ruby H P Law, David L Steer, Partha P Das, Jeffrey R Mann, Lee H Wong

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 74 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Hsiao P J VoonDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Maheshi UdugamaDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Wendi LinDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Linda HiiDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Ruby H P LawDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
David L SteerBiomedical Proteomics Facility, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Partha P DasAnatomy and Developmental Biology, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Jeffrey R MannGenome Modification Platform, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia.
Lee H WongDepartment of Biochemistry and Molecular Biology, Cancer Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia. lee.wong@monash.edu.
Monash University · AUAustralian Regenerative Medicine Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An array of oncogenic histone point mutations have been identified across a number of different cancer studies. It has been suggested that some of these mutant histones can exert their effects by inhibiting epigenetic writers. Here, we report that the H3.3 G34R (glycine to arginine) substitution mutation, found in paediatric gliomas, causes widespread changes in H3K9me3 and H3K36me3 by interfering with the KDM4 family of K9/K36 demethylases. Expression of a targeted single-copy of H3.3 G34R at endogenous levels induced chromatin alterations that were comparable to a KDM4 A/B/C triple-knockout. We find that H3.3 G34R preferentially binds KDM4 while simultaneously inhibiting its enzymatic activity, demonstrating that histone mutations can act through inhibition of epigenetic erasers. These results suggest that histone point mutations can exert their effects through interactions with a range of epigenetic readers, writers and erasers.

Indexed as

MutationPoint MutationAnimalsArginineBiotinylationBrain NeoplasmsChildChromatinDisease Models, AnimalEmbryonic Stem CellsEpigenesis, GeneticGene Expression Regulation, NeoplasticGlioblastomaGlycineHistonesHumansArginineChromatinGlycineHistones

Identifiers

PMID30087349
PMCPMC6081460
OpenAlexW2887461697

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.