Evidence map›Paper›PMID 33287886›Full record

ArticleActa neuropathologica communications2020

Effects of H3.3G34V mutation on genomic H3K36 and H3K27 methylation patterns in isogenic pediatric glioma cells.

Tina Yi-Ting Huang, Andrea Piunti, Jin Qi, Marc Morgan, Elizabeth Bartom, Ali Shilatifard, Amanda M Saratsis

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Oncohistones: Hijacking the histone code.Annual review of cancer biology · 2022
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  19. The correlation between polymorphisms in theTranslational pediatrics · 2021
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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

7 authors at 1 institution in 1 country.

Tina Yi-Ting HuangDepartment of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Andrea PiuntiDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Jin QiDepartment of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Marc MorganDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Elizabeth BartomDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Ali ShilatifardDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Amanda M SaratsisDepartment of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA. asaratsis@luriechildrens.org.ORCID 0000-0002-4913-2771
Northwestern University · US

Funding

Bioinformatics Analysis of Next Generation Sequencing Data from Cancer CellsR50CA221848 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Elizabeth Thomas Bartom · 2017 to 2026
$1.8M
NCI NIH HHS R50 CA221848NINDS NIH HHS K08NS097264
6 · The paper itself

Abstract

Histone H3.3 mutation (H3F3A) occurs in 50% of cortical pediatric high-grade gliomas. This mutation replaces glycine 34 with arginine or valine (G34R/V), impairing SETD2 activity (H3K36-specific trimethyltransferase). Consequently, reduced H3K36me3 is observed on H3.3G34V nucleosomes relative to wild-type, contributing to genomic instability and driving a distinct gene expression signature associated with tumorigenesis. However, it is not known if this differential H3K36me3 enrichment is due to H3.3G34V mutant protein alone. Therefore, we set to elucidate the effect of H3.3G34V mutant protein in pediatric glioma on H3K36me3, H3K27me3 and H3.3 enrichment in vitro. We found that the doxycycline-inducible shRNA knockdown of mutant H3F3A encoding the H3.3G34V protein resulted in loss of H3.3G34V enrichment and increased H3K36me3 enrichment throughout the genome. After knockdown, H3.3G34V enrichment was preserved at loci observed to have the greatest H3.3G34V and H3K36me3 enrichment prior to knockdown. Induced expression of mutant H3.3G34V protein in vitro was insufficient to induce genomic H3K36me3 enrichment patterns observed in H3.3G34V mutant glioma cells. We also observed strong co-enrichment of H3.3G34V and wild-type H3.3 protein, as well as greater H3K27me3 enrichment, in cells expressing H3.3G34V. Taken together, our study demonstrates the effects of H3.3G34V mutant protein on genomic H3K36me3, H3K27me3 and H3.3 enrichment patterns in isogenic cell lines.

Indexed as

AstrocytesBrain NeoplasmsCell Line, TumorCell ProliferationCell SurvivalChildChromatin ImmunoprecipitationChromatin Immunoprecipitation SequencingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGliomaHigh-Throughput Nucleotide SequencingHistone CodeHistonesHumansMethylationH3-3A protein, humanHistonesH3K36me3Histone H3 mutationsPediatric high-grade gliomaPost-translational modifications

Identifiers

PMID33287886
PMCPMC7722426
OpenAlexW3112502359

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.