Evidence map›Paper›PMID 32109204›Full record

ArticleeLife2020

Integrated analysis of H2A.Z isoforms function reveals a complex interplay in gene regulation.

Assala Lamaa, Jonathan Humbert, Marion Aguirrebengoa, Xue Cheng, Estelle Nicolas, Jacques Côté, Didier Trouche

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
2.9field-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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Key regulatory elements of the TGFβ-LRRC15 axis predict disease progression and immunotherapy resistance across cancer types.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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 2 institutions in 2 countries.

Assala LamaaLBCMCP, Centre de Biologie Intégrative, Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0001-7706-1694
Jonathan HumbertSt-Patrick Research Group in Basic Oncology, Laval University Cancer Research Center and Oncology Division of CHU de Québec-Université Laval Research Center, Quebec, Canada.ORCID 0000-0002-1090-6207
Marion AguirrebengoaBigA Core Facility, Centre de Biologie Intégrative, Université de Toulouse, CNRS, UPS, Toulouse, France.
Xue ChengSt-Patrick Research Group in Basic Oncology, Laval University Cancer Research Center and Oncology Division of CHU de Québec-Université Laval Research Center, Quebec, Canada.
Estelle NicolasLBCMCP, Centre de Biologie Intégrative, Université de Toulouse, CNRS, UPS, Toulouse, France.
Jacques CôtéSt-Patrick Research Group in Basic Oncology, Laval University Cancer Research Center and Oncology Division of CHU de Québec-Université Laval Research Center, Quebec, Canada.ORCID 0000-0001-6751-555X
Didier TroucheLBCMCP, Centre de Biologie Intégrative, Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0003-1398-6481
Centre National de la Recherche Scientifique · FRUniversité Laval · CA

Funding

CIHR FDN-143314
6 · The paper itself

Abstract

The H2A.Z histone variant plays major roles in the control of gene expression. In human, H2A.Z is encoded by two genes expressing two isoforms, H2A.Z.1 and H2A.Z.2 differing by three amino acids. Here, we undertook an integrated analysis of their functions in gene expression using endogenously-tagged proteins. RNA-Seq analysis in untransformed cells showed that they can regulate both distinct and overlapping sets of genes positively or negatively in a context-dependent manner. Furthermore, they have similar or antagonistic function depending on genes. H2A.Z.1 and H2A.Z.2 can replace each other at Transcription Start Sites, providing a molecular explanation for this interplay. Mass spectrometry analysis showed that H2A.Z.1 and H2A.Z.2 have specific interactors, which can mediate their functional antagonism. Our data indicate that the balance between H2A.Z.1 and H2A.Z.2 at promoters is critically important to regulate specific gene expression, providing an additional layer of complexity to the control of gene expression by histone variants.

Indexed as

Gene Expression RegulationCell LineGenesHistonesHumansPromoter Regions, GeneticProtein IsoformsTranscription, Genetichistone H2A.F-ZHistonesProtein Isoformschromosomesgene expressiongenome-wide analysesH2A.Z histone varianthuman

Identifiers

PMID32109204
PMCPMC7048395
OpenAlexW3007648883

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.