Evidence map›Paper›PMID 28489069›Full record

ArticleNature communications2017

Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression.

Kévin Contrepois, Clément Coudereau, Bérénice A Benayoun, Nadine Schuler, Pierre-François Roux, Oliver Bischof, Régis Courbeyrette, Cyril Carvalho, Jean-Yves Thuret, Zhihai Ma and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
9.3field-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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.

  1. Pooled it
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  12. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
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57 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

23 authors at 7 institutions in 3 countries.

Kévin ContrepoisInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Clément CoudereauInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Bérénice A BenayounDepartment of Genetics, Stanford University, Stanford, California 94305-5120, USA.
Nadine SchulerDepartment of Radiation Oncology, Saarland University, 66421 Homburg (Saar), Germany.
Pierre-François RouxInstitut Pasteur/INSERM U933, Laboratory of Nuclear Organization and Oncogenesis, Department of Cell Biology and Infection, 75015 Paris, France.
Oliver BischofInstitut Pasteur/INSERM U933, Laboratory of Nuclear Organization and Oncogenesis, Department of Cell Biology and Infection, 75015 Paris, France.
Régis CourbeyretteInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Cyril CarvalhoInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Jean-Yves ThuretInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Zhihai MaDepartment of Genetics, Stanford University, Stanford, California 94305-5120, USA.
Céline DerboisCEA, CNG, 91057 Evry, France.
Marie-Claire NeversCEA, Service de Pharmacologie et Immunoanalyse (SPI), INRA, Université Paris-Saclay, F-91191 Gif-sur-Yvette, France.
Hervé VollandCEA, Service de Pharmacologie et Immunoanalyse (SPI), INRA, Université Paris-Saclay, F-91191 Gif-sur-Yvette, France.
Christophe E RedonLaboratory of Molecular Pharmacology, C.C.R., N.C.I., N.I.H., Bethesda, Maryland 20892, USA.
William M BonnerLaboratory of Molecular Pharmacology, C.C.R., N.C.I., N.I.H., Bethesda, Maryland 20892, USA.
Jean-François DeleuzeCEA, CNG, 91057 Evry, France.
Clotilde WielInserm U1052, Centre de Recherche en Cancérologie de Lyon, CNRS UMR5286, Centre Léon Bérard, Université de Lyon 69008, Lyon, France.
David BernardInserm U1052, Centre de Recherche en Cancérologie de Lyon, CNRS UMR5286, Centre Léon Bérard, Université de Lyon 69008, Lyon, France.ORCID 0000-0002-1557-2074
Michael P SnyderDepartment of Genetics, Stanford University, Stanford, California 94305-5120, USA.
Claudia E RübeDepartment of Radiation Oncology, Saarland University, 66421 Homburg (Saar), Germany.
Robert OlasoCEA, CNG, 91057 Evry, France.
François FenailleCEA, IBITECS, Service de Pharmacologie et d'Immunoanalyse, UMR 0496, Laboratoire d'Etude du Métabolisme des Médicaments, MetaboHUB-Paris, Université Paris Saclay, F-91191 Gif-sur-Yvette cedex, France.
Carl MannInstitute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay, 91198 Gif-sur-Yvette cedex, France.
Commissariat à l'Énergie Atomique et aux Énergies Alternatives · FRUniversité Paris-Sud · FRStanford University · USInserm · FRSaarland University · DEUnited States Nuclear Regulatory Commission · USUniversité Claude Bernard Lyon 1 · FR

Funding

Regulation of transcriptional consistency by broad H3K4me3 domains in young cells and during agingR00AG049934 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BENAYOUN, BERENICE ANATH · 2017 to 2019
$717k
Regulation of transcriptional consistency by broad H3K4me3 domains in young cells and during agingK99AG049934 · NIA · STANFORD UNIVERSITY · PI BENAYOUN, BERENICE ANATH · 2015 to 2016
$191k
6 · The paper itself

Abstract

The senescence of mammalian cells is characterized by a proliferative arrest in response to stress and the expression of an inflammatory phenotype. Here we show that histone H2A.J, a poorly studied H2A variant found only in mammals, accumulates in human fibroblasts in senescence with persistent DNA damage. H2A.J also accumulates in mice with aging in a tissue-specific manner and in human skin. Knock-down of H2A.J inhibits the expression of inflammatory genes that contribute to the senescent-associated secretory phenotype (SASP), and over expression of H2A.J increases the expression of some of these genes in proliferating cells. H2A.J accumulation may thus promote the signalling of senescent cells to the immune system, and it may contribute to chronic inflammation and the development of aging-associated diseases.

Indexed as

Age FactorsAnimalsCell LineCell ProliferationCellular SenescenceCytokinesDNA DamageFibroblastsGene Expression ProfilingGenetic VariationHistonesHumansInflammation MediatorsMice, Inbred C57BLSkinCytokinesHistonesInflammation Mediators

Identifiers

PMID28489069
PMCPMC5436145
OpenAlexW2613773167

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.