Evidence map›Paper›PMID 32546717›Full record

ArticleNature communications2020

Intragenic recruitment of NF-κB drives splicing modifications upon activation by the oncogene Tax of HTLV-1.

Lamya Ben Ameur, Paul Marie, Morgan Thenoz, Guillaume Giraud, Emmanuel Combe, Jean-Baptiste Claude, Sebastien Lemaire, Nicolas Fontrodona, Hélène Polveche, Marine Bastien and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 14% 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, 37 citations in OpenAlex.

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  10. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
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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

15 authors at 2 institutions in 3 countries.

Lamya Ben AmeurLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.ORCID http://orcid.org/0000-0002-2975-8822
Paul Marie *Laboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.ORCID http://orcid.org/0000-0003-2987-7917
Morgan Thenoz *Laboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Guillaume Giraud *Laboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Emmanuel CombeLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.ORCID http://orcid.org/0000-0003-3349-6615
Jean-Baptiste ClaudeLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Sebastien LemaireLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Nicolas FontrodonaLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Hélène PolvecheCECS, I-Stem, Corbeil-Essonnes, 91100, France.
Marine BastienLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.
Antoine GessainUnité d'Epidémiologie et Physiopathologie des Virus Oncogénes, Institut Pasteur, Paris, France.
Eric WattelUniversité Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Faculté de Médecine Lyon Sud, ENS - HCL, Pierre Bénite, France.ORCID http://orcid.org/0000-0003-4254-1692
Cyril F BourgeoisLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France.ORCID http://orcid.org/0000-0002-0756-5501
Didier AuboeufLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France. didier.auboeuf@inserm.fr.ORCID http://orcid.org/0000-0002-3757-0002
Franck MortreuxLaboratory of Biology and Modelling of the Cell, Univ Lyon, ENS de Lyon, Univ Claude Bernard, CNRS UMR 5239, INSERM U1210, 46 Allée d'Italie Site Jacques Monod, 69007, Lyon, France. franck.mortreux@ens-lyon.fr.ORCID http://orcid.org/0000-0002-4840-021X
Université Claude Bernard Lyon 1 · FRInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic NF-κB activation in inflammation and cancer has long been linked to persistent activation of NF-κB-responsive gene promoters. However, NF-κB factors also massively bind to gene bodies. Here, we demonstrate that recruitment of the NF-κB factor RELA to intragenic regions regulates alternative splicing upon NF-κB activation by the viral oncogene Tax of HTLV-1. Integrative analyses of RNA splicing and chromatin occupancy, combined with chromatin tethering assays, demonstrate that DNA-bound RELA interacts with and recruits the splicing regulator DDX17, in an NF-κB activation-dependent manner. This leads to alternative splicing of target exons due to the RNA helicase activity of DDX17. Similar results were obtained upon Tax-independent NF-κB activation, indicating that Tax likely exacerbates a physiological process where RELA provides splice target specificity. Collectively, our results demonstrate a physical and direct involvement of NF-κB in alternative splicing regulation, which significantly revisits our knowledge of HTLV-1 pathogenesis and other NF-κB-related diseases.

Indexed as

Alternative SplicingDEAD-box RNA HelicasesGene Expression RegulationGene Products, taxHumansHuman T-lymphotropic virus 1Leukocytes, MononuclearNF-kappa BOncogenesTranscription Factor RelADDX17 protein, humanDdx5 protein, humanDEAD-box RNA HelicasesGene Products, taxNF-kappa BRELA protein, humantax protein, Human T-lymphotrophic virus 1Transcription Factor RelA

Identifiers

PMID32546717
PMCPMC7298006
OpenAlexW3035739326

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.