Evidence map›Paper›PMID 28685753›Full record

ArticleNature communications2017

Nucleolin directly mediates Epstein-Barr virus immune evasion through binding to G-quadruplexes of EBNA1 mRNA.

María José Lista, Rodrigo Prado Martins, Olivier Billant, Marie-Astrid Contesse, Sarah Findakly, Pierre Pochard, Chrysoula Daskalogianni, Claire Beauvineau, Corinne Guetta, Christophe Jamin and 4 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 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 128 citations in OpenAlex.

  1. Increasing intrinsic protein disorder improves CD8+ immunogenicity for a SARS CoV2 vaccine candidate antigen.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 2 countries.

María José ListaInstitut National de la Santé et de la Recherche Médicale UMR1078; Université de Bretagne Occidentale, Faculté de Médecine et des Sciences de la Santé; Etablissement Français du Sang (EFS) Bretagne; CHRU Brest, Hôpital Morvan, Laboratoire de Génétique Moléculaire, 22 avenue Camille Desmoulins, Brest F-29200, France.
Rodrigo Prado MartinsCibles Thérapeutiques, Institut National de la Santé et de la Recherche Médicale UMR1162, Institut de Génétique Moléculaire, Université Paris 7, Hôpital St Louis, 27 rue Juliette Dodu, Paris F-75010, France.
Olivier BillantInstitut National de la Santé et de la Recherche Médicale UMR1078; Université de Bretagne Occidentale, Faculté de Médecine et des Sciences de la Santé; Etablissement Français du Sang (EFS) Bretagne; CHRU Brest, Hôpital Morvan, Laboratoire de Génétique Moléculaire, 22 avenue Camille Desmoulins, Brest F-29200, France.
Marie-Astrid ContesseInstitut National de la Santé et de la Recherche Médicale UMR1078; Université de Bretagne Occidentale, Faculté de Médecine et des Sciences de la Santé; Etablissement Français du Sang (EFS) Bretagne; CHRU Brest, Hôpital Morvan, Laboratoire de Génétique Moléculaire, 22 avenue Camille Desmoulins, Brest F-29200, France.
Sarah FindaklyCibles Thérapeutiques, Institut National de la Santé et de la Recherche Médicale UMR1162, Institut de Génétique Moléculaire, Université Paris 7, Hôpital St Louis, 27 rue Juliette Dodu, Paris F-75010, France.
Pierre PochardInserm UMR 1227, Lymphocytes B et Autoimmunité; Université de Bretagne Occidentale; CHRU Brest, Hôpital Morvan, Laboratoire d'Immunologie, Brest F-29200, France.
Chrysoula DaskalogianniCibles Thérapeutiques, Institut National de la Santé et de la Recherche Médicale UMR1162, Institut de Génétique Moléculaire, Université Paris 7, Hôpital St Louis, 27 rue Juliette Dodu, Paris F-75010, France.
Claire BeauvineauChemistry, Modelling and Imaging for Biology, CNRS UMR9187 - Inserm U1196, Institut Curie, Université Paris-Sud, Campus universitaire, Bat. 110, Orsay F-91405, France.
Corinne GuettaChemistry, Modelling and Imaging for Biology, CNRS UMR9187 - Inserm U1196, Institut Curie, Université Paris-Sud, Campus universitaire, Bat. 110, Orsay F-91405, France.
Christophe JaminInserm UMR 1227, Lymphocytes B et Autoimmunité; Université de Bretagne Occidentale; CHRU Brest, Hôpital Morvan, Laboratoire d'Immunologie, Brest F-29200, France.
Marie-Paule Teulade-FichouChemistry, Modelling and Imaging for Biology, CNRS UMR9187 - Inserm U1196, Institut Curie, Université Paris-Sud, Campus universitaire, Bat. 110, Orsay F-91405, France.
Robin FåhraeusCibles Thérapeutiques, Institut National de la Santé et de la Recherche Médicale UMR1162, Institut de Génétique Moléculaire, Université Paris 7, Hôpital St Louis, 27 rue Juliette Dodu, Paris F-75010, France.
Cécile VoissetInstitut National de la Santé et de la Recherche Médicale UMR1078; Université de Bretagne Occidentale, Faculté de Médecine et des Sciences de la Santé; Etablissement Français du Sang (EFS) Bretagne; CHRU Brest, Hôpital Morvan, Laboratoire de Génétique Moléculaire, 22 avenue Camille Desmoulins, Brest F-29200, France.
Marc BlondelInstitut National de la Santé et de la Recherche Médicale UMR1078; Université de Bretagne Occidentale, Faculté de Médecine et des Sciences de la Santé; Etablissement Français du Sang (EFS) Bretagne; CHRU Brest, Hôpital Morvan, Laboratoire de Génétique Moléculaire, 22 avenue Camille Desmoulins, Brest F-29200, France.
Inserm · FRÉtablissement Français du Sang · FRInstitut Cochin · FRUniversité de Bretagne Occidentale · FRInstitut National de Recherche en Santé Publique · MLUniversité Paris Cité · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oncogenic Epstein-Barr virus (EBV) evades the immune system but has an Achilles heel: its genome maintenance protein EBNA1, which is essential for viral genome maintenance but highly antigenic. EBV has seemingly evolved a system in which the mRNA sequence encoding the glycine-alanine repeats (GAr) of the EBNA1 protein limits its expression to the minimal level necessary for function while minimizing immune recognition. Here, we identify nucleolin (NCL) as a host factor required for this process via a direct interaction with G-quadruplexes formed in GAr-encoding mRNA sequence. Overexpression of NCL enhances GAr-based inhibition of EBNA1 protein expression, whereas its downregulation relieves the suppression of both expression and antigen presentation. Moreover, the G-quadruplex ligand PhenDC3 prevents NCL binding to EBNA1 mRNA and reverses GAr-mediated repression of EBNA1 expression and antigen presentation. Hence the NCL-EBNA1 mRNA interaction is a relevant therapeutic target to trigger an immune response against EBV-carrying cancers.

Indexed as

Host-Pathogen InteractionsAminoquinolinesAnimalsB-LymphocytesCell Line, TumorEpstein-Barr Virus Nuclear AntigensG-QuadruplexesHCT116 CellsHerpesvirus 4, HumanHumansImmune EvasionLeontopithecusLigandsNucleolinPhosphoproteinsPicolinic AcidsAminoquinolinesEBV-encoded nuclear antigen 1Epstein-Barr Virus Nuclear AntigensLigandsNucleolinPhosphoproteinsPicolinic AcidspyridostatinQuinolinesRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID28685753
PMCPMC5504353
OpenAlexW2725779950

What OpenQuestion holds

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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.