Evidence map›Paper›PMID 29382845›Full record

ArticleNature communications2018

HTLV-1 Tax plugs and freezes UPF1 helicase leading to nonsense-mediated mRNA decay inhibition.

Francesca Fiorini, Jean-Philippe Robin, Joanne Kanaan, Malgorzata Borowiak, Vincent Croquette, Hervé Le Hir, Pierre Jalinot, Vincent Mocquet

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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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

8 authors at 7 institutions in 2 countries.

Francesca FioriniMolecular Microbiology and Structural Biochemistry, MMSB-IBCP UMR5086 CNRS, Univ Lyon1, 7 passage du Vercors, 69367, Lyon Cedex 7, France.
Jean-Philippe RobinLaboratory of Biology and Modelling of the Cell, ENS de Lyon, Univ Claude Bernard Lyon 1, CNRS UMR 5239, INSERM U1210, 46 allée d'Italie, 69364, Lyon, France.
Joanne KanaanInstitut de Biologie de l'Ecole Normale Supérieure, CNRS UMR8197, Inserm, Ecole Normale Supérieure, PSL Research University, 46 rue d'Ulm, 75005, Paris, France.
Malgorzata BorowiakLaboratory of Biology and Modelling of the Cell, ENS de Lyon, Univ Claude Bernard Lyon 1, CNRS UMR 5239, INSERM U1210, 46 allée d'Italie, 69364, Lyon, France.
Vincent CroquetteLaboratoire de Physique Statistique, École Normale Supérieure, PSL Research University, Univ Paris Diderot Sorbonne Paris-Cité, Sorbonne Univ UPMC Univ Paris 06, CNRS, 24 rue Lhomond, 75005, Paris, France.
Hervé Le HirInstitut de Biologie de l'Ecole Normale Supérieure, CNRS UMR8197, Inserm, Ecole Normale Supérieure, PSL Research University, 46 rue d'Ulm, 75005, Paris, France.
Pierre JalinotLaboratory of Biology and Modelling of the Cell, ENS de Lyon, Univ Claude Bernard Lyon 1, CNRS UMR 5239, INSERM U1210, 46 allée d'Italie, 69364, Lyon, France. pjalinot@ens-lyon.fr.
Vincent MocquetLaboratory of Biology and Modelling of the Cell, ENS de Lyon, Univ Claude Bernard Lyon 1, CNRS UMR 5239, INSERM U1210, 46 allée d'Italie, 69364, Lyon, France. vincent.mocquet@ens-lyon.fr.
Inserm · FRCenter for Integrated Protein Science Munich · DEÉcole Normale Supérieure de Lyon · FRÉcole Normale Supérieure - PSL · FRInstitut de Biologie de l'École Normale Supérieure · FRSorbonne Université · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Up-Frameshift Suppressor 1 Homolog (UPF1) is a key factor for nonsense-mediated mRNA decay (NMD), a cellular process that can actively degrade mRNAs. Here, we study NMD inhibition during infection by human T-cell lymphotropic virus type I (HTLV-1) and characterise the influence of the retroviral Tax factor on UPF1 activity. Tax interacts with the central helicase core domain of UPF1 and might plug the RNA channel of UPF1, reducing its affinity for nucleic acids. Furthermore, using a single-molecule approach, we show that the sequential interaction of Tax with a RNA-bound UPF1 freezes UPF1: this latter is less sensitive to the presence of ATP and shows translocation defects, highlighting the importance of this feature for NMD. These mechanistic insights reveal how HTLV-1 hijacks the central component of NMD to ensure expression of its own genome.

Indexed as

Nonsense Mediated mRNA DecayAdenosine TriphosphateGene Products, taxHeLa CellsHost-Pathogen InteractionsHumansHuman T-lymphotropic virus 1MutationProtein DomainsProtein TransportRNA HelicasesTrans-ActivatorsAdenosine TriphosphateGene Products, taxRNA Helicasestax protein, Human T-lymphotrophic virus 1Trans-ActivatorsUPF1 protein, human

Identifiers

PMID29382845
PMCPMC5789848
OpenAlexW2793826746

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.