Evidence map›Paper›PMID 25246653›Full record

ArticleRNA (New York, N.Y.)2014

Functional analysis of Kaposi's sarcoma-associated herpesvirus vFLIP expression reveals a new mode of IRES-mediated translation.

Zulkefley Othman, Mariam K Sulaiman, Margaret M Willcocks, Nathalie Ulryck, David J Blackbourn, Bruno Sargueil, Lisa O Roberts, Nicolas Locker

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Translational Control in Virus-Infected Cells.Cold Spring Harbor perspectives in biology · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A researcher's guide to the galaxy of IRESs.Cellular and molecular life sciences : CMLS · 2017
    Review
  12. Small molecules targeting viral RNA.Wiley interdisciplinary reviews. RNA · 2016
    Review
  13. Review
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 2 institutions in 2 countries.

Zulkefley OthmanFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom.
Mariam K SulaimanFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom.
Margaret M WillcocksFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom.
Nathalie UlryckFaculté des Sciences Pharmaceutiques et Biologiques, UMR8015, Université Paris Descartes, 75270 Paris, France.
David J BlackbournFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom.
Bruno SargueilFaculté des Sciences Pharmaceutiques et Biologiques, UMR8015, Université Paris Descartes, 75270 Paris, France.
Lisa O RobertsFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom.
Nicolas LockerFaculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU27HE, United Kingdom n.locker@surrey.ac.uk.
University of Surrey · GBDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic virus, the etiological agent of Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL). One of the key viral proteins that contributes to tumorigenesis is vFLIP, a viral homolog of the FLICE inhibitory protein. This KSHV protein interacts with the NFκB pathway to trigger the expression of antiapoptotic and proinflammatory genes and ultimately leads to tumor formation. The expression of vFLIP is regulated at the translational level by an internal ribosomal entry site (IRES) element. However, the precise mechanism by which ribosomes are recruited internally and the exact location of the IRES has remained elusive. Here we show that a 252-nt fragment directly upstream of vFLIP, within a coding region, directs translation. We have established its RNA structure and demonstrate that IRES activity requires the presence of eIF4A and an intact eIF4G. Furthermore, and unusually for an IRES, eIF4E is part of the complex assembled onto the vFLIP IRES to direct translation. These molecular interactions define a new paradigm for IRES-mediated translation.

Indexed as

Binding SitesCell Line, TumorGene Expression Regulation, ViralHEK293 CellsHerpesvirus 8, HumanHumansModels, MolecularNucleic Acid ConformationRibosomesRNA, ViralTranscription, GeneticViral ProteinsRNA, Viralviral FLIP protein, Human herpesvirus 8Viral ProteinseIF4EIRESRNA structuretranslationviruses

Identifiers

PMID25246653
PMCPMC4201831
OpenAlexW2163714351

What OpenQuestion holds

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LicenceCC BY-NC
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.