Evidence map›Paper›PMID 19726500›Full record

ArticleJournal of virology2009

General and target-specific RNA binding properties of Epstein-Barr virus SM posttranscriptional regulatory protein.

Zhao Han, Dinesh Verma, Chelsey Hilscher, Dirk P Dittmer, Sankar Swaminathan

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Epstein-Barr virus co-opts TFIIH component XPB to specifically activate essential viral lytic promoters.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. Spironolactone blocks Epstein-Barr virus production by inhibiting EBV SM protein function.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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

5 authors at 3 institutions in 1 country.

Zhao HanDivision of Infectious Diseases, Department of Medicine, and University of Florida Shands Cancer Center, University of Florida, Gainesville, Florida, USA.
Dinesh Verma
Chelsey Hilscher
Dirk P Dittmer
Sankar Swaminathan
University of Florida Health · USUniversity of North Carolina at Chapel Hill · USUF Health Cancer Center

Funding

ART Modulation of Viral Pathogenesis in Oral EpitheliaR01DE018304 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2007 to 2025
$6.9M
POSTTRANSCRIPTIONAL GENE REGULATION BY EBV SM PROTEINR01CA081133 · NCI · UNIVERSITY OF UTAH · PI SWAMINATHAN, SANKAR · 1999 to 2022
$4.9M
Viral and cellular gene regulation during lytic KSHV replicationR01CA119905 · NCI · UNIVERSITY OF UTAH · PI SWAMINATHAN, SANKAR · 2006 to 2010
$1.1M
NCI NIH HHS R01 CA081133NCI NIH HHS R01 CA119905NCI NIH HHS R01 CA81133NIDCR NIH HHS DE018304NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) SM protein is an essential nuclear shuttling protein expressed by EBV early during the lytic phase of replication. SM acts to increase EBV lytic gene expression by binding EBV mRNAs and enhancing accumulation of the majority of EBV lytic cycle mRNAs. SM increases target mRNA stability and nuclear export, in addition to modulating RNA splicing. SM and its homologs in other herpesvirus have been hypothesized to function in part by binding viral RNAs and recruiting cellular export factors. Although activation of gene expression by SM is gene specific, it is unknown whether SM binds to mRNA in a specific manner or whether its RNA binding is target independent. SM-mRNA complexes were isolated from EBV-infected B-lymphocyte cell lines induced to permit lytic EBV replication, and a quantitative measurement of mRNAs corresponding to all known EBV open reading frames was performed by real-time quantitative reverse transcription-PCR. The results showed that although SM has broad RNA binding properties, there is a clear hierarchy of affinities among EBV mRNAs with respect to SM complex formation. In vitro binding assays with two of the most highly SM-associated transcripts suggested that SM binds preferentially to specific sequences or structures present in noncoding regions of some EBV mRNAs. Furthermore, the presence of these sequences conferred responsiveness to SM. These data are consistent with a mechanism of action similar to that of hnRNPs, which exert sequence-specific effects on gene expression despite having multiple degenerate consensus binding sites common to a large number of RNAs.

Indexed as

AnimalsBlotting, NorthernCallithrixCell Line, TumorGene Expression Regulation, ViralHerpesvirus 4, HumanHumansImmediate-Early ProteinsOligonucleotide Array Sequence AnalysisRNA Processing, Post-TranscriptionalRNA, ViralTrans-ActivatorsTranscriptional ActivationBRLF1 protein, Human herpesvirus 4Immediate-Early ProteinsRNA, ViralTrans-Activators

Identifiers

PMID19726500
PMCPMC2772688
OpenAlexW2014925436

What OpenQuestion holds

Textmetadata
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.