Evidence map›Paper›PMID 26207799›Full record

ArticleVirology2015

Differential effects of Sp cellular transcription factors on viral promoter activation by varicella-zoster virus (VZV) IE62 protein.

Mohamed I Khalil, William T Ruyechan, John Hay, Ann Arvin

Abstract read
In one paragraph

Article in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 6 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

4 authors at 3 institutions in 2 countries.

Mohamed I KhalilDepartments of Pediatrics and Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, United States; Department of Molecular Biology, National Research Center EL-Buhouth St., Dokki, Cairo, Egypt. Electronic address: mkhalil2@stanford.edu.
William T RuyechanDepartment of Microbiology and Immunology and the Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, NY, United States.
John HayDepartment of Microbiology and Immunology and the Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, NY, United States.
Ann ArvinDepartments of Pediatrics and Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, United States.
University at Buffalo, State University of New York · USNational Research Centre · EGStanford University · US

Funding

Varicella-Zoster Virus: T Cell/Skin Tropisms &ImmunityR01AI020459 · NIAID · STANFORD UNIVERSITY · PI OLIVER, STEFAN LYNE · 1985 to 2023
$6.4M
Varicella-zoster Virus: Tegument Proteins in PathogenesisR01AI053846 · NIAID · STANFORD UNIVERSITY · PI ARVIN, ANN · 2003 to 2012
$4.1M
Varicella-Zoster Virus: T Cell/Skin Tropisms & ImmunityR37AI020459 · NIAID · STANFORD UNIVERSITY · PI ARVIN, ANN · 2016 to 2020
$2.0M
Structure/Function of Varicella Zoster Virus DNAR01AI018449 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI RUYECHAN, WILLIAM T · 1985 to 2007
$1.8M
Structure/Function of Varicella Zoster Virus DNA.R56AI018449 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI HAY, JOHN I. · 2008 to 2009
$788k
Structure/Function of Varicella Zoster Virus DNAR21AI018449 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI RUYECHAN, WILLIAM T · 2002 to 2002
$304k
NIAID NIH HHS AI018449NIAID NIH HHS AI020459NIAID NIH HHS AI053846NIAID NIH HHS R01 AI018449NIAID NIH HHS R01 AI020459NIAID NIH HHS R01 AI053846NIAID NIH HHS R21 AI018449NIAID NIH HHS R37 AI020459NIAID NIH HHS R56 AI018449
6 · The paper itself

Abstract

The immediate early (IE) 62 protein is the major varicella-zoster virus (VZV) regulatory factor. Analysis of the VZV genome revealed 40 predicted GC-rich boxes within 36 promoters. We examined effects of ectopic expression of Sp1-Sp4 on IE62- mediated transactivation of three viral promoters. Ectopic expression of Sp3 and Sp4 enhanced IE62 activation of ORF3 and gI promoters while Sp3 reduced IE62 activation of ORF28/29 promoter and VZV DNA replication. Sp2 reduced IE62 transactivation of gI while Sp1 had no significant influence on IE62 activation with any of these viral promoters. Electrophoretic mobility shift assays (EMSA) confirmed binding of Sp1 and Sp3 but not Sp2 and Sp4 to the gI promoter. Sp1-4 bound to IE62 and amino acids 238-258 of IE62 were important for the interaction with Sp3 and Sp4 as well as Sp1. This work shows that Sp family members have differential effects on IE62-mediated transactivation in a promoter-dependent manner.

Indexed as

Gene Expression Regulation, ViralBase CompositionBase SequenceCell Line, TumorEpithelial CellsGenome, ViralHerpesvirus 3, HumanHost-Pathogen InteractionsHumansImmediate-Early ProteinsMolecular Sequence DataOpen Reading FramesPromoter Regions, GeneticProtein BindingSp1 Transcription FactorSp2 Transcription FactorIE62 protein, Human herpesvirus 3Immediate-Early ProteinsSP1 protein, humanSp1 Transcription FactorSP2 protein, humanSp2 Transcription FactorSP3 protein, humanSp3 Transcription FactorSP4 protein, humanSp4 Transcription FactorTrans-ActivatorsViral Envelope ProteinsIE62PromotersSp1Sp2Sp3Sp4TranscriptionVZV

Identifiers

PMID26207799
PMCPMC4619144
OpenAlexW937839387

What OpenQuestion holds

Textmetadata
LicenceTDM
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.