Evidence map›Paper›PMID 9811691›Full record

ArticleJournal of virology1998

A cis repression sequence adjacent to the transcription start site of the human cytomegalovirus US3 gene is required to down regulate gene expression at early and late times after infection.

P E Lashmit, M F Stinski, E A Murphy, G C Bullock

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 32 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 1 institution in 1 country.

P E LashmitDepartment of Microbiology, College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.
M F Stinski
E A Murphy
G C Bullock
University of Iowa · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
THE GENES THAT REGULATE HUMAN CYTOMEGALOVIRUS EXPRESSIONR01AI013562 · NIAID · UNIVERSITY OF IOWA · PI STINSKI, MARK F · 1985 to 2005
$1.4M
REGULATION OF HUMAN CYTOMEGALOVIRUS GENE EXPRESSIONR21AI013562 · NIAID · UNIVERSITY OF IOWA · PI STINSKI, MARK F · 2000 to 2000
$294k
NIAID NIH HHS AI-13562NIAID NIH HHS R01 AI013562NIAID NIH HHS R21 AI013562NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

Human cytomegalovirus has two enhancer-containing immediate-early (IE) promoters with a cis repression sequence (CRS) positioned immediately upstream of the transcription start site, designated the major IE (MIE) promoter and the US3 promoter. The role of the CRS upstream of the US3 transcription start site in the context of the viral genome was determined by comparing the levels of transcription from these two enhancer-containing promoters in recombinant viruses with a wild-type or mutant CRS. Upstream of the CRS of the US3 promoter was either the endogenous enhancer (R2) or silencer (R1). The downstream US3 gene was replaced with the indicator gene chloramphenicol acetyltransferase (CAT). Infected permissive human fibroblast cells or nonpermissive, undifferentiated monocytic THP-1 cells were analyzed for expression from the US3 promoter containing either the wild-type or mutant CRS. With the wild-type CRS, the maximum level of transcription in permissive cells was detected within 4 to 6 h after infection and then declined. With the mutant CRS and the R2 enhancer upstream, expression from the US3 promoter continued to increase throughout the viral replication cycle to levels 20- to 40-fold higher than for the wild type. In nonpermissive or permissive monocytic THP-1 cells, expression from the US3 promoter was also significantly higher when the CRS was mutated. Less expression was obtained when only the R1 element was present, but expression was higher when the CRS was mutated. Thus, the CRS in the enhancer-containing US3 promoter appears to allow for a short burst of US3 gene expression followed by repression at early and late times after infection. Overexpression of US3 may be detrimental to viral replication, and its level of expression must be stringently controlled. The role of the CRS and the viral IE86 protein in controlling enhancer-containing promoters is discussed.

Indexed as

Genes, ViralMembrane GlycoproteinsTrans-ActivatorsViral Envelope ProteinsViral ProteinsBase SequenceCell LineChloramphenicol O-AcetyltransferaseCytomegalovirusDNA PrimersDNA, ViralDown-RegulationEnhancer Elements, GeneticGene Expression Regulation, ViralGenes, RegulatorGenes, ReporterChloramphenicol O-AcetyltransferaseDNA PrimersDNA, Viralglycoprotein H, Cytomegalovirusglycoprotein H, Human cytomegalovirusglycoprotein O, cytomegalovirusGlycoproteinsIE2 protein, CytomegalovirusImmediate-Early ProteinsMembrane GlycoproteinsMembrane ProteinsTrans-ActivatorsUL115 protein, Human herpesvirus 5US3 protein, cytomegalovirusViral Envelope ProteinsViral Proteins

Identifiers

PMID9811691
PMCPMC110467
OpenAlexW2170116065

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.