ArticleJournal of virology2004
Differential cellular requirements for activation of herpes simplex virus type 1 early (tk) and late (gC) promoters by ICP4.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Identification of Phage RNA Polymerases That Minimize Double-Stranded RNA By-Product Formation and Their Characterization via In Vitro Transcription.Microorganisms · 2026Article
- An Epstein-Barr Virus-Encoded Protein Complex Requires an Origin of Lytic Replication In Cis to Mediate Late Gene Transcription.PLoS pathogens · 2016Article
- Full trans-activation mediated by the immediate-early protein of equine herpesvirus 1 requires a consensus TATA box, but not its cognate binding sequence.Virus research · 2016Article
- Herpesvirus Late Gene Expression: A Viral-Specific Pre-initiation Complex Is Key.Frontiers in microbiology · 2016Review
- Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Journal of virology · 2014Article
- Murine cytomegalovirus protein pM79 is a key regulator for viral late transcription.Journal of virology · 2013Article
- mRNA decay during herpes simplex virus (HSV) infections: mutations that affect translation of an mRNA influence the sites at which it is cleaved by the HSV virion host shutoff (Vhs) protein.Journal of virology · 2013Article
- Herpes simplex virus 1 ICP4 forms complexes with TFIID and mediator in virus-infected cells.Journal of virology · 2011Article
- HSV-1 Cgal+ infection promotes quaking RNA binding protein production and induces nuclear-cytoplasmic shuttling of quaking I-5 isoform in human hepatoma cells.Molecular & cellular proteomics : MCP · 2011Article
- VEGF-A expression by HSV-1-infected cells drives corneal lymphangiogenesis.The Journal of experimental medicine · 2010Article
- Factors modulating expression of Renilla luciferase from control plasmids used in luciferase reporter gene assays.Analytical biochemistry · 2010Review
- PMA induces expression from the herpes simplex virus thymidine kinase promoter via the activation of JNK and ERK in the presence of adenoviral E1A proteins.Archives of biochemistry and biophysics · 2009Article
- Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.Journal of virology · 2009Article
- Induction of cellular stress overcomes the requirement of herpes simplex virus type 1 for immediate-early protein ICP0 and reactivates expression from quiescent viral genomes.Journal of virology · 2008Article
- Stabilized binding of TBP to the TATA box of herpes simplex virus type 1 early (tk) and late (gC) promoters by TFIIA and ICP4.Journal of virology · 2008Article
- Binding of ICP4, TATA-binding protein, and RNA polymerase II to herpes simplex virus type 1 immediate-early, early, and late promoters in virus-infected cells.Journal of virology · 2008Article
- Reactivation of expression from quiescent herpes simplex virus type 1 genomes in the absence of immediate-early protein ICP0.Journal of virology · 2007Article
- DNA-dependent oligomerization of herpes simplex virus type 1 regulatory protein ICP4.Journal of virology · 2007Article
- Herpes simplex virus immediate-early protein ICP22 triggers loss of serine 2-phosphorylated RNA polymerase II.Journal of virology · 2007Article
- Phosphorylation of the varicella-zoster virus (VZV) major transcriptional regulatory protein IE62 by the VZV open reading frame 66 protein kinase.Journal of virology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The herpes simplex virus type 1 immediate-early protein, ICP4, activates the transcription of viral early and late genes and is essential for viral growth. It has been shown to bind DNA and interact with components of the general transcription machinery to activate or repress viral transcription, depending upon promoter context. Since early and late gene promoters have different architectures and cellular metabolism may be very different at early and late times after infection, the cellular requirements for ICP4-mediated activation of early and late genes may differ. This hypothesis was tested using tk and gC as representative early and late promoters, respectively. Nuclear extracts and phosphocellulose column fractions derived from nuclear extracts were able to reconstitute basal and ICP4-activated transcription of both promoters in vitro. When examining the contribution of the general transcription factors on the ability of ICP4 to activate transcription, the fraction containing the general transcription factor TFIIA was not essential for ICP4 activation of the gC promoter, but it was required for efficient activation of the tk promoter. The addition of recombinant TFIIA restored the ability of ICP4 to efficiently activate the tk promoter, but it had no net effect on activation of the gC promoter. The dispensability of TFIIA for ICP4 activation of the gC promoter required an intact INR element. In addition, microarray and Northern blot analysis indicated that TFIIA abundance may be reduced at late times of infection. This decrease in TFIIA expression during infection and its dispensability for activation of late but not early genes suggest one of possibly many mechanisms for the transition from viral early to late gene expression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.