ArticleCell research2007
Early growth response gene 1 (Egr-1) regulates HSV-1 ICP4 and ICP22 gene expression.
Article in Cell research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- EGR Proteins Mediate Interferon-Independent Anti-HSV-1 Responses Through Viral and Host Targets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Early Transcriptomic Response of Human Iris Stromal Cells During Herpes Simplex Virus Entry Reveals Interplay Between Cell Glycocalyx and Viral Exploitation.International journal of molecular sciences · 2026Article
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- The expression and function of HSV ICP47 and its promoter in mice.Journal of virology · 2023Article
- Examining the role of EGR1 during viral infections.Frontiers in microbiology · 2022Review
- Transcriptional study reveals a potential leptin-dependent gene regulatory network in zebrafish brain.Fish physiology and biochemistry · 2021Article
- Host signaling and EGR1 transcriptional control of human cytomegalovirus replication and latency.PLoS pathogens · 2019Article
- Egr-1 regulates RTA transcription through a cooperative involvement of transcriptional regulators.Oncotarget · 2017Article
- Overexpression of thyroid hormone receptor β1 altered thyroid hormone-mediated regulation of herpes simplex virus-1 replication in differentiated cells.Journal of neurovirology · 2016Article
- Functional Characterization of the Serine-Rich Tract of Varicella-Zoster Virus IE62.Journal of virology · 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
- A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.SOJ pharmacy & pharmaceutical sciences · 2014Article
- Construction and Characterization of Recombinant HSV-1 Expressing Early Growth Response-1.ISRN virology · 2014Article
- Induction of Transcription Factor Early Growth Response Protein 1 during HSV-1 Infection Promotes Viral Replication in Corneal Cells.British microbiology research journal · 2013Article
- Small interfering RNA targeting for infected-cell polypeptide 4 inhibits herpes simplex virus type 1 replication in retinal pigment epithelial cells.Clinical & experimental ophthalmology · 2012Article
- A wide extent of inter-strain diversity in virulent and vaccine strains of alphaherpesviruses.PLoS pathogens · 2011Article
- Article
- A5-positive primary sensory neurons are nonpermissive for productive infection with herpes simplex virus 1 in vitro.Journal of virology · 2011Article
- Lytic HSV-1 infection induces the multifunctional transcription factor Early Growth Response-1 (EGR-1) in rabbit corneal cells.Virology journal · 2011Article
- A common neuronal response to alphaherpesvirus infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms mediating herpes simplex virus type 1 (HSV-1) gene silencing during latent infection are not clear. Five copies of early growth response gene 1 (Egr-1) binding elements were identified in the intron of HSV-1 ICP22 (infected cell protein No. 22) gene, leading to the hypothesis that Egr-1 binds to the viral genome and regulates the viral gene expression. Transient co-transfection assays indicated that Egr-1 negatively regulated the transcription of both full-length and intron-removed ICP22 promoters. The same assays also revealed that Egr-1 repressed ICP4 (infected cell protein No. 4) promoter activity in a dose-dependent manner but showed less inhibition when the intron was removed. Histone deacetylation was not involved in this regulation since histone deacetylase inhibitor trichostatin A did not exhibit any effect on Egr-1-mediated repression. Chromatin immunoprecipitation assays showed that Egr-1 reduced the binding of Sp1 to the promoters and that the co-repressor Nab2 (NGFI-A/EGR1-binding protein) was recruited to the proximity of ICP4 in the presence of Egr-1. These results suggested that the multifunctional transcription factor Egr-1 can repress HSV-1 immediate-early gene expression through the recruitment of co-repressor Nab2 and reduction of Sp1 occupancy, and thus may play a critical role in HSV-1 gene silencing during latency.
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