ArticleJournal of virology2000
Herpes simplex virus type 1 ICP4 promotes transcription preinitiation complex formation by enhancing the binding of TFIID to DNA.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
- Targeted mutagenesis of the ICP4 transactivation domain generates a protective DIVA vaccine against duck plague.Poultry science · 2026Article
- Transcription factor VIB-1 activates catalase-3 expression by promoting PIC assembly in Neurospora crassa.Nucleic acids research · 2025Article
- Sp1 facilitates continued HSV-1 gene expression in the absence of key viral transactivators.mBio · 2024Article
- A CRISPR-based rapid DNA repositioning strategy and the early intranuclear life of HSV-1.eLife · 2023Article
- Herpes Simplex Virus 1 (HSV-1) Infected Cell Protein 0 (ICP0) Targets of Ubiquitination during Productive Infection of Primary Adult Sensory Neurons.International journal of molecular sciences · 2023Article
- Full Viral Genome Sequencing and Phylogenomic Analysis of Feline Herpesvirus Type 1 (FHV-1) in Cheetahs (Viruses · 2021Article
- The Herpes Simplex Virus 1 Protein ICP4 Acts as both an Activator and a Repressor of Host Genome Transcription during Infection.Molecular and cellular biology · 2021Article
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- Noncytotoxic functions of killer cell granzymes in viral infections.PLoS pathogens · 2021Review
- Parallel G-quadruplexes recruit the HSV-1 transcription factor ICP4 to promote viral transcription in herpes virus-infected human cells.Communications biology · 2021Article
- Viral Involvement in Alzheimer's Disease.ACS chemical neuroscience · 2021Article
- The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment.Oncolytic virotherapy · 2021Review
- Single AAV-Mediated CRISPR-SaCas9 Inhibits HSV-1 Replication by Editing ICP4 in Trigeminal Ganglion Neurons.Molecular therapy. Methods & clinical development · 2020Article
- RNA Polymerase II Promoter-Proximal Pausing and Release to Elongation Are Key Steps Regulating Herpes Simplex Virus 1 Transcription.Journal of virology · 2020Article
- Article
- 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
- Proteomic analysis of the herpes simplex virus 1 virion protein 16 transactivator protein in infected cells.Proteomics · 2015Article
- Epstein-Barr virus late gene transcription depends on the assembly of a virus-specific preinitiation complex.Journal of virology · 2014Article
- Glycoprotein targeted therapeutics: a new era of anti-herpes simplex virus-1 therapeutics.Reviews in medical virology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Infected-cell polypeptide 4 (ICP4) of herpes simplex virus type 1 (HSV-1) activates the expression of many HSV genes during infection. It functions along with the cellular general transcription factors to increase the transcription rates of genes. In this study, an HSV late promoter consisting of only a TATA box and an INR element was immobilized on a magnetic resin and incubated with nuclear extracts or purified TFIID in the presence and absence of ICP4. Analysis of the complexes formed on these promoters revealed that ICP4 increased the formation of transcription preinitiation complexes (PICs) in a TATA box-dependent manner, as determined by the presence of ICP4, TFIID, TFIIB, and polymerase II on the promoter. With both nuclear extract and purified TFIID, it was determined that ICP4 helped TFIID bind to the promoter and the TATA box. These observations differed from those for the activator Gal4-VP16. As previously observed by others, Gal4-VP16 also increased the formation of PICs without helping TFIID bind to the promoter, suggesting that ICP4 and VP16 differ in their mechanism of activation and that ICP4 functions to facilitate PIC formation at an earlier step in the formation of PICs. We also observed that the DNA binding activity of ICP4 was not sufficient to help TFIID bind to the promoter and that the region of ICP4 that was responsible for this activity is located between residues 30 and 274. Taken together these results demonstrate that a specific region of ICP4 helps TFIID bind to the TATA box and that this in turn facilitates the formation of transcription PICs.
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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.