ArticleJournal of virology2004
Cellular repressor inhibits human cytomegalovirus transcription from the UL127 promoter.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
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- NFκB and Cyclic AMP Response Element Sites Mediate the Valproic Acid and UL138 Responsiveness of the Human Cytomegalovirus Major Immediate Early Enhancer and Promoter.Journal of virology · 2023Article
- The human cytomegalovirus decathlon: Ten critical replication events provide opportunities for restriction.Frontiers in cell and developmental biology · 2022Review
- Epigenetic reprogramming of host and viral genes by Human Cytomegalovirus infection in Kasumi-3 myeloid progenitor cells at early times post-infection.Journal of virology · 2021Article
- Regulation of the MIE Locus During HCMV Latency and Reactivation.Pathogens (Basel, Switzerland) · 2020Review
- Bright and Early: Inhibiting Human Cytomegalovirus by Targeting Major Immediate-Early Gene Expression or Protein Function.Viruses · 2020Review
- The 5' Untranslated Region of the Major Immediate Early mRNA Is Necessary for Efficient Human Cytomegalovirus Replication.Journal of virology · 2018Article
- Immediate-Early (IE) gene regulation of cytomegalovirus: IE1- and pp71-mediated viral strategies against cellular defenses.Virologica Sinica · 2014Review
- Functional annotation of human cytomegalovirus gene products: an update.Frontiers in microbiology · 2014Review
- Early inhibitors of human cytomegalovirus: state-of-art and therapeutic perspectives.Pharmacology & therapeutics · 2011Review
- Histone deacetylase 3, not histone deacetylase 2, interacts with the major immediate early locus of human cytomegalovirus.Virology journal · 2011Article
- Alternative splicing of the human cytomegalovirus major immediate-early genes affects infectious-virus replication and control of cellular cyclin-dependent kinase.Journal of virology · 2011Article
- The CREB site in the proximal enhancer is critical for cooperative interaction with the other transcription factor binding sites to enhance transcription of the major intermediate-early genes in human cytomegalovirus-infected cells.Journal of virology · 2009Article
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- Role of the cytomegalovirus major immediate early enhancer in acute infection and reactivation from latency.Medical microbiology and immunology · 2008Review
- Reversal of human cytomegalovirus major immediate-early enhancer/promoter silencing in quiescently infected cells via the cyclic AMP signaling pathway.Journal of virology · 2007Article
- The autoregulatory and transactivating functions of the human cytomegalovirus IE86 protein use independent mechanisms for promoter binding.Journal of virology · 2007Article
- High-efficiency promoter-dependent transduction by adeno-associated virus type 6 vectors in mouse lung.Human gene therapy · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The region of the human cytomegalovirus (HCMV) genome between the UL127 promoter and the major immediate-early (MIE) enhancer is referred to as the unique region. The role of this region during a viral infection is not known. In wild-type HCMV-infected permissive fibroblasts, there is no transcription from the UL127 promoter at any time during productive infection. Our investigators previously reported that the region upstream of the UL127 TATA box repressed expression from the UL127 promoter (C. A. Lundquist et al., J. Virol. 73:9039-9052, 1999). The region was reported to contain functional NF1 DNA binding sites (L. Hennighausen and B. Fleckenstein, EMBO J. 5:1367-1371, 1986). Sequence analysis of this region detected additional consensus binding sites for three transcriptional regulatory proteins, FoxA (HNF-3), suppressor of Hairy wing, and CAAT displacement protein. The cis-acting elements in the unique region prevented activation of the early UL127 promoter by the HCMV MIE proteins. In contrast, deletion of the region permitted very high activation of the UL127 promoter by the viral MIE proteins. Mutation of the NF1 sites had no effect on the basal activity of the promoter. To determine the role of the other sites in the context of the viral genome, recombinant viruses were generated in which each putative repressor site was mutated and the effect on the UL127 promoter was analyzed. Mutation of the putative Fox-like site resulted in a significant increase in expression from the viral early UL127 promoter. Insertion of wild-type Fox-like sites between the HCMV immediate-early (IE) US3 TATA box and the upstream NF-kappaB-responsive enhancer (R2) also significantly decreased gene expression, but mutated Fox-like sites did not. The wild-type Fox-like site inhibits activation of a viral IE enhancer-containing promoter. Cellular protein, which is present in uninfected or infected permissive cell nuclear extracts, binds to the wild-type Fox-like site but not to mutated sites. Reasons for repression of UL127 gene transcription during productive infection are discussed.
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