ArticleJournal of virology2010
The Elk-1 and serum response factor binding sites in the major immediate-early promoter of human cytomegalovirus are required for efficient viral replication in quiescent cells and compensate for inactivation of the NF-kappaB sites in proliferating cells.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Sensing the storm: how inflammatory signalling drives reactivation of the human cytomegalovirus major immediate-early promoter.The Journal of general virology · 2026Review
- SARS-CoV-2 encoded ORF3a interacts with YY1 to promote latent HCMV reactivation.PLoS pathogens · 2025Article
- 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
- Regulation of the MIE Locus During HCMV Latency and Reactivation.Pathogens (Basel, Switzerland) · 2020Review
- Activator protein-1 transactivation of the major immediate early locus is a determinant of cytomegalovirus reactivation from latency.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cytomegalovirus Latency and Reactivation: An Intricate Interplay With the Host Immune Response.Frontiers in cellular and infection microbiology · 2020Review
- SAMHD1 Modulates Early Steps during Human Cytomegalovirus Infection by Limiting NF-κB Activation.Cell reports · 2019Article
- Loss of the Human Cytomegalovirus US16 Protein Abrogates Virus Entry into Endothelial and Epithelial Cells by Reducing the Virion Content of the Pentamer.Journal of virology · 2017Article
- Human cytomegalovirus reactivation from latency: validation of a "switch" model in vitro.Virology journal · 2016Article
- Human Cytomegalovirus Latency: Approaching the Gordian Knot.Annual review of virology · 2016Article
- Bioactive Molecules Released From Cells Infected with the Human Cytomegalovirus.Frontiers in microbiology · 2016Review
- Differentiation-Coupled Induction of Human Cytomegalovirus Replication by Union of the Major Enhancer Retinoic Acid, Cyclic AMP, and NF-κB Response Elements.Journal of virology · 2015Article
- Demonstration of Tightly Radiation-Controlled Molecular Switch Based on CArG Repeats by In Vivo Molecular Imaging.Molecular imaging and biology · 2015Article
- A temporal gate for viral enhancers to co-opt Toll-like-receptor transcriptional activation pathways upon acute infection.PLoS pathogens · 2015Article
- Real-time transcriptional profiling of cellular and viral gene expression during lytic cytomegalovirus infection.PLoS pathogens · 2012Article
- The US16 gene of human cytomegalovirus is required for efficient viral infection of endothelial and epithelial cells.Journal of virology · 2012Article
- The activator protein 1 binding motifs within the human cytomegalovirus major immediate-early enhancer are functionally redundant and act in a cooperative manner with the NF-{kappa}B sites during acute infection.Journal of virology · 2011Article
- Phorbol ester-induced human cytomegalovirus major immediate-early (MIE) enhancer activation through PKC-delta, CREB, and NF-kappaB desilences MIE gene expression in quiescently infected human pluripotent NTera2 cells.Journal of virology · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major immediate-early promoter (MIEP) region of human cytomegalovirus (HCMV) plays a critical role in the regulation of lytic and latent infections by integrating multiple signals supplied by the infecting virus, the type and physiological state of the host cell, and its extracellular surroundings. The interaction of cellular transcription factors with their cognate binding sites, which are present at high densities within the enhancer upstream from the MIEP core promoter, regulate the rate of IE gene transcription and thus affect the outcome of HCMV infection. We have shown previously that the NF-kappaB binding sites within the MIEP enhancer and cellular NF-kappaB activity induced by HCMV infection are required for efficient MIEP activity and viral replication in quiescent cells (P. Caposio, A. Luganini, G. Hahn, S. Landolfo, and G. Gribaudo, Cell. Microbiol. 9:2040-2054, 2007). We now show that the inactivation of either the Elk-1 or serum response factor (SRF) binding site within the enhancer also reduces MIEP activation and viral replication of recombinant HCMV viruses in quiescent fibroblasts. In these cells, we show that the expression of either Elk-1 or SRF is required for optimal IE gene expression, and that the HCMV-stimulated activation of the MEK1/2-ERK1/2 signaling axis leads to Elk-1 transcriptional competency. Furthermore, the replication kinetics of recombinant viruses in which NF-kappaB, Elk-1, and SRF binding sites all are inactivated demonstrate that the higher levels of Elk-1 and SRF binding to MIEP in proliferating cells can compensate even for a lack of HCMV-induced NF-kappaB-mediated MIEP transactivation. These observations highlight the importance of the combination of different MIEP binding sites to optimize IE gene expression in cells in different physiological states.
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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.