ArticleJournal of virology2007
Reversal of human cytomegalovirus major immediate-early enhancer/promoter silencing in quiescently infected cells via the cyclic AMP signaling pathway.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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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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.
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Who cites it
44 citing papers in PubMed, 60 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
- Review
- iTRAQ-Based Proteomics Analysis of Human Cytomegalovirus Latency and Reactivation in T98G Cells.Journal of virology · 2022Article
- Modulation of host cell signaling during cytomegalovirus latency and reactivation.Virology journal · 2021Review
- Review
- CMV-encoded GPCR pUL33 activates CREB and facilitates its recruitment to the MIE locus for efficient viral reactivation.Journal of cell science · 2021Article
- 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
- FOXO transcription factors activate alternative major immediate early promoters to induce human cytomegalovirus reactivation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Human cytomegalovirus major immediate early transcripts arise predominantly from the canonical major immediate early promoter in reactivating progenitor-derived dendritic cells.The Journal of general virology · 2020Article
- Bright and Early: Inhibiting Human Cytomegalovirus by Targeting Major Immediate-Early Gene Expression or Protein Function.Viruses · 2020Review
- Cytomegalovirus Latency and Reactivation: An Intricate Interplay With the Host Immune Response.Frontiers in cellular and infection microbiology · 2020Review
- Src family kinase activity drives cytomegalovirus reactivation by recruiting MOZ histone acetyltransferase activity to the viral promoter.The Journal of biological chemistry · 2019Article
- Alternative promoters drive human cytomegalovirus reactivation from latency.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Molecular Determinants and the Regulation of Human Cytomegalovirus Latency and Reactivation.Viruses · 2018Review
- Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency.Virology · 2017Article
- Differential control of retrovirus silencing in embryonic cells by proteasomal regulation of the ZFP809 retroviral repressor.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cytomegalovirus latency and reactivation: recent insights into an age old problem.Reviews in medical virology · 2016Review
- Human Cytomegalovirus US28 Is Important for Latent Infection of Hematopoietic Progenitor Cells.Journal of virology · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The human cytomegalovirus (HCMV) major immediate-early (MIE) enhancer contains five functional cyclic AMP (cAMP) response elements (CRE). Because the CRE in their native context do not contribute appreciably to MIE enhancer/promoter activity in lytically infected human fibroblasts and NTera2 (NT2)-derived neurons, we postulated that they might have a role in MIE enhancer/promoter reactivation in quiescently infected cells. Here, we show that stimulation of the cAMP signaling pathway by treatment with forskolin (FSK), an adenylyl cyclase activator, greatly alleviates MIE enhancer/promoter silencing in quiescently infected NT2 neuronal precursors. The effect is immediate, independent of de novo protein synthesis, associated with the phosphorylation of ATF-1 serine 63 and CREB serine 133, dependent on protein kinase A (PKA) and the enhancer's CRE, and linked to viral-lytic-cycle advancement. Coupling of FSK treatment with the inhibition of either histone deacetylases or protein synthesis synergistically activates MIE gene expression in a manner suggesting that MIE enhancer/promoter silencing is optimally relieved by an interplay of multiple regulatory mechanisms. In contrast, MIE enhancer/promoter silence is not overcome by stimulation of the gamma interferon (IFN-gamma) signaling pathway, despite the enhancer having two IFN-gamma-activated-site-like elements. We conclude that stimulation of the cAMP/PKA signaling pathway drives CRE-dependent MIE enhancer/promoter activation in quiescently infected cells, thus exposing a potential mode of regulation in HCMV reactivation.
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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.