ArticleJournal of virology2004
RBP-J (CSL) is essential for activation of the K14/vGPCR promoter of Kaposi's sarcoma-associated herpesvirus by the lytic switch protein RTA.
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 46 papers.
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Who cites it
46 citing papers in PubMed, 83 citations in OpenAlex.
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- Gallic acid inhibits Kaposi's Sarcoma-associated herpesvirus lytic reactivation by suppressing RTA transcriptional activities.Food science & nutrition · 2021Article
- Sp3 Transcription Factor Cooperates with the Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein To Synergistically Activate Specific Viral and Cellular Gene Promoters.Journal of virology · 2020Article
- Review
- Article
- KSHV and the Role of Notch Receptor Dysregulation in Disease Progression.Pathogens (Basel, Switzerland) · 2017Review
- Hijacking GPCRs by viral pathogens and tumor.Biochemical pharmacology · 2016Review
- Modulation of cellular signaling by herpesvirus-encoded G protein-coupled receptors.Frontiers in pharmacology · 2015Review
- Herpesvirus-encoded GPCRs: neglected players in inflammatory and proliferative diseases?Nature reviews. Drug discovery · 2014Review
- Kaposi's Sarcoma-Associated Herpesvirus Subversion of the Anti-Inflammatory Response in Human Skin Cells Reveals Correlates of Latency and Disease Pathogenesis.Journal of skin cancer · 2014Article
- Abortive lytic reactivation of KSHV in CBF1/CSL deficient human B cell lines.PLoS pathogens · 2013Article
- Quantitative analysis of the bidirectional viral G-protein-coupled receptor and lytic latency-associated nuclear antigen promoter of Kaposi's sarcoma-associated herpesvirus.Journal of virology · 2012Article
- An alternative Kaposi's sarcoma-associated herpesvirus replication program triggered by host cell apoptosis.Journal of virology · 2012Article
- Multiple defects, including premature apoptosis, prevent Kaposi's sarcoma-associated herpesvirus replication in murine cells.Journal of virology · 2012Article
- Cooperation between viral interferon regulatory factor 4 and RTA to activate a subset of Kaposi's sarcoma-associated herpesvirus lytic promoters.Journal of virology · 2012Article
- KSHV Rta Promoter Specification and Viral Reactivation.Frontiers in microbiology · 2012Article
- The RBP-Jκ binding sites within the RTA promoter regulate KSHV latent infection and cell proliferation.PLoS pathogens · 2012Article
- Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen induction by hypoxia and hypoxia-inducible factors.Journal of virology · 2012Article
- Notch1 regulates the expression of the multidrug resistance gene ABCC1/MRP1 in cultured cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Replication and transcription activator (RTA) of murine gammaherpesvirus 68 binds to an RTA-responsive element and activates the expression of ORF18.Journal of virology · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Kaposi's sarcoma-associated herpesvirus (KSHV) gene product virally encoded G protein-coupled receptor (vGPCR) is a homolog of cellular GPCRs and has been proposed to play important roles in KSHV-induced angiogenesis. The most abundant vGPCR-containing transcripts are K14/vGPCR bicistronic RNAs that are strongly induced during lytic reactivation. Here we show that the promoter governing this transcript is strongly responsive to activation by the viral lytic switch protein RTA. By deletion mapping and scanning mutation analyses, we have identified three putative RTA response elements (A, B, and C) in this promoter. However, none of these sites appear to directly bind RTA in electrophoretic mobility shift assays (EMSA). Site C corresponds to a canonical binding site for RBP-J, a sequence-specific transcriptional repressor that is normally the target of Notch signaling. RBP-J can bind RTA and recruit it to its cognate recognition site; when this happens, the activation function of RTA can relieve RBP-J-mediated repression and upregulate expression of the targeted gene. EMSA studies reveal that both sites A and C can bind to RBP-J; sequence inspection reveals that site A is a novel functional variant of known RBP-J recognition sites. (Site B corresponds to an as-yet-unknown host DNA-binding protein.) The importance of sites A and C in vivo is underscored by the observation that K14/vGPCR promoter function is dramatically inhibited in cells genetically deficient in RBP-J. The regulation of K14/vGPCR transcripts by RBP-J raises the possibility that other modulators of Notch signaling might be able to induce expression of this RNA outside the context of lytic KSHV replication.
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