ArticleJournal of virology2002
Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) replication and transcription factor activates the K9 (vIRF) gene through two distinct cis elements by a non-DNA-binding mechanism.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- KSHV ORF20 Promotes Coordinated Lytic Reactivation for Increased Infectious Particle Production.Viruses · 2024Article
- Application of the CDK9 inhibitor FIT-039 for the treatment of KSHV-associated malignancy.BMC cancer · 2023Article
- The ORF45 Protein of Kaposi Sarcoma-Associated Herpesvirus Is an Inhibitor of p53 Signaling during Viral Reactivation.Journal of virology · 2021Article
- Nucleolar stress enhances lytic reactivation of the Kaposi's sarcoma-associated herpesvirus.Oncotarget · 2018Article
- Importance of Promyelocytic Leukema Protein (PML) for Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Frontiers in microbiology · 2018Article
- Restoring PU.1 induces apoptosis and modulates viral transactivation via interferon-stimulated genes in primary effusion lymphoma.Oncogene · 2017Article
- The Modulation of Apoptotic Pathways by Gammaherpesviruses.Frontiers in microbiology · 2016Review
- Preparation and characterization of polyclonal antibody against Kaposi's sarcoma-associated herpesvirus lytic gene encoding RTA.Folia microbiologica · 2015Article
- Mechanism of angiopoietin-1 upregulation in Kaposi's sarcoma-associated herpesvirus-infected PEL cell lines.Journal of virology · 2015Article
- Viral Bcl-2 Encoded by the Kaposi's Sarcoma-Associated Herpesvirus Is Vital for Virus Reactivation.Journal of virology · 2015Article
- Molecular biology of KSHV lytic reactivation.Viruses · 2015Review
- Fluorescent tagging and cellular distribution of the Kaposi's sarcoma-associated herpesvirus ORF45 tegument protein.Journal of virology · 2014Article
- Distinct roles of Kaposi's sarcoma-associated herpesvirus-encoded viral interferon regulatory factors in inflammatory response and cancer.Journal of virology · 2013Review
- 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
- Kaposi's Sarcoma-Associated Herpesvirus Genome Replication, Partitioning, and Maintenance in Latency.Frontiers in microbiology · 2012Article
- KSHV Rta Promoter Specification and Viral Reactivation.Frontiers in microbiology · 2012Article
- Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation.Advances in virology · 2011Article
- Article
- Enhancement of autophagy during lytic replication by the Kaposi's sarcoma-associated herpesvirus replication and transcription activator.Journal of virology · 2010Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The replication and transcription activator (RTA) of Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8, a homologue of Epstein-Barr virus BRLF1 or Rta, is a strong transactivator and inducer of lytic replication. RTA acting alone can induce lytic replication of KSHV in infected cell lines that originated from primary effusion lymphomas, leading to virus production. During the lytic replication process, RTA activates many kinds of genes, including polyadenylated nuclear RNA, K8, K9 (vIRF), ORF57, and so on. We focused here on the mechanism of how RTA upregulates the K9 (vIRF) promoter and identified two independent cis-acting elements in the K9 (vIRF) promoter that responded to RTA. These elements were finally confined to the sequence 5'-TCTGGGACAGTC-3' in responsive element (RE) I-2B and the sequence 5'-GTACTTAAAATA-3' in RE IIC-2, both of which did not share sequence homology. Multiple factors bound specifically with these elements, and their binding was correlated with the RTA-responsive activity. Electrophoretic mobility shift assay with nuclear extract from infected cells and the N-terminal part of RTA expressed in Escherichia coli, however, did not show that RTA interacted directly with these elements, in contrast to the RTA responsive elements in the PAN/K12 promoter region, the ORF57/K8 promoter region. Thus, it was likely that RTA could transactivate several kinds of unique cis elements without directly binding to the responsive elements, probably through cooperation with other DNA-binding factors.
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