ArticleJournal of virology2006
Kaposi's Sarcoma-associated herpesvirus lytic switch protein stimulates DNA binding of RBP-Jk/CSL to activate the Notch pathway.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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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Who cites it
42 citing papers in PubMed, 58 citations in OpenAlex.
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- MicroRNA let-7 and viral infections: focus on mechanisms of action.Cellular & molecular biology letters · 2022Review
- NDRG1 facilitates lytic replication of Kaposi's sarcoma-associated herpesvirus by maintaining the stability of the KSHV helicase.PLoS pathogens · 2021Article
- Review
- A herpesvirus transactivator and cellular POU proteins extensively regulate DNA binding of the host Notch signaling protein RBP-Jκ to the virus genome.The Journal of biological chemistry · 2019Article
- Genome-Wide Identification of Direct RTA Targets Reveals Key Host Factors for Kaposi's Sarcoma-Associated Herpesvirus Lytic Reactivation.Journal of virology · 2019Article
- Upregulation of MicroRNA 711 Mediates HIV-1 Vpr Promotion of Kaposi's Sarcoma-Associated Herpesvirus Latency and Induction of Pro-proliferation and Pro-survival Cytokines by Targeting the Notch/NF-κB-Signaling Axis.Journal of virology · 2018Article
- EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells.PLoS pathogens · 2017Article
- An easily transfectable cell line that produces an infectious reporter virus for routine and robust quantitation of Kaposi's sarcoma-associated herpesvirus reactivation.Journal of virological methods · 2017Article
- KSHV and the Role of Notch Receptor Dysregulation in Disease Progression.Pathogens (Basel, Switzerland) · 2017Review
- Reactivation and Lytic Replication of Kaposi's Sarcoma-Associated Herpesvirus: An Update.Frontiers in microbiology · 2017Review
- Kaposi's Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA.Journal of virology · 2016Article
- Molecular biology of KSHV lytic reactivation.Viruses · 2015Review
- KSHV reactivation and novel implications of protein isomerization on lytic switch control.Viruses · 2015Review
- The cellular peptidyl-prolyl cis/trans isomerase Pin1 regulates reactivation of Kaposi's sarcoma-associated herpesvirus from latency.Journal of virology · 2014Article
- Endogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?Retrovirology · 2013Review
- Oxygen-dependent expression of cytochrome c oxidase subunit 4-2 gene expression is mediated by transcription factors RBPJ, CXXC5 and CHCHD2.Nucleic acids research · 2013Article
- 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
Corrections and comments
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Authors and funding
8 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) lytic switch protein, Rta, is a ligand-independent inducer of the Notch signal transduction pathway, and KSHV cannot reactivate from latency in cells null for the Notch target protein RBP-Jk. Here we show that Rta promotes DNA binding of RBP-Jk, a mechanism that is fundamentally different from that established for the RBP-Jk-activating proteins, Notch intracellular domain (NICD) and Epstein-Barr virus EBNA2. Although constitutively active RBP-Jk and NICD do not transactivate KSHV promoters independently, cotransfection of an Rta mutant lacking its transactivation domain robustly restores transcriptional activation. Cooperation requires intact DNA binding sites for Rta and RBP-Jk and trimeric complex formation between the three molecules in vitro. In infected cells, RBP-Jk is virtually undetectable on a series of viral and cellular promoters during KSHV latency but is significantly enriched following Rta expression during viral reactivation. Accordingly, Rta, but not EBNA2 and NICD, reactivates the complete viral lytic cycle.
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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.