ReviewViruses2015
KSHV reactivation and novel implications of protein isomerization on lytic switch control.
Review in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Generation of iVero.219-mcRTA: a doxycycline-inducible high-titer KSHV producer cell line with multicopyFrontiers in cellular and infection microbiology · 2026Article
- Review
- Inhibiting KSHV replication by targeting the essential activities of KSHV processivity protein, PF-8.Journal of medical virology · 2024Review
- KSHV RTA utilizes the host E3 ubiquitin ligase complex RNF20/40 to drive lytic reactivation.Journal of virology · 2023Article
- Insight into the Epigenetics of Kaposi's Sarcoma-Associated Herpesvirus.International journal of molecular sciences · 2023Review
- Multicentric Castleman disease and the evolution of the concept.Pathologica · 2021Review
- Article
- Viruses and Skin Cancer.International journal of molecular sciences · 2021Review
- Autophagy in Viral Development and Progression of Cancer.Frontiers in oncology · 2021Review
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
- NCOA2 promotes lytic reactivation of Kaposi's sarcoma-associated herpesvirus by enhancing the expression of the master switch protein RTA.PLoS pathogens · 2019Article
- Genome-Wide Identification of Direct RTA Targets Reveals Key Host Factors for Kaposi's Sarcoma-Associated Herpesvirus Lytic Reactivation.Journal of virology · 2019Article
- Molecular mechanisms of viral oncogenesis in humans.Nature reviews. Microbiology · 2018Review
- Article
- KSHV inhibits stress granule formation by viral ORF57 blocking PKR activation.PLoS pathogens · 2017Article
- The replication and transcription activator of murine gammaherpesvirus 68 cooperatively enhances cytokine-activated, STAT3-mediated gene expression.The Journal of biological chemistry · 2017Article
- KSHV and the Role of Notch Receptor Dysregulation in Disease Progression.Pathogens (Basel, Switzerland) · 2017Review
- Deregulation of KSHV latency conformation by ER-stress and caspase-dependent RAD21-cleavage.PLoS pathogens · 2017Article
- RTA Occupancy of the Origin of Lytic Replication during Murine Gammaherpesvirus 68 Reactivation from B Cell Latency.Pathogens (Basel, Switzerland) · 2017Article
- Nuclear Localization and Cleavage of STAT6 Is Induced by Kaposi's Sarcoma-Associated Herpesvirus for Viral Latency.PLoS pathogens · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In Kaposi's sarcoma-associated herpesvirus (KSHV) oncogenesis, both latency and reactivation are hypothesized to potentiate tumor growth. The KSHV Rta protein is the lytic switch for reactivation. Rta transactivates essential genes via interactions with cofactors such as the cellular RBP-Jk and Oct-1 proteins, and the viral Mta protein. Given that robust viral reactivation would facilitate antiviral responses and culminate in host cell lysis, regulation of Rta's expression and function is a major determinant of the latent-lytic balance and the fate of infected cells. Our lab recently showed that Rta transactivation requires the cellular peptidyl-prolyl cis/trans isomerase Pin1. Our data suggest that proline‑directed phosphorylation regulates Rta by licensing binding to Pin1. Despite Pin1's ability to stimulate Rta transactivation, unchecked Pin1 activity inhibited virus production. Dysregulation of Pin1 is implicated in human cancers, and KSHV is the latest virus known to co-opt Pin1 function. We propose that Pin1 is a molecular timer that can regulate the balance between viral lytic gene expression and host cell lysis. Intriguing scenarios for Pin1's underlying activities, and the potential broader significance for isomerization of Rta and reactivation, are highlighted.
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Identifiers
What OpenQuestion holds
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.