ArticleFrontiers in microbiology2012
KSHV Rta Promoter Specification and Viral Reactivation.
Article in Frontiers in microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 105 citations in OpenAlex.
- Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.Nature microbiology · 2026Article
- Phospholipase Cβ regulates negative associative memory through calcium dependent and independent mechanisms.The Journal of biological chemistry · 2026Article
- Stage-specific regulation of KSHV infection by HIF-1α.Journal of virology · 2026Article
- Oral Neisseria gonorrhoeae Promotes KSHV Lytic Replication.Journal of medical virology · 2025Article
- RNA helicases, DDX5 and DDX17, facilitate lytic reactivation of gammaherpesviruses.PLoS pathogens · 2025Article
- RNA Modifications and Their Role in Regulating KSHV Replication and Pathogenic Mechanisms.Journal of medical virology · 2025Review
- Review
- Conserved cysteine residues in Kaposi's sarcoma herpesvirus ORF34 are necessary for viral production and viral pre-initiation complex formation.Journal of virology · 2024Article
- Linear ubiquitination regulates the KSHV replication and transcription activator protein to control infection.Nature communications · 2024Article
- From enhancers to genome conformation: complex transcriptional control underlies expression of a single herpesviral gene.bioRxiv : the preprint server for biology · 2024Article
- Conserved cysteine residues in Kaposi's sarcoma herpesvirus ORF34 are necessary for viral production and viral pre-initiation complex formation.bioRxiv : the preprint server for biology · 2024Article
- KSHV 3.0: a state-of-the-art annotation of the Kaposi's sarcoma-associated herpesvirus transcriptome using cross-platform sequencing.mSystems · 2024Article
- KSHV 3.0: A State-of-the-Art Annotation of the Kaposi's Sarcoma-Associated Herpesvirus Transcriptome Using Cross-Platform Sequencing.bioRxiv : the preprint server for biology · 2023Article
- mViruses · 2023Article
- Kaposi's sarcoma-associated herpesvirus replication and transcription activator protein activates CD274/PD-L1 gene promoter.Cancer science · 2023Article
- Kaposi's Sarcoma-Associated Herpesvirus Immediate Early Proteins Trigger FOXQ1 Expression in Oral Epithelial Cells, Engaging in a Novel Lytic Cycle-Sustaining Positive Feedback Loop.Journal of virology · 2023Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein Represses Cellular MDM2 Expression via Suppressing the Sp1- and p53-Mediated Transactivation.International journal of molecular sciences · 2022Article
- Investigating the structural changes due to adenosine methylation of the Kaposi's sarcoma-associated herpes virus ORF50 transcript.PLoS computational biology · 2022Article
- Caspase-Mediated Cleavage of the Transcription Factor Sp3: Possible Relevance to Cancer and the Lytic Cycle of Kaposi's Sarcoma-Associated Herpesvirus.Microbiology spectrum · 2022Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Viruses are obligate intracellular pathogens whose biological success depends upon replication and packaging of viral genomes, and transmission of progeny viruses to new hosts. The biological success of herpesviruses is enhanced by their ability to reproduce their genomes without producing progeny viruses or killing the host cells, a process called latency. Latency permits a herpesvirus to remain undetected in its animal host for decades while maintaining the potential to reactivate, or switch, to a productive life cycle when host conditions are conducive to generating viral progeny. Direct interactions between many host and viral molecules are implicated in controlling herpesviral reactivation, suggesting complex biological networks that control the decision. One viral protein that is necessary and sufficient to switch latent Kaposi's sarcoma-associated herpesvirus (KSHV) into the lytic infection cycle is called K-Rta. K-Rta is a transcriptional activator that specifies promoters by binding DNA directly and interacting with cellular proteins. Among these cellular proteins, binding of K-Rta to RBP-Jk is essential for viral reactivation. In contrast to the canonical model for Notch signaling, RBP-Jk is not uniformly and constitutively bound to the latent KSHV genome, but rather is recruited to DNA by interactions with K-Rta. Stimulation of RBP-Jk DNA binding requires high affinity binding of Rta to repetitive and palindromic "CANT DNA repeats" in promoters, and formation of ternary complexes with RBP-Jk. However, while K-Rta expression is necessary for initiating KSHV reactivation, K-Rta's role as the switch is inefficient. Many factors modulate K-Rta's function, suggesting that KSHV reactivation can be significantly regulated post-Rta expression and challenging the notion that herpesviral reactivation is bistable. This review analyzes rapidly evolving research on KSHV K-Rta to consider the role of K-Rta promoter specification in regulating the progression of KSHV 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.