ArticleJournal of virology2007
The minimal replicator element of the Kaposi's sarcoma-associated herpesvirus terminal repeat supports replication in a semiconservative and cell-cycle-dependent manner.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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
29 citing papers in PubMed, 35 citations in OpenAlex.
- Bypass of LANA-DNA crosslinks by Polη ensures KSHV genome maintenance and tumor growth.Cell reports · 2026Article
- Review
- Latently KSHV-Infected Cells Promote Further Establishment of Latency upon Superinfection with KSHV.International journal of molecular sciences · 2021Article
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
- KSHV-encoded LANA protects the cellular replication machinery from hypoxia induced degradation.PLoS pathogens · 2019Article
- Towards Better Understanding of KSHV Life Cycle: from Transcription and Posttranscriptional Regulations to Pathogenesis.Virologica Sinica · 2019Review
- LANA oligomeric architecture is essential for KSHV nuclear body formation and viral genome maintenance during latency.PLoS pathogens · 2019Article
- BET-Inhibitors Disrupt Rad21-Dependent Conformational Control of KSHV Latency.PLoS pathogens · 2017Article
- G-quadruplex-interacting compounds alter latent DNA replication and episomal persistence of KSHV.Nucleic acids research · 2016Article
- Kaposi's Sarcoma Herpesvirus Genome Persistence.Frontiers in microbiology · 2016Review
- KSHV Genome Replication and Maintenance.Frontiers in microbiology · 2016Review
- Review
- Identification of properties of the Kaposi's sarcoma-associated herpesvirus latent origin of replication that are essential for the efficient establishment and maintenance of intact plasmids.Journal of virology · 2014Article
- The origin recognition complex in human diseases.Bioscience reports · 2013Review
- Comprehensive analysis of LANA interacting proteins essential for viral genome tethering and persistence.PloS one · 2013Article
- Monitoring plasmid replication in live mammalian cells over multiple generations by fluorescence microscopy.Journal of visualized experiments : JoVE · 2012Article
- Kaposi's sarcoma-associated herpesvirus-encoded LANA recruits topoisomerase IIβ for latent DNA replication of the terminal repeats.Journal of virology · 2012Article
- The latency-associated nuclear antigen, a multifunctional protein central to Kaposi's sarcoma-associated herpesvirus latency.Future microbiology · 2011Review
- Single molecule analysis of replicated DNA reveals the usage of multiple KSHV genome regions for latent replication.PLoS pathogens · 2011Article
- Analysis of DNA methylation in human BK virus.Virus genes · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) persists as episomes in infected cells by circularizing at the terminal repeats (TRs). The KSHV episome carries multiple reiterated copies of the terminal repeat, and each copy is capable of supporting replication. Expression of the latency-associated nuclear antigen (LANA) is critical for the replication of TR-containing plasmids. A 32-bp sequence upstream of LANA binding site 1 (LBS1), referred to as RE (replication element), along with LANA binding sites 1 and 2 (RE-LBS1/2), is sufficient to support replication (J. Hu and R. Renne, J. Virol. 79:2637-2642, 2005). In this report we demonstrate that the minimal replicator element (RE-LBS1/2) replicates in synchrony with the host cellular DNA, and only once, in a cell-cycle-dependent manner. Overexpression of the mammalian replication inhibitor geminin blocked replication of the plasmid containing the minimal replicator element, confirming the involvement of the host cellular replication control mechanism, and prevented rereplication of the plasmid in the same cell cycle. Overexpression of Cdt1 also rescued the replicative ability of the RE-LBS1/2-containing plasmids. A chromatin immunoprecipitation assay performed using anti-origin recognition complex 2 (alpha-ORC2) and alpha-LANA antibodies from cells transfected with RE-LBS1/2, RE-LBS1, LBS1, or RE showed the association of ORC2 with the RE region. Expression of LANA increased the number of copies of chromatin-bound DNA of replication elements, suggesting that LANA is important for the recruitment of ORCs and may contribute to the stabilization of the replication protein complexes at the RE site.
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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.