ArticleVirology2009
Identification and functional characterization of the left origin of lytic replication of murine gammaherpesvirus 68.
Article in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- RNF213 modulates γ-herpesvirus infection and reactivation via targeting the viral Replication and Transcription Activator.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Comparative Analysis of Gammaherpesvirus Circular RNA Repertoires: Conserved and Unique Viral Circular RNAs.Journal of virology · 2019Article
- Multiple Lytic Origins of Replication Are Required for Optimal Gammaherpesvirus Fitness In Vitro and In Vivo.PLoS pathogens · 2016Article
- Murine Gammaherpesvirus 68 ORF48 Is an RTA-Responsive Gene Product and Functions in both Viral Lytic Replication and Latency during In Vivo Infection.Journal of virology · 2015Article
- CTCF and Sp1 interact with the Murine gammaherpesvirus 68 internal repeat elements.Virus genes · 2012Article
- Replication and transcription activator (RTA) of murine gammaherpesvirus 68 binds to an RTA-responsive element and activates the expression of ORF18.Journal of virology · 2011Article
- CCAAT/enhancer binding proteins play a role in oriLyt-dependent genome replication during MHV-68 de novo infection.Protein & cell · 2011Article
- Initiation of lytic DNA replication in Epstein-Barr virus: search for a common family mechanism.Future virology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Murine gammaherpesvirus 68 (MHV-68) replicates robustly in cell culture, providing a model for studying viral genome replication during de novo infection of tumor-associated herpesviruses. We have previously identified a 1.25-kb origin of lytic replication (oriLyt) for MHV-68. To further investigate the molecular mechanism of viral genome replication, we first fine-mapped essential cis-elements from this oriLyt fragment using a transposon-mediated high-density mutagenesis method. The result provided information for us to identify a second oriLyt located towards the left end of MHV-68 genome using a de novo infection-replication assay. We further characterized this left oriLyt by scanning deletion analysis and site-directed mutations, and showed that several CCAAT motifs are essential for oriLyt function, whereas an AT-rich region enhances replication. However, GC-rich repeats are not important cis-element. Moreover, we identified a cellular transcription factor, NF-Y, which binds to CCAAT boxes in EMSA and associates with oriLyt in ChIP assay. Using a dominant negative expression plasmid, we demonstrated that NF-Y plays an important role in mediating MHV-68 genome replication during de novo infection.
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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.