ArticleJournal of virology2012
Murine gammaherpesvirus 68 LANA acts on terminal repeat DNA to mediate episome persistence.
Article in Journal of virology, 2012. 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
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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
26 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- The amplitude of gammaherpesvirus lytic replication dictates adaptive immune activation: Potential implications for KSHV LANA in immune evasion.bioRxiv : the preprint server for biology · 2026Article
- Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome.Nucleic acids research · 2024Article
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- Virus-Host Interplay Between Poly (ADP-Ribose) Polymerase 1 and Oncogenic Gammaherpesviruses.Frontiers in microbiology · 2021Review
- Deletion of Murine Gammaherpesvirus GeneJournal of virology · 2020Article
- Brd/BET Proteins Influence the Genome-Wide Localization of the Kaposi's Sarcoma-Associated Herpesvirus and Murine Gammaherpesvirus Major Latency Proteins.Frontiers in microbiology · 2020Article
- A comparative epigenome analysis of gammaherpesviruses suggests cis-acting sequence features as critical mediators of rapid polycomb recruitment.PLoS pathogens · 2019Article
- Article
- Article
- Conditional mutagenesis in vivo reveals cell type- and infection stage-specific requirements for LANA in chronic MHV68 infection.PLoS pathogens · 2018Article
- The Critical Role of Genome Maintenance Proteins in Immune Evasion During Gammaherpesvirus Latency.Frontiers in microbiology · 2018Review
- Murine Gammaherpesvirus 68 Expressing Kaposi Sarcoma-Associated Herpesvirus Latency-Associated Nuclear Antigen (LANA) Reveals both Functional Conservation and Divergence in LANA Homologs.Journal of virology · 2017Article
- Cross-species conservation of episome maintenance provides a basis for in vivo investigation of Kaposi's sarcoma herpesvirus LANA.PLoS pathogens · 2017Article
- Latency-Associated Nuclear Antigen E3 Ubiquitin Ligase Activity Impacts Gammaherpesvirus-Driven Germinal Center B Cell Proliferation.Journal of virology · 2016Article
- Identification of Viral and Host Proteins That Interact with Murine Gammaherpesvirus 68 Latency-Associated Nuclear Antigen during Lytic Replication: a Role for Hsc70 in Viral Replication.Journal of virology · 2016Article
- Kaposi's Sarcoma Herpesvirus Genome Persistence.Frontiers in microbiology · 2016Review
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- The Kaposi Sarcoma Herpesvirus Latency-associated Nuclear Antigen DNA Binding Domain Dorsal Positive Electrostatic Patch Facilitates DNA Replication and Episome Persistence.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Murine gammaherpesvirus 68 (MHV68) ORF73 (mLANA) has sequence homology to Kaposi's sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen (LANA). LANA acts on the KSHV terminal repeat (TR) elements to mediate KSHV episome maintenance. Disruption of mLANA expression severely reduces the ability of MHV68 to establish latent infection in mice, consistent with the possibility that mLANA mediates episome persistence. Here we assess the roles of mLANA and MHV68 TR (mTR) elements in episome persistence. mTR-associated DNA persisted as an episome in latently MHV68-infected tumor cells, demonstrating that the mTR elements can serve as a cis-acting element for MHV68 episome maintenance. In some cases, both control vector and mTR-associated DNAs integrated into MHV68 episomal genomes. Therefore, we also assessed the roles of mTRs as well as mLANA in the absence of infection. DNA containing both mLANA and mTRs in cis persisted as an episome in murine A20 or MEF cells. In contrast, mTR DNA never persisted as an episome in the absence of mLANA. mLANA levels were increased when mLANA was expressed from its native promoters, and episome maintenance was more efficient with higher mLANA levels. Increased numbers of mTRs conferred more efficient episome maintenance, since DNA containing mLANA and eight mTR elements persisted more efficiently in A20 cells than did DNA with mLANA and two or four mTRs. Similar to KSHV LANA, mLANA broadly associated with mitotic chromosomes but relocalized to concentrated dots in the presence of episomes. Therefore, mLANA acts on mTR elements to mediate MHV68 episome persistence.
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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.