ArticleFuture microbiology2011
The Ying-Yang of the virus-host interaction: control of the DNA damage response.
Article in Future microbiology, 2011. 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
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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Establishment of a nasopharyngeal carcinoma cell line capable of undergoing lytic Epstein-Barr virus reactivation.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
- Phosphoproteomic Profiling Reveals Epstein-Barr Virus Protein Kinase Integration of DNA Damage Response and Mitotic Signaling.PLoS pathogens · 2015Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- SUMO binding by the Epstein-Barr virus protein kinase BGLF4 is crucial for BGLF4 function.Journal of virology · 2012Article
- Induction of DNA damage signaling upon Rift Valley fever virus infection results in cell cycle arrest and increased viral replication.The Journal of biological chemistry · 2012Article
- E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.PLoS pathogens · 2012Article
- Conserved herpesvirus kinases target the DNA damage response pathway and TIP60 histone acetyltransferase to promote virus replication.Cell host & microbe · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Evaluation of: Nikitin PA, Yan CM, Forte E et al.: An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells. Cell. Host Microbe 8(6), 510-522 (2010). Viruses have evolved elegant strategies to manipulate the host while the host counters with defense systems including the interferon response, apoptosis and the DNA damage response (DDR). Viruses have multiple strategies for manipulating the DDR and the same virus can even activate or inhibit the DDR at different stages of infection. Epstein-Barr virus (EBV) is implicated in several human cancers, including Burkitt's lymphoma, nasopharyngeal carcinoma, post-transplant lymphoproliferative disease and HIV-associated lymphomas. Although multiple viral proteins have been implicated in EBV-associated malignancies, the cellular pathways that control EBV-induced transformation and tumorigenesis remain incompletely understood. In this study, Nikitin et al. demonstrate that early EBV infection induces a cellular DDR that restricts virus-mediated transformation. The EBV-encoded EBNA3C protein subsequently attenuates this response to favor transformation and immortalization of host cells.
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.