ArticleRNA (New York, N.Y.)2010
A p53-dependent promoter associated with polymorphic tandem repeats controls the expression of a viral transcript encoding clustered microRNAs.
Article in RNA (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- High-fidelity long-read sequencing of an avian herpesvirus reveals extensive intrapopulation diversity in tandem repeat regions.PLoS pathogens · 2025Article
- Critical roles of non-coding RNAs in lifecycle and biology of Marek's disease herpesvirus.Science China. Life sciences · 2023Review
- Marek's Disease Virus Virulence Genes Encode Circular RNAs.Journal of virology · 2022Article
- Alternative splicing of a viral mirtron differentially affects the expression of other microRNAs from its cluster and of the host transcript.RNA biology · 2016Article
- In vivo expression patterns of microRNAs of Gallid herpesvirus 2 (GaHV-2) during the virus life cycle and development of Marek's disease lymphomas.Virus genes · 2015Article
- Role of virus-encoded microRNAs in Avian viral diseases.Viruses · 2014Review
- The p53-microRNA-34a axis regulates cellular entry receptors for tumor-associated human herpes viruses.Medical hypotheses · 2013Article
- The oncogenic microRNA OncomiR-21 overexpressed during Marek's disease lymphomagenesis is transactivated by the viral oncoprotein Meq.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor protein p53 plays a role in cellular responses to cancer-initiating events by regulating progress through the cell cycle. Several recent studies have shown that p53 transactivates expression of the members of the proapoptotic microRNA-34 family, which are underexpressed in several cancers. We demonstrate here that the latency-associated cluster of microRNAs (miRNA) encoded by an oncogenic herpesvirus, gallid herpesvirus 2 (GaHV-2), is a direct target of p53. Robust transcriptional activity was induced in three avian cell lines by a sequence mapping 600 base pairs (bp) upstream of the cluster of miRNAs. We found transcription start sites for the pri-miRNA transcript at the 3' end of this transcription-inducing sequence. The promoter has no consensus core promoter element, but is organized into a variable number of tandem repeats of 60-bp harboring p53-responsive elements (RE). The minimal functional construct consists of two tandem repeats. Mutagenesis to change the sequence of the p53 RE abolished transcriptional activity, whereas p53 induction enhanced mature miRNA expression. The identification of a viral miRNA promoter regulated by p53 is biologically significant, because all avirulent GaHV-2 strains described to date lack the corresponding regulatory sequence, whereas all virulent, very virulent, and hypervirulent strains possess at least two tandem repeats harboring the p53 RE.
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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.