ArticleVirology journal2008
HDAC inhibitors stimulate viral transcription by multiple mechanisms.
Article in Virology journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 19 citations in OpenAlex.
- Histone deacetylase III interactions with BK polyomavirus large tumor antigen may affect protein stability.Virology journal · 2023Article
- Seleno-aspirin compound AS-10 promotes histone acetylation ahead of suppressing androgen receptor transcription, G1 arrest, and apoptosis of prostate cancer cells.The Prostate · 2023Article
- Article
- Directed Nucleosome Sliding during the Formation of the Simian Virus 40 Particle Exposes DNA Sequences Required for Early Transcription.Journal of virology · 2019Article
- Epigenetic Regulation of Viral Biological Processes.Viruses · 2017Review
- Epigenetic Analysis of SV40 Minichromosomes.Current protocols in microbiology · 2017Article
- Transcriptional repression is epigenetically marked by H3K9 methylation during SV40 replication.Clinical epigenetics · 2014Article
- Transient CD8-memory contraction: a potential contributor to latent cytomegalovirus reactivation.Journal of leukocyte biology · 2012Article
- Dual agarose magnetic (DAM) ChIP.BMC research notes · 2009Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe effects of histone deacetylase inhibitor (HDACi) treatment on SV40 transcription and replication were determined by monitoring the levels of early and late expression, the extent of replication, and the percentage of SV40 minichromosomes capable of transcription and replication following treatment with sodium butyrate (NaBu) and trichostatin A (TSA).
resultsThe HDACi treatment was found to maximally stimulate early transcription at early times and late transcription at late times through increased numbers of minichromosomes which carry RNA polymerase II (RNAPII) transcription complexes and increased occupancy of the transcribing minichromosomes by RNAPII. HDACi treatment also partially relieved the normal down-regulation of early transcription by T-antigen seen later in infection. The increased recruitment of transcribing minichromosomes at late times was correlated to a corresponding reduction in SV40 replication and the percentage of minichromosomes capable of replication.
conclusionThese results suggest that histone deacetylation plays a critical role in the regulation of many aspects of an SV40 lytic 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.