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Modulation of hepatitis B virus pregenomic RNA stability and splicing by histone deacetylase 5 enhances viral biosynthesis
Taha Y Taha 1 , Varada Anirudhan 2 , Umaporn Limothai 3 , Daniel D Loeb 4 , Pavel A Petukhov 1 , Alan McLachlan 2
Affiliations
Affiliations
1
Department of Pharmaceutical Sciences, College of Pharmacy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
2
Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America.
3
Center of Excellence in Hepatitis and Liver Cancer, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
4
McArdle Laboratory for Cancer Research, University of Wisconsin - Madison, Madison, Wisconsin, United States of America.
PMID: 32822428 DOI: 10.1371/journal.ppat.1008802
Abstract
Hepatitis B virus (HBV) is a worldwide health problem without curative treatments. Investigation of the regulation of HBV biosynthesis by class I and II histone deacetylases (HDACs) demonstrated that catalytically active HDAC5 upregulates HBV biosynthesis. HDAC5 expression increased both the stability and splicing of the HBV 3.5 kb RNA without altering the translational efficiency of the viral pregenomic or spliced 2.2 kb RNAs. Together, these observations point to a broader role of HDAC5 in regulating RNA splicing and transcript stability while specifically identifying a potentially novel approach toward antiviral HBV therapeutic development.
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发表于 2020-8-22 18:19