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- Title
- Hepatitis B virus-X protein recruits histone deacetylase 1 to repress insulin-like growth factor binding protein 3 transcription
- Author(s)
- J K Shon; Bo Hwa Shon; In-Young Park; Su Ui Lee; L Fa; K Y Chang; J H SHin; Young Ik Lee
- Bibliographic Citation
- Virus Research, vol. 139, no. 1, pp. 14-21
- Publication Year
- 2009
- Abstract
- Hepatitis B virus (HBV), a major causative agent of hepatocelluar carcinoma (HCC), encodes an oncogenic X-protein (HBx) which has been known as a transcriptional transactivator on multiple viral and celluar promoters. In the report, we verified that HBx transcriptionally repress insulin-like growth factor binding protein-3 (IGFBP-3) by promoting HBx/histone deacetylase 1 (HDAC1) complex formation. HBx recruited HDAC1 forms complex with Sp1 in a p53-independent manner) and deacetylates Sp1 which resulted in the diminished binding of Sp1 on targeted DNA during transcriptional repression. Deacetylation of Sp1 by HBx recruited HDAC1 likely to be a part of the mechanism that controls HBx induced IGFBP-3 repression and the modification of chromatin structure.
- Keyword
- chromatin immunoprecipitationhistone deacetylase 1immunoprecipitationinsulin-like growth factor binding protein-3insulin-like growth factor type 1trichostatin A
- ISSN
- 0168-1702
- Publisher
- Elsevier
- DOI
- http://dx.doi.org/10.1016/j.virusres.2008.09.006
- Type
- Article
- Appears in Collections:
- Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
- Files in This Item:
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