Hepatitis B virus-X protein recruits histone deacetylase 1 to repress insulin-like growth factor binding protein 3 transcription.
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.
Mesh Terms:
Cells, Cultured, Gene Expression Regulation, Neoplastic, Gene Expression Regulation, Viral, Hepatitis B virus, Histone Deacetylase 1, Histone Deacetylases, Insulin-Like Growth Factor Binding Protein 3, Promoter Regions, Genetic, Protein Binding, Repressor Proteins, Trans-Activators, Transcription, Genetic
Cells, Cultured, Gene Expression Regulation, Neoplastic, Gene Expression Regulation, Viral, Hepatitis B virus, Histone Deacetylase 1, Histone Deacetylases, Insulin-Like Growth Factor Binding Protein 3, Promoter Regions, Genetic, Protein Binding, Repressor Proteins, Trans-Activators, Transcription, Genetic
Virus Res.
Date: Jan. 01, 2009
PubMed ID: 18948152
View in: Pubmed Google Scholar
Download Curated Data For This Publication
105747
Switch View:
- Interactions 1