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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cells, Cultured
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Gene Expression Regulation, Neoplastic / physiology*
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Gene Expression Regulation, Viral
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Hepatitis B virus / genetics
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Hepatitis B virus / physiology*
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Histone Deacetylase 1
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Histone Deacetylases / metabolism*
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Insulin-Like Growth Factor Binding Protein 3 / antagonists & inhibitors*
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Promoter Regions, Genetic
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Protein Binding
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Repressor Proteins / genetics
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Repressor Proteins / metabolism
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Trans-Activators / metabolism*
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Transcription, Genetic*
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Viral Regulatory and Accessory Proteins
Substances
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Insulin-Like Growth Factor Binding Protein 3
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Repressor Proteins
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Trans-Activators
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Viral Regulatory and Accessory Proteins
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hepatitis B virus X protein
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HDAC1 protein, human
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Histone Deacetylase 1
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Histone Deacetylases