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Updated: Jun 28, 2026

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System
Published on: December 21, 2019
Hepatitis B virus-X protein recruits histone deacetylase 1 to repress insulin-like growth factor binding protein 3
Jin Kyung Shon1, Bo Hwa Shon, In Young Park
1Liver Cell Signal Transduction Laboratory, Metabolic Syndrome Research Center, Korea Research Institute of Bioscience and Biotechnology, Liver Research Division, Lee's Biotechnology Institute of Research and Development, Taejeon 305-606, Republic of Korea.
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.
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