Project description:As HBx has been reported to interact with p53 and alter the recruitment of p53 to its binding sites, we would like to identify p53-associated genes that were deregulated by HBx. We employed whole genome microarray expression profiling to identify genes that were deregulated by HBx protein.
Project description:As HBx has been reported to interact with p53 and alter the recruitment of p53 to its binding sites, we obtained a comprehensive genome-wide profile of deregulated p53 transcription complex-DNA binding by the HBx protein using massively parallel deep sequencing coupled to p53 chromatin immunoprecipitation (ChIP-Seq) on HBx-expressing and control HepG2 liver cell culture model system.
Project description:Hepatitis B virus (HBV) has been clearly recognized as an etiological factor for hepatocellular carcinoma (HCC). HBV encodes the potentially oncogenic HBx protein. We aimed to elucidate the molecular mechanism of HCC caused by HBx and to discover the biomarker related to HCC by HBx. Three experimental groups, 3, 9 and 13 month aged HBx Tg mice and age matched normal wild type B6 mouse which have same background of HBx Tg mice were used to find differentially expressed genes during HCC. Keywords: Genetic modification
Project description:Hepatitis B virus (HBV) has been clearly recognized as an etiological factor for hepatocellular carcinoma (HCC). HBV encodes the potentially oncogenic HBx protein. We aimed to elucidate the molecular mechanism of HCC caused by HBx and to discover the biomarker related to HCC by HBx. Three experimental groups, 3, 9 and 13 month aged HBx Tg mice and age matched normal wild type B6 mouse which have same background of HBx Tg mice were used to find differentially expressed genes during HCC. Keywords: Genetic modification 3-month-old, 9-month-old, 13-month-old wild type B6 mice vs 3-month-old, 9-month-old, 13-month-old HBx transfected mice; Biological replicates at each timepoint; 9 controls vs 9 HBx-mice
Project description:Hepatitis B Virus (HBV) remains a major public health problem, and is a major cause liver cancer worldwide. HBV infection in vivo requires the function of the HBx protein, which facilitates expression of viral genes from the episomal genome by an unknown mechanism. Evidence suggests that HBx functions as a targeting subunit for the CRL4 E3 ubiquitin ligase, redirecting the complex to target and degrade an unknown host restriction factor. We used substrate trapping proteomics to search for ubiquitylation substrates of HBx. We used MLN4924 to block CRL activity and stabilize interactions between HBx and its substrates. We then performed APMS to identify bound proteins and potential substrates.
Project description:Hepatoarcinogenesis is a slow and multistep process. We used Hepatitis B virus X antigen (HBx) induced Hepatocellular carcinoma (HCC) as model. We also identify the biomarkers, the pathways and networks underlying HCC formation in this animal model. We analyzed the events from the early, middle, and late stages, in order to predict and prevent the development of cancer. At each specific stage, we analyzed the expression level that differed at least two-fold between HBx transgenic and wild-type mouse liver. Statistical approaches were used to identify genes displaying an increasing or decreasing trend throughout hepatocarcinogenesis. The liver was excised from 6-week-, 8-month-, 12-month-, 14-month-, and 16-month-old HBx transgenic mice (A106 strain) and RNA samples were isolated. In both 14-month- and 16-month-old mice, samples were obtained from both the tumor tissue and the normal.