Project description:Chronic hepatitis B virus (HBV) infection is the main etiology of liver fibrosis (LF), leading to cirrhosis and liver tumors. DNA methylation caused by HBV protein changes the liver microenvironment and activates hepatic stellate cells, which is an important mechanism of liver fibrosis. However, the exact mechanism remains unclear. DNA methyltransferase 3A (DNMT3A) is a major enzyme that promotes DNA methylation. HBV infection promotes the expression of DNMT3A. To determine the specific roles of DNMT3A, we used lentivirus to overexpress DNMT3A in hepatocellular carcinoma cell line (HepG2). And the changes of transcriptome were analysed by RNA-seq.
Project description:Chronic hepatitis B virus (HBV) infection is the main etiology of liver fibrosis (LF), leading to cirrhosis and liver tumors. DNA methylation caused by HBV protein changes the liver microenvironment and activates hepatic stellate cells, which is an important mechanism of liver fibrosis. However, the exact mechanism remains unclear. DNA methyltransferase 3A (DNMT3A) is a major enzyme that promotes DNA methylation. HBV infection promotes the expression of DNMT3A. To determine the specific roles of DNMT3A, we used lentivirus to overexpress DNMT3A in hepatocellular carcinoma cell line (HepG2). And the changes of epigenome were analysed by RRBS.
Project description:Nuclear extracts were collected from HepG2 cells overexpressing JMJD1C after 30 min insulin treatment. Nuclear extracts were immunoprecipitated and purified protein was sent for mass spec analysis.
Project description:This SuperSeries is composed of the following subset Series: GSE36242: Transcriptomic response to benzo[a]pyrene treatment in HepG2 cells (RNA-Seq) GSE36243: Transcriptomic response to benzo[a]pyrene treatment in HepG2 cells (Affymetrix) Refer to individual Series