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:DNA methylation occurs as 5-methylcytosines mainly at cytosine-guanine dinucleotides, so-called CpG sites, and such methylation is a well-studied epigenetic mechanism for transcriptional regulation. Genomic DNA methylation patterns are established by the actions of the de novo methyltransferases Dnmt3a and Dnmt3b, and are maintained by the methyltransferase Dnmt1. Expression of Dnmt3a mRNA is relatively high in skeletal muscle, suggesting a major role in transcriptional regulation. Thus, we created transgenic mice specifically overexpressing Dnmt3a in skeletal muscle (Dnmt3a Tg mice). In this study, we performed a microarray analysis of skeletal muscle in wild-type control and Dnmt3a Tg mice. The microarray data shows upregulation of a set of slow-twitch myofiber-specific genes and downregulation of fast-twitch myofiber-specific genes in Dnmt3a-Tg muscle compared with WT muscle.
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:DNA methylation occurs as 5-methylcytosines mainly at cytosine-guanine dinucleotides, so-called CpG sites, and such methylation is a well-studied epigenetic mechanism for transcriptional regulation. Genomic DNA methylation patterns are established by the actions of the de novo methyltransferases Dnmt3a and Dnmt3b, and are maintained by the methyltransferase Dnmt1. Expression of Dnmt3a mRNA is relatively high in skeletal muscle, suggesting a major role in transcriptional regulation. Thus, we created transgenic mice specifically overexpressing Dnmt3a in skeletal muscle (Dnmt3a Tg mice). In this study, we performed a microarray analysis of skeletal muscle in wild-type control and Dnmt3a Tg mice (young: 3 months of age, female, and old: 26 months of age, female). The microarray data shows upregulation of a set of slow-twitch myofiber-specific genes and downregulation of fast-twitch myofiber-specific genes in Dnmt3a-Tg muscle compared with WT muscle.
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