Expression data from HepG2 (liver hepatocellular cells)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Giancarlo Chesi
PROVIDER: E-GEOD-51818 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Mature microRNA expression profiling of HBx-expressing HepG2 cells versus Control cells under UV stress The mature microRNA expression profile of HBx-expressing HepG2 cells versus control cells in three independent biological repeated experiments. This study focuses only on human sequences. The complete data matrix is linked below as a supplementary file.
2010-05-16 | E-GEOD-15554 | biostudies-arrayexpress
Project description:Mature microRNA expression profiling of HBx-expressing HepG2 cells versus Control cells. Free of UV sensitization. The mature microRNA expression profile of HBx-expressing HepG2 cells versus control cells in three independent biological repeated experiments (no UV). This study focuses only on human sequences. The complete data matrix is linked below as a supplementary file.
2010-05-24 | E-GEOD-17474 | biostudies-arrayexpress
Project description:PGC-1 transcription factor was customized to limit its interations to ERRalpha. This mutant (2x9) was used to dissect the transcription activation patterns that are attributable to the PGC1-ERR interaction and PGC-1 actions that are independent of ERR. Inactive mutant with the deleted LLXXL motifs (L2L3) and wt PGC-1 were used as negative and positive controls respectively. BGAL-expressing construct was used to control for non-specific effects of adenoviral infection. Experiment Overall Design: Expression constructs for BGAL control and three variants of PGC-1 were introduced into HepG2 cells via adenoviral infection. RNA was isolated 24 hrs post infection and the changes in gene expression were detected using GeneChip technology (Affymetrix). Hybridization was performed on the HG-133 plus 2 platform. The experiment was performed in three biological replicates. Raw expression data were normalized using MAS5.0 algorithm.
2008-06-14 | E-GEOD-5968 | biostudies-arrayexpress
Project description:A time course of the effect of overexpressing GPI-PLD on global gene expression in HepG2 cells was compared to control virus. Experiment Overall Design: This experiment compares the global gene expression in HepG2 cells that were either transduced with an adenovirus expressing GPI-phospholipase D or an adenovirus expressing beta galactosidase as a control. Treatment was for 6 or 12 hrs. Four replicates for each condition were used. 10 micrograms of total RNA was assayed per genechip using standard Affymetrix protocols. CONTEXT: Recent studies demonstrated that de novo lipogenesis is increased in patients with nonalcoholic fatty liver disease (NAFLD). Patients with NAFLD also have plasma lipid abnormalities. These lipid abnormalities may in part be related to insulin resistance, which is common in patients with NAFLD. Insulin resistance is associated with alterations in proteins involved in lipid metabolism including glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), which is involved in triglyceride metabolism. OBJECTIVE: The objective of the study was to determine whether alterations in serum and hepatic levels of GPI-PLD occur in patients with NAFLD. DESIGN AND PATIENTS: We examined the following: 1) levels of serum GPI-PLD in nondiabetics with nonalcoholic steatohepatitis, compared with matched controls; 2) hepatic expression of GPI-PLD mRNA in patients with normal liver or NAFLD; and 3) effect of overexpressing GPI-PLD vs. beta-galactosidase (control) on global gene expression in a human hepatoma cell line. RESULTS: The serum levels of GPI-PLD were significantly higher in patients with nonalcoholic steatohepatitis than in matched controls (119 +/- 24 vs.105 +/- 15 microg/ml, P = 0.047). The hepatic expression of GPI-PLD mRNA was increased nearly 3-fold in NAFLD patients, compared with patients with normal liver (3.1 +/- 2.6 vs. 1.1 +/- 1.0 arbitrary units per microgram total RNA, P = 0.026). Finally, overexpressing GPI-PLD was associated with an increase in de novo lipogenesis genes. CONCLUSIONS: Patients with NAFLD have elevated serum levels and hepatic expression of GPI-PLD, and its overexpression in vitro is associated with increased expression of de novo lipogenesis genes. These results suggest that GPI-PLD may play a role in the pathogenesis of NAFLD and/or its metabolic features and warrants further investigation.
2007-10-26 | E-GEOD-4731 | biostudies-arrayexpress
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Project description:In order to identify the effects of transcription factor EB (TFEB) overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments on injected mice overexpressing TFEB specifically in the liver. For the analysis of the injected mice overexpressing TFEB, total RNA was extracted from the liver of three mice. RNA extracted from the liver of 3 not-injected mice was used as a control.
2013-04-20 | E-GEOD-35015 | biostudies-arrayexpress
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.
2020-01-02 | MSV000084745 | MassIVE
Project description:The microarray results showed that linalool sitimulation of lipid-loaded HepG2 cells rewired the hepatic transcriptome profile, with linalool being comparable to those of fenofibrate. Total of 8,988 genes that were commonly and significantly expressed in all experimental groups, including control hepatocytes, lipid-loaded hepatocytes, and lipid-loaded hepatocyted stimulated with linalool or fenofibrate, respectively, to compare the transcriptome profile of linalool (1mM) with those of hypotriglyceridemic drug, fenofibrate (100 ?M). Lipid loading of hepatocytes notably changed hepatic transcriptome profile, where 77 % of the selected genes showed >20% changes in expression (fold change > 1.2 or fold change <0.8). However, linalool stimulation of lipid-loaded cells showed that 48 % of the selected genes had expression changes of >20%. Thus, 29 % of the selected genes became to show less than 20% changes in expression after linalool stimulation compared to the lipid-loaded condition. Fenofibrate showed 46 % of the selected gene expression changes of >20%. Thus, 31 % of the seleted genes fell into the <20% change category compared to the lipid-loaded condition after fenofibrate stimulation. Untreated control vs. lipid-loaded HepG2 cells (3 biological replicates), untreated control vs. lipid-loaded HepG2 cells treated with fenofibrate (3 biological replicates), untreated control vs. lipid-loaded HepG2 cells treated with linalool (2 biological replicates). One replicate per array
2013-04-11 | E-GEOD-45961 | biostudies-arrayexpress
Project description:Objective - The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease (CAD) in humans. The lipid associated SNPs identified by genome-wide association studies (GWAS) are located ~ 30 kb downstream from TRIB1 suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits. Methods & Results - Characterization of the risk locus reveals that it encompasses a gene, TRIB1 associated locus (TRIBAL) comprised of a well conserved promoter region and an alternatively spliced transcript. Bioinformatic analysis and re-sequencing identified a single nucleotide polymorphism (SNP), rs2001844, within the promoter region that associates with increased plasma triglycerides, reduced HDL-C and CAD risk. Furthermore, we show that rs2001844 is an expression trait locus (eQTL) for TRIB1 expression in blood and alters TRIBAL promoter activity in a reporter assay model. The TRIBAL transcript has features typical of long noncoding RNAs (lncRNA), including poor sequence conservation. Modulation of TRIBAL expression had limited impact on either TRIB1 or lipid regulatory genes mRNA levels in human hepatocyte models. In contrast, TRIB1 knockdown markedly increased TRIBAL expression in HepG2 cells and primary human hepatocytes. Conclusions - These studies demonstrate an interplay between a novel locus,TRIBAL, and TRIB1. TRIBAL is located in the GWAS identified risk locus, responds to altered expression of TRIB1, harbors a risk SNP that is an eQTL for TRIB1 expression and associates with plasma triglyceride concentrations. HepG2 hepatoma cells were stably infected with TRIBAL1 or no insert carrying lentiviruses
2014-02-14 | E-GEOD-54937 | biostudies-arrayexpress
Project description:Here we report a comprehensive proteomic analysis of purified human hepatocytes and a human hepatoma cell line HepG2. The complete dataset comprises 9,400 proteins and provides quantitative depiction of the proteomes of hepatocytes and HepG2 cells at the protein titer and copy number dimensions.
2016-01-26 | PXD001874 | Pride