Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profile analysis of inflammatory response regulated by hepatocyte nuclear factor 4α

ABSTRACT: To obtain a genomic view of hepatocyte nuclear factor-4α (HNF-4α) in the regulation of the inflammatory response, microarray analysis was used to probe the expression profile of an inflammatory response induced by cytokines in a model of knock-down HNF-4α HepG2 cells. The results indicate an extensive role for HNF-4α plays in the regulation of a large number of the liver-specific genes. Majority of genes (71%) affected by cytokine treatment are also affected by HNF-4α knock-down. This significant overlap suggests that HNF-4α may play a role in regulating the cytokine-induced inflammatory response.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15991 | GEO | 2009/05/06

SECONDARY ACCESSION(S): PRJNA115349

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

shRNA profiling of human hepatocyte HepG2 cells knocked down for HNF4 to investigate its role in inflammatory response

Project description:To obtain a genomic view of hepatocyte nuclear factor-4Î± (HNF-4Î±) in the regulation of the inflammatory response, microarray analysis was used to probe the expression profile of an inflammatory response induced by cytokines in a model of knock-down HNF-4Î± HepG2 cells. The results indicate an extensive role for HNF-4Î± plays in the regulation of a large number of the liver-specific genes. Majority of genes (71%) affected by cytokine treatment are also affected by HNF-4Î± knock-down. This significant overlap suggests that HNF-4Î± may play a role in regulating the cytokine-induced inflammatory response. Experiment Overall Design: The different treated HepG2 cells were grouped into 4 groups (four replicates in each group): Group1, Control; Group2, HNF-4Î± shRNA treated cells; Group3, cytokine treated group; Group4, HNF-4Î± shRNA and cytokine treatments. RNA extraction and hybridization on Affymetrix microarrays were processed. The expression profiles between different groups were analyzed and compared. In order to explore the function of HNF-4Î± in the inflammatory response, a set of 170 genes annotated as inflammatory response was obtained from GO (geneotology.org), the enrichments of these inflammatory genes were analyzed in different treated groups.

2009-05-16 | E-GEOD-15991 | biostudies-arrayexpress

Gene expression profiles for genetically engineered human hepatoma HepG2/8F_HS cells with or without heat treatment, cultured as monolayer or spheroids

Project description:We developed genetically engineered HepG2/8F_HS cells, in which eight liver-enriched transcription factor (LETF) genes—hepatocyte nuclear factor (HNF)-1α, HNF-1β, HNF-3β, HNF-4α, HNF-6, CCAAT/enhancer binding protein (C/EBP)-α, C/EBP-β and C/EBP-γ— under the control of TRE/PCMVmin promoter were introduced into a previously developed human hepatoma cell line (HepG2-HSP). The heat-inducible synthetic promoter system was introduced into HepG2 cells and tetracycline-responsive transactivator (tTA) and enhanced green fluorescent protein (EGFP) were expressed via positive feedback of tTA transcription in response to heat treatment. HepG2/8F_HS cells can induce high liver functions by heat treatment via overexpression of LETF genes.

2022-04-04 | E-MTAB-11486 | biostudies-arrayexpress

Gene expression profiles for genetically engineered murine hepatoma Hepa8F5 cells treated with or without doxycycline, cultured as monolayer or spheroids

Project description:We developed genetically engineered Hepa/8F5 cells (available from RIKEN BioResource Center [RCB4661]), in which genes of eight liver-enriched transcription factors (LETFs)—hepatocyte nuclear factor (HNF)-1α, HNF-1β, HNF-3β [FOXA2], HNF-4α, HNF-6, CCAAT/enhancer binding protein (C/EBP)-α, C/EBP-β and C/EBP-γ—were transduced into murine hepatoma Hepa1-6 cells as drug-inducible expression cassettes [Biochem. Eng. J., 60, 67–73 (2012)]. Hepa/8F5 cells can induce high liver functions by the addition of an inducer drug (doxycycline; Dox) via overexpression of LETF genes.

2017-11-15 | E-MTAB-5770 | biostudies-arrayexpress

Hepatocyte nuclear factor 1β gene regulation in E14.5 ureteric bud cells

Project description:HNF-1β mutations are one of the most common single-gene mutations that underlie kidney developmental disease. Hepatocyte nuclear factor 1β (HNF-1β) is essential for kidney development, but its functions in ureteric bud (UB) branching morphogenesis are incompletely understood. We isolated E14.5 UB cells using fluorescence-activated cell sorting, and performed RNA-sequencing to compare gene expression in wild-type and HNF-1β deficient UB cells. 1632 genes have significantly lower expression in the HNF-1β deficient UB cells and 2223 genes have significantly higher expression in HNF-1β deficient UB cells.

2022-10-20 | GSE205217 | GEO

Hepatocyte nuclear factor 1β binding in E14.5 kidney

Project description:HNF-1β mutations are one of the most common single-gene mutations that underlie kidney developmental disease. Hepatocyte nuclear factor 1β (HNF-1β) is essential for kidney development, but its functions in kidney development are incompletely understood. We identified 8284 HNF-1β binding sites using ChIP-sequencing. The majority of these peaks map to promoter (26%), intron (34%) or distal intergenic regions (37.4%) of the mouse genome. 61% of peaks map to protein coding genes, 12% map to long-noncoding RNAs, and 2% map to miRNAs.

2022-10-20 | GSE205189 | GEO

Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor

Project description:Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is essential for normal kidney development and renal tubular function. Mutations of HNF-1β produce cystic kidney disease, a phenotype associated with deregulation of canonical (β-catenin-dependent) Wnt signaling. Here, we show that ablation of HNF-1β in mIMCD3 renal epithelial cells produces hyperresponsiveness to Wnt ligands and increases expression of Wnt target genes, including Axin2, Ccdc80, and Rnf43. Levels of β-catenin and expression of Wnt target genes are also increased in HNF-1β mutant mouse kidneys. Genome-wide ChIP-seq in wild-type and mutant cells showed that ablation of HNF-1β increases by five-fold the number of sites on chromatin that are occupied by β-catenin. Remarkably, 50% of the sites that are occupied by β-catenin in HNF-1β mutant cells colocalize with HNF-1β binding sites in wild-type cells, indicating widespread reciprocal binding. We found that the Wnt target genes Ccdc80 and Rnf43 contain a novel composite DNA element comprising a β-catenin/lymphoid enhancer binding factor (LEF) site overlapping with an HNF-1β half-site. HNF-1β directly competes with the binding of β-catenin/LEF complexes to this element and thereby inhibits β-catenin-dependent transcription. Collectively, these studies reveal a novel mechanism whereby a transcription factor constrains canonical Wnt signaling through direct inhibition of β-catenin/LEF chromatin binding.

2019-11-11 | GSE130164 | GEO

Homo sapiens

Project description:Expression profile analysis of inflammatory response regulated by hepatocyte nuclear factor 4α

| PRJNA115349 | ENA

Genome-wide gene expression prolifing post GNL3 knockdown in human neural progenitor cells

Project description:We used two siRNAs to knock down GNL3 in human neural progenitor cells which were derived from normal human induced pluripotent stem cells (ATCC, ACS-1011). GNL3 knockdown experiments were done in three biological replicates. Total RNA was extracted from GNL3 knockdown and control groups for RNA sequencing (Illumina Hiseq2000, paired-end 100 bp). Genes that affected by both siRNAs were considered differentially expressed genes between GNL3 knockdown and control groups (adjusted P value < 0.05). Using Gene Ontology and KEGG pathway analysis, we found that those differentially exrepssed genes were mainly related to immune response, response to cytokine, cell cycle, and p53 signaling pathway.

2020-05-21 | GSE150945 | GEO

Itaconate Negatively Regulates Innate Signaling through Modification of IRAK4, Degradation of NFκB, and the Modulation of Global Ubiquitination

Project description:A wide variety of electrophilic derivatives of the Kreb’s cycle-derived metabolite, itaconate, are immunomodulatory, yet these derivatives have overlapping and sometimes contradictory activities. Therefore, we generated a genetic system to interrogate the immunomodulatory functions of endogenously produced itaconate in human macrophages. Endogenous itaconate is driven by multiple innate signals restraining inflammatory cytokine production. Endogenous itaconate directly targets cysteine 13 in IRAK4 disrupting IRAK4 autophosphorylation and activation, drives the degradation of NFκB, and modulates global ubiquitination patterns. As a result, cells unable to make itaconate overproduce inflammatory cytokines such as TNFα, IL6, and IL-1β in response to these innate activators. In contrast, the production of IFNβ, downstream of LPS, requires the production of itaconate. These data demonstrate that itaconate is a critical arbiter of inflammatory cytokine production downstream of multiple innate signaling pathways laying the groundwork for the development of itaconate mimetics for the treatment of autoimmunity.

2024-07-16 | PXD053956 | JPOST Repository

Project description:TAL1 knock down

| PRJNA125301 | ENA