Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin immunoprecipitation and transcription of mouse liver in the presence or absence of exogenous glucocorticoid to identify direct targets of the glucocorticoid receptor

ABSTRACT: The purpose of this study was to identify direct targets of the glucocorticoid receptor (GR) using an orthogonal analysis. An expression study of mouse livers in the presence or absence of exogenous glucocorticoid complemented a genome-wide location analysis on chromatin from the same livers. These were hybridized to the BCBC Mouse PancChip 5.0 and the Mouse PromoterChip BCBC-3.0 respectively.

ORGANISM(S): Mus musculus

SUBMITTER: Klaus Kaestner

PROVIDER: E-CBIL-38 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Glucocorticoid receptor-dependent gene regulatory networks.

Phuc Le Phillip P Friedman Joshua R JR Schug Jonathan J Brestelli John E JE Parker J Brandon JB Bochkis Irina M IM Kaestner Klaus H KH

PLoS genetics 20050805 2

While the molecular mechanisms of glucocorticoid regulation of transcription have been studied in detail, the global networks regulated by the glucocorticoid receptor (GR) remain unknown. To address this question, we performed an orthogonal analysis to identify direct targets of the GR. First, we analyzed the expression profile of mouse livers in the presence or absence of exogenous glucocorticoid, resulting in over 1,300 differentially expressed genes. We then executed genome-wide location anal ...[more]

PMID: 16110340

Similar Datasets

Chromatin immunoprecipitation of wild type and Foxa2 knock-out mouse liver using anti-HNF6 anitbodies to test whether Foxa2 inhibits HNF6-mediated transcription in the liver

Project description:The aim of this study was to test, in vivo, if Foxa2 inhibits HNF6-mediated transcription in the liver. We utilized hepatocyte-specific gene ablation of Foxa2 and the Mouse PromoterChip BCBC 3.0 and Mouse PancChip 5.0 cDNA microarrays to investigate HNF6 binding to its target promoters in vivo in the presence or absence of Foxa2. For the mouse promoter microarray analysis, chromatin immunoprecipitation using anti-HNF6 antibodies was performed on chromatin isolated from Foxa2loxP/loxP Alfp.Cre and control mouse livers. Along with sheared genomic DNA (common reference), the immunoprecipitated DNA was amplified, labeled and hybridized to the Mouse PromoterChip BCBC 3.0. For microarray analysis of gene expression, liver RNAs were isolated from three Foxa2loxP/loxP Alfp.Cre and three control mice. RNAs were reverse transcribed, labeled, and hybridized to the Mouse PancChip 5.0. Overall, our studies demonstrate that HNF6 binds to and regulates its target promoters in vivo in the presence and absence of Foxa2 and that the expression levels of HNF6 targets are not influenced by Foxa2.

2007-09-14 | E-CBIL-36 | biostudies-arrayexpress

ChIP-Chip and SACO Analysis of Pdx-1 binding in NIT-1 Insulinoma Cells

Project description:The BCBC Promoter Chip 5B was used to identify genomic targets of Pdx-1 binding. Genomic DNA from mouse NIT-1 insulinoma cells was immunoprecipitated with a Pdx-1 Antibody, PCR amplified, and labeled to the chip. All hybridizations were versus a common reference sample which was a labeled IgG IP. Additionally a Pdx1 SACO library for NIT-1 cells was generated.

2014-11-21 | E-MTAB-3126 | biostudies-arrayexpress

Transcription profiling of mouse Ngn3-expressing pancreatic cells in a time series through embryonic development and adult islet cells

Project description:Neurogenin3 (Ngn3) is a basic helix-loop-helix transcription factor which is expressed in scattered cells in the embryonic pancreas. Mice deficient for Ngn3 fail to produce any pancreatic endocrine cells and die shortly after birth. Expression of transcription factors critical to pancreatic development (Isl1, NeuroD, Pax4, and Pax6) is missing and endocrine precursors are absent in mutant pancreatic epithelium. This study utilizes mice which were engineered to contain EGFP (Enhanced Green Fluorescent Protein) under the control of the Ngn3 promoter. In this way, cells which express Ngn3 can be FACS sorted and studied throughout embryonic development (E13.5, E14.5, E15.5, E16.5, and E17.5). EGFP positive cells from the embryonic time-points in addition to adult islets (no cells expressing Ngn3) were hybridized to the BCBC PancChip 6.0 expression microarray, thus generating a profile of gene expression during this critical stage of development of the endocrine pancreas.

2007-12-15 | E-CBIL-40 | biostudies-arrayexpress

Transcription profiling of wild type and Foxa2 knock out mouse mature beta cells

Project description:The winged helix transcription factor Foxa2 regulates Pdx1 gene expression and fetal endocrine pancreas development. We show here by inducible gene ablation that Foxa2 inactivation in mature beta-cells induces hyperinsulinemic hypoglycemia in Foxa2loxP/loxP, Pdx1-CreERT2 adult mice. Mutant beta-cells exhibited a markedly increased pool of docked insulin granules, some of which were engaged in sequential or compound exocytosis, consistent with an increased first phase glucose-stimulated insulin secretion. Expression of multiple genes involved in vesicular trafficking, membrane targeting and fuel-secretion pathways is dependent on Foxa2. In addition, impaired cytosolic Ca2+ oscillations and elevated intracellular cAMP production accompanied this secretory defect, and were likely contributors to the sensitization of the exocytotic machinery. Thus, in the absence of Foxa2, alterations in intracellular second messenger signaling redistribute the insulin granules into the readily releasable pool. We conclude that Foxa2 is required both for the fetal pancreas development and for the function of mature beta-cells.

2007-09-22 | E-CBIL-39 | biostudies-arrayexpress

Transcription profiling of mouse islet growth after partial pancreatectomy and exendin-4 Treatment

Project description:Diabetes mellitus results from an inadequately functioning beta-cell mass. In the adult pancreas, beta-cell mass is dynamic, increasing to meet metabolic demands and decreasing with metabolic or injury insults. Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor agonist that augments beta-cell mass by increasing beta-cell neogenesis and proliferation and by reducing apoptosis. We utilized a cDNA microarray approach to identify genes that are differentially regulated during islet growth after Ex-4 treatment or a partial pancreatectomy (Ppx). Mice underwent 50% Ppx or sham operation and received Ex-4 or vehicle every 24 hours. cDNA prepared from total pancreatic RNA isolated at 12, 24 and 48 hrs after surgery was hybridized to the PancChip 4.0 microarray.

2005-12-01 | E-CBIL-5 | biostudies-arrayexpress

Gene expression profiling of MafA, MafB, and MafA/MafB Mutants in E18.5 pancreas

Project description:MafA and MafB transcription factors have been shown to be key regulators of insulin and glucagon transcription. MafB is essential for alpha and beta cell differentiation, as MafB deficient mice produced fewer insulin+ and glucagon+ cells during development, with MafA expressed in remaining insulin+ cells. In contrast, beta cell development was reported to be normal in a total MafA knock out, although the animals developed beta cell dysfunction and diabetes as adults. However, we have found that MafB expression is elevated during development and retained in adult insulin+ cells after conditional removal of MafA in the pancreas. These studies will evaluate the broader significance of these insulin and glucagon regulators in alpha and beta cell development and function. Our efforts will focus on determining if the concerted actions of MafA and MafB factors are significant to beta cell formation, and we specifically plan to: Determine how alpha and beta cell differentiation is affected in MafA/MafB compound mutant mice during pancreas development. cDNA microarray studies (pancchip 6.0) with wild type, MafAKO, MafB-/-, and MafAKOMafB-/- mutant E18.5 pancreata will be performed to comprehensively identify genes controlled by MafA and MafB in developing alpha and beta cells.

2014-11-04 | E-MTAB-3070 | biostudies-arrayexpress

Transcription profiling of wild type and C/EBPbeta deficient mice during a partial hepatectomy time series to identify transcriptional targets of C/EBPbeta

Project description:The aim of this experiment was to use microarray analysis to compare the response of wild type (WT) and C/EBPbeta deficient (KO) mice during a partial hepatectomy time course in hopes of identifying transcriptional targets of C/EBPbeta. In addition, the WT time course alone was examined to analyze mammalian cellular proliferation in vivo. In the partial hepatectomy model, quiescent hepatocytes reenter the cell cycle and progress in a synchronous fashion. This allows for the elucidation of regulatory networks operative in mammalian cell cycle. (Identification of transcriptional networks during liver regeneration (2004) Journal of Biological Chemistry)

2006-10-03 | E-CBIL-16 | biostudies-arrayexpress

Transcription profiling of rat insulinoma (INS-1 derived) cell lines that vary in their glucose responsiveness

Project description:The aim of this study was to identify the gene expression changes associated with glucose responsiveness in Rat INS-1 derived cell lines. RNA was prepared from cell lines which were shown to be highly glucose responsive and also lines which were shown to be poorly glucose responsive. Dr. Chris Newgard's lab quantified the RNA and sent it frozen in water. 3 biological replicates per condition were sent for the following conditions: (i) 832/13 and 833/15, robust glucose responsiveness; (ii)832/1 and 832/2 showed poor glucose responsiveness.

2007-09-11 | E-CBIL-35 | biostudies-arrayexpress

Cytotoxicity Study of Rat INS1 cell lines

Project description:Cytokines IL-1 and IFN-gamma have been shown to be the primary effectors of beta-cell destruction during the immune response. The aim of this study was to identify the gene expression changes that are associated with resistance of beta cells to cytokines. INS-1 rat insulinoma cells were grown in increasing doses of cytokines until a resistance phenotype had developed. RNA was prepared from these cytokine resistant sublines as well as the original, cytokine-sensitive parental INS-1 cells in Dr. Chris Newgard's lab, quantified and sent frozen in water. 3-7 biological replicates per condition were sent for the following three conditions: (i) 834/40, Cytokine-sensitive (CS), (ii) 833/15 and 833/117, Cytokine resistant grown in the absence of cytokines (CRu), (iii) 833/15C and 833/117C: Cytokine Resistant Grown in the Presence of Cytokines (CRt)

2014-07-22 | E-MTAB-2776 | biostudies-arrayexpress

Transcription profiling of mouse islets treated with PANcreatic DERived factor for 48 or 72 h to elucidate the genetic mechanisms of PANDER-induced cell death

Project description:Expression profiling using the UPenn Mouse PancChip 5.0 was used to elucidate the genetic mechanisms of PANDER-induced cell death in pancreatic islets. Murine islets were treated with PANDER (PANcreatic DERived factor) for 48 or 72 h (n=4 and n=3 respectively). Following linear amplification, the RNA was matched for purity using Quantitative PCR.

2006-05-24 | E-CBIL-7 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data