Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

ABSTRACT: To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells Total RNA was prepared from enterocytes obtained from small intestines of IKKb(EE)IEC and WT littermates. Two biological replicates were performed for each experimental condition.

ORGANISM(S): Mus musculus

SUBMITTER: monica guma

PROVIDER: E-GEOD-29701 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Constitutive intestinal NF-κB does not trigger destructive inflammation unless accompanied by MAPK activation.

Guma Monica M Stepniak Dariusz D Shaked Helena H Spehlmann Martina E ME Shenouda Steve S Cheroutre Hilde H Vicente-Suarez Ildelfonso I Eckmann Lars L Kagnoff Martin F MF Karin Michael M

The Journal of experimental medicine 20110808 9

Nuclear factor (NF)-κB, activated by IκB kinase (IKK), is a key regulator of inflammation, innate immunity, and tissue integrity. NF-κB and one of its main activators and transcriptional targets, tumor necrosis factor (TNF), are up-regulated in many inflammatory diseases that are accompanied by tissue destruction. The etiology of many inflammatory diseases is poorly understood, but often depends on genetic factors and environmental triggers that affect NF-κB and related pathways. It is unknown, ...[more]

PMID: 21825016

Similar Datasets

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

Project description:To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells

2011-06-09 | GSE29701 | GEO

Gene expression in IL-10-deficient and wild-type mice following Citrobacter rodentium infection

Project description:To further understand immune mechanims involved in regulating intestinal inflammation, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating inflammation in the absence of IL-10. Whole colon tissue from IL-10-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Citrobacter rodentium infection and from uninfected controls. Consistent with the histological and cellular analysis, expression levels of many chemokines and cytokines involved in recruiting leukocytes and promoting inflammation were, on average, lower in IL-10 deficient compared to wild-type mice after infection. An exception to this general trend was IL-27, a cytokine with both pro- and anti-inflammatory properties. Two weeks after Citrobacter rodentium challenge, total RNA was extracted and analyzed from whole colon tissue of infected IL-10-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 4-5 female mice which were pooled and used in the experiment.

2014-03-12 | E-GEOD-55812 | biostudies-arrayexpress

Expression profile of colon crypts from WT and GMCSF-/- mice with or without DSS treatment

Project description:To discover possible molecular mechanisms mediated by GM-CSF that may be involved in regeneration of the colon epithelium after DSS-induced injury we performed whole-genome wide mRNA microchip analysis of isolated crypt epithelial cells from unchallenged and DSS-challenged WT and GM-CSF-/- mice. Total RNA was prepared from isolated crypts obtained from colons of GM-CSF deficient mice and WT littermates treated or untreated with 1.5%DSS for 6 days. Three biological replicates were performed for each experimental condition.

2012-11-21 | E-GEOD-42173 | biostudies-arrayexpress

Expression data from colon samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic colitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137281 | GEO

Expression data from ileum samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic ileitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137280 | GEO

Expression data from jejunum IEC deleted for both HDAC1 and HDAC2

Project description:Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the intrinsic specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC-deficient for Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between normal IEC and HDAC1/2 deleted jejunum IEC.

2020-12-31 | GSE158522 | GEO

HO-1/BMMSCs exosomes treating inflammatory injured IEC-6 cells LC-MSMS

Project description:In this study, we established a rat small intestinal cell (IEC-6) injury model with tumor necrosis factor-α (TNF-α). Then, we added the exosomes from TNF- α damaged IEC-6 (TNF-α-exo), co-cultured with BMMSCs exosomes (BM-exo) and heme oxygenase-1 modified BMMSCs (HBM-exo) system exosomes into IEC-6 cells injured by TNF- α inflammation. After 48 hours, IEC-6 cells were collected for proteomic detection.

2020-06-29 | PXD017002 | Pride

Mus musculus

Project description:Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

| PRJNA141187 | ENA

Gene expression in IL-17RA-deficient and wild-type mice following Giardia muris infection

Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection. Two weeks after Giardia muris challenge, total RNA was extracted and analyzed from tissue of the small intestines of infected IL-17RA-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 6 female mice which were pooled and used in the experiment.

2015-05-15 | E-GEOD-68868 | biostudies-arrayexpress

Quantitative proteomic TandemMassTag analysis of intestinal epithelial cells (IEC) deleted for both Hdac1 and Hdac2

Project description:We have performed quantitative proteomic TandemMassTag to investigate proteomic changes after deletion of epigenetic eraser genes Hdac1 and Hdac2 in intestinal epithelial cells. Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC deficient in Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between Hdac1 and Hdac2 in IEC.

2021-09-09 | PXD022558 | Pride

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