Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

XBP1 links ER stress to intestinal inflammation

ABSTRACT: XBP1 is the transcriptino factor that is activated by the ER stress. XBP1 is known to induce the ER dexpansion and increase the expression of the ER chaperone genes to prtect the cell from the ER stress. We generated a mouse strain that lacked XBP1 specifically in the mouse intestine by breeding the XBP1flox mice with Villin-cre mice. Here we examined genes that are differentially expressed between WT and XBP1 KO mouse intestine to identify genes that are downstream of XBP1.

ORGANISM(S): Mus musculus

PROVIDER: GSE12038 | GEO | 2008/07/10

SECONDARY ACCESSION(S): PRJNA113359

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse XBP1 knockouts vs. wild type intestine reveals XBP1 links ER stress to intestinal inflammation

Project description:XBP1 is the transcriptino factor that is activated by the ER stress. XBP1 is known to induce the ER dexpansion and increase the expression of the ER chaperone genes to prtect the cell from the ER stress. We generated a mouse strain that lacked XBP1 specifically in the mouse intestine by breeding the XBP1flox mice with Villin-cre mice. Here we examined genes that are differentially expressed between WT and XBP1 KO mouse intestine to identify genes that are downstream of XBP1. Experiment Overall Design: Total RNAs were pooled from three mice of indicated genotypes. Microarray experiments were performed by using Affymetrix GeneChipÂ® Mouse Genome 430 2.0 Array in Biopolymers Facility at Harvard Medical School.

2008-10-21 | E-GEOD-12038 | biostudies-arrayexpress

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator XBP1 for tunicamycin treatment

Project description:To further development of our miRNA expression approach to ER stress, we have employed miRNA microarray expression profiling as a discovery platform to identify ER stress-responsible ones. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted. Among them, expression of three miRNAs (miR-23a, miR-27a, miR-24-2) was quantified in the RNA samples from the same as the microarray, and COS7 cells by real-time PCR, confirming existence of similar mechanisms of trancriptional repression in ER stress by tunicamycin treatment. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed at each time (untreated, 12 or 24 hrs). miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted.

2015-01-18 | E-GEOD-35174 | biostudies-arrayexpress

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator XBP1 for tunicamycin treatment

2015-01-18 | GSE35174 | GEO

Analysis of the IRE1/XBP1 unfolded protein response (UPR) pathway in Schmid metaphyseal chondrodysplasia hypertrophic chondrocyte endoplasmic reticulum (ER) stress

Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1Cart?Ex2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1Cart?Ex2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1Cart?Ex2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR. Entire growth plate hypertrophic zones were microdissected from one tibia from each of three 2-week old wildtype mice, three 2-week old mice carrying a COL10A1 p.N617K mutation (ColXN617K), three 2-week old mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), and three 2-week old mice resulting from a cross between ColXN617K and Xbp1Cart?Ex2 (C/X).

2015-08-21 | E-GEOD-72261 | biostudies-arrayexpress

Analysis of the IRE1/XBP1 unfolded protein response (UPR) pathway in Schmid metaphyseal chondrodysplasia hypertrophic chondrocyte endoplasmic reticulum (ER) stress

Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1CartΔEx2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1CartΔEx2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1CartΔEx2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1CartΔEx2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR.

2015-08-21 | GSE72261 | GEO

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [CUT&RUN]

Project description:Cancer cells exploit adaptive responses such as endoplasmic reticulum (ER) stress to support their survival. ER stress response is mediated in part by the ER-localized transmembrane sensor IRE1α endoribonuclease and its substrate XBP1 to regulate XBP1 target gene expression. However, the mechanism that controls the IRE1α/XBP1 pathway remains poorly understood. CARM1 is an oncogene that is often overexpressed in a number of cancer types including ovarian cancer. Here we report that CARM1 determines ER stress response by controlling the IRE1α/XBP1 pathway. Genome-wide profiling revealed that CARM1 regulates XBP1 target gene expression during ER stress response. CARM1 directly interacts with XBP1. Inhibition of the IRE1α/XBP1 pathway was effective in ovarian cancer in a CARM1-dependent manner both in vitro and in vivo in orthotopic and patient-derived xenograft models. In addition, IRE1α inhibitor B-I09 synergizes with immune checkpoint blockade anti-PD1 antibody in an immunocompetent CARM1-expressing ovarian cancer model.

2021-08-11 | GSE157117 | GEO

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [RNA-seq]

2021-08-11 | GSE157116 | GEO

Activation of XBP1 but not ATF6α rescues heart failure induced by persistent ER stress in medaka fish

Project description:To investigate contribution of different UPR pathways to ER stress-induced abnormal heart phenotype in medaka, we generated constitutive XBP1(S) or ATF6(N) expression medaka lines. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different genotype medaka hearts.

2022-10-14 | GSE215040 | GEO

Targeting the IRE1α/XBP1 endoplasmic reticulum stress response pathway in ARID1Amutant ovarian cancers

Project description:xenograft, patientderived xenograft and the genetic Arid1aflox/flox/Pik3caH1047R mouse models. Finally, B-I09 synergizes with inhibition of HDAC6, a known regulator of the ER stress response, in suppressing the growth of ARID1A-inactivated OCCCs. These studies reveal a promising therapeutic strategy for ARID1A-mutant OCCCs and define the IRE1?-XBP1 axis of the ER stress response as a targetable vulnerability for ARID1A-mutant OCCCs. Our findings indicate that pharmacological inhibition of the IRE1?-XBP1 pathway alone or in combination with HDAC6 inhibition represents an urgently needed therapeutic strategy for ARID1A-mutant ovarian cancers.

2021-08-10 | GSE180468 | GEO

The role of hepatic XBP1 in FXR null mice

Project description:X-box binding protein 1 (XBP1) is a key component of the unfolded protein response that is activated in response to ER stress. Farnesoid X receptor (FXR) null (Fxr-/-) mice have elevated bile acid levels and progressive liver injury. Hepatic XBP1 pathway is activated in older Fxr-/- mice. This project is to investigate the role of liver XBP1 in Fxr-/- mice.

2022-09-19 | GSE201902 | GEO

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