Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

ABSTRACT: Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

PROVIDER: PRJNA755990 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15510523.fastq.gz	Fastqsanger.gz
	SRR15510524.fastq.gz	Fastqsanger.gz
	SRR15510525.fastq.gz	Fastqsanger.gz
	SRR15510526.fastq.gz	Fastqsanger.gz
	SRR15510527.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

Project description:We assessed the impact of intestinal epithelial XBP1 in coordinating epithelial DNA damage responses. As our data revealed that low XBP1 activity in the context of chronic DNA damage is associated with both reduced p53 pathway activity and formation of tumors with metastaic potential in-vivo, we performed RNA sequencing of intestinal organoids (H2b/Xbp1fl/fl, H2bΔIEC, H2b/Xbp1ΔIEC, H2b/p53∆IEC) to identify a transcriptional program downstream of p53 that drives the tumorigenic in-vivo phenotype.

2021-09-01 | GSE182353 | GEO

Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

Project description:Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

| PRJNA612190 | ENA

Expression data from IRE1a or XBP1 deficient mouse liver

Project description:IRE1a and XBP1 are key regulators of the unfolded protein response (UPR). XBP1 ablation causes profound hypolipidemia in mice, and triggers feedback activation of its upstream enzyme IRE1a, instigating regulated IRE1-dependent decay (RIDD), an mRNA degradation mechanism dependent on IRE1a's endoribonuclease activity. Comprehensive microarray analysis of XBP1 and/or IRE1a deficient liver identified genes involved in lipogenesis and lipoprotein metabolism as RIDD substrates, which might contribute to the suppression of plasma lipid levels by activated IRE1a. To identify RIDD substrate mRNAs and direct XBP1 targets in the liver, we performed a comprehensive comparative microarray analysis of three groups of RNA samples: WT and XBP1 deficient mice, WT and IRE1a deficient mice untreated or injected with tunicamycin, and XBP1 deficient mice injected with luciferase or IRE1a siRNA.

2012-10-17 | E-GEOD-40515 | biostudies-arrayexpress

Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

Project description:Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

| PRJNA866374 | ENA

Expression data from IRE1a or XBP1 deficient mouse liver

2012-10-17 | GSE40515 | GEO

Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression [scRNA-seq]

Project description:Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression [scRNA-seq]

| PRJNA867672 | ENA

Regulatory T Cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis

Project description:Regulatory T Cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis

| PRJNA590272 | ENA

Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

Project description:Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

| PRJNA528597 | ENA

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

IRE1α-XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

Project description:Tumors evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function. However, it remains unclear how intratumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer (OvCa), an aggressive malignancy refractory to standard treatments and current immunotherapies, induces Endoplasmic Reticulum (ER) stress and activation of the IRE1α-XBP1 arm of the Unfolded Protein Response (UPR)10,11 in T cells to control their mitochondrial respiration and anti-tumor function. XBP1 upregulation in T cells isolated from human OvCa specimens was associated with decreased intratumoral T cell infiltration and reduced IFNG mRNA expression. Malignant ascites fluid obtained from OvCa patients inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, leading to IRE1α/XBP1-driven suppression of mitochondrial activity and IFN- production. Mechanistically, XBP1 induction limited the influx of glutamine necessary to sustain T cell mitochondrial respiration under glucose-deprived conditions by regulating the abundance of glutamine carriers. Restoring N-linked protein glycosylation, abrogating IRE1α-XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to OvCa ascites. XBP1-deficient T cells in the metastatic OvCa milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, OvCa-bearing mice lacking XBP1 selectively in T cells demonstrated superior anti-tumor immunity, delayed malignant progression and increased overall survival. Therefore, controlling ER stress or targeting IRE1α-XBP1 signaling may help restore T cell metabolic fitness and anti-tumor capacity in cancer hosts.

2018-10-18 | GSE118430 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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