Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126971 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE21549: Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice. GSE21576: Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice Refer to individual Series
2010-09-01 | E-GEOD-21603 | biostudies-arrayexpress
Project description:To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling. Total RNA of three samples of EDTA-dissociated colon epithelial cells of wild-type mice and three samples of vil-Cre-Bcl9-/-/Bcl9l-/- mice, each sample consisting of material of two or three different mice, was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_PoolID _UniqueID_NumberOfMice.
2010-09-01 | E-GEOD-21549 | biostudies-arrayexpress
Project description:Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice
| PRJNA129317 | ENA
Project description:Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice.
| PRJNA129513 | ENA
Project description:To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling.
2010-09-01 | GSE21549 | GEO
Project description:To investigate the impact of ablating Bcl9/Bcl9l on tumorigenesis, 6-8- week-old mice were exposed first to a single dose dimethylhydrazine (DMH, 44 mg/kg body weight), which is metabolized in the liver to carcinogenic azoxymethane (AOM), followed by 7 days oral administration of 2 % dextrane sulfate sodium (DSS) in the drinking water. This regimen results in the emergence of dysplastic adenomas, which progress to differentiated adenocarcinomas that are morphologically similar to human colorectal adenocarcinomas and typically harbor β-catenin stabilizing mutations of GSK3ß phosphorylation sites. Accordingly, these tumors present hallmarks of active Wnt signaling such as accumulation of nuclear β-catenin and expression of Wnt target genes. Total RNA of laser dissected samples from five different tumors each of two wild-type mice and three vil-Cre-Bcl9-/-/Bcl9l-/- mice was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_TumorID_MouseID_UniqueID.
2010-09-01 | E-GEOD-21576 | biostudies-arrayexpress
Project description:The Runx1 transcription factor plays an important role in tissue homeostasis through its effects on stem/progenitor cell populations and differentiation. The effect of Runx1 on epithelial differentiation of the secretory cell lineage of the colon was recently demonstrated. This study aimed to examine the role of Runx1 in tumor development in epithelial cells of the gastrointestinal tract. Conditional knockout mice were generated that lacked Runx1 expression in epithelial cells of the GI tract. These mice were crossed onto the ApcMin background, sacrificed, and their intestinal tumor phenotypes were compared with ApcMin Runx1 wildtype control mice. Apc-wildtype Runx1-mutant mice were also examined for tumor development. Colons from Runx1 knockout and wildtype mice were used for genome-wide mRNA expression analyses followed by gene-specific quantitative RT-PCR of whole colon and colon epithelium, to identify Runx1 target genes. Runx1 deficiency in intestinal epithelial cells significantly enhanced tumorigenesis in ApcMin mice. Notably, epithelial Runx1 deficiency in Apc-wildtype mice was sufficient to cause tumor development. Absence of Runx1 was associated with global changes in expression of genes involved in inflammation and intestinal metabolism, and with gene sets indicative of metastatic phenotype and poor prognosis. Gene-specific analysis of Runx1 deficient colon epithelium revealed increased expression of genes linked to an expansion of the stem/progenitor cell population. These results identify Runx1 as a novel tumor suppressor gene for gastrointestinal tumors and support a role for Runx1 in maintaining the balance between the intestinal stem/progenitor cell population and epithelial differentiation of the GI tract. A total of 8 colon tissue RNA samples were analyzed, comprising 4 colon samples from wild-type mice (Villin-Cre negative / Runx1-floxed) and 4 colon samples from mice that lack epithelial expression of Runx1 (Villin-Cre positive/Runx1-floxed).
2012-09-13 | E-GEOD-34292 | biostudies-arrayexpress
Project description:Purpose : The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of colon samples of intestinal epithelial cell specific Axin1 Knockout mice and WT controls that were submitted to DSS-induced colitis and AOM/DSS-induced colorectal carcinogenesis. Methods : DSS-induced colitis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice by giving 3% DSS dissolved in drinking water for 7 days and subsequently placed on regular water for recovery before sacrifice at Day 7 and D13. Methods : AOM/DSS-induced colorectal tumorigenesis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice that were sacrificed at day 100 post-AOM injection to collect colorectal tumors. Methods : Colonic mRNA profiles of WT and Axin1KOΔIEC mice were generated by deep sequencing using Illumina NextSeq 500 instrument (150base-lengths read V2 chemistry in a paired-end mode)
2022-02-09 | GSE196220 | GEO
Project description:The intestinal epithelial barrier plays critical role in the intestinal homeostasis and dysfunction of the epithelial barrier causes microbial invasion that would lead to inflammation in the gut. Antimicrobial peptides (AMPs) are essential components of the epithelial barrier to inhibit bacterial invasion. The regulatory mechanisms of the expression of AMPs are not fully characterized. Here, we report a cell-type-specific role of ovarian tumor family deubiquitinase 4 (OTUD4) in experimental colitis and bacterial infection. OTUD4 is upregulated in the inflamed mucosa of IBD patients and in the colon of mice treated with dextran sulfate sodium salt (DSS). Knockout of OTUD4 in intestinal organoids promotes the expression of AMPs after the stimulation with lipopolysaccharide (LPS), peptidoglycan (PGN), or Salmonella typhimurium (S.t.). In addition, the expression of AMPs was upregulated in intestinal epithelial cells (IECs) after DSS treatment or S.t. infection. Consistently, Vil-Cre;Otud4fl/fl mice and Def-Cre;Otud4fl/fl mice exhibit hyper-resistance to DSS-induced colitis and S.t. infection compared to Otud4fl/fl mice. Mechanistically, Knockout of OTUD4 results in hyper K63-linked ubiquitination of MyD88 and increases the activation of the NF-κB signaling pathway and MAPK signaling pathway to promote the expression of AMPs. These finds collectively highlight an indispensable role of OTUD4 in paneth cells to modulate AMPs production, indicating OTUD4 as a promoter and potential druggable target for gastrointestinal inflammation and bacterial infection.
2023-03-01 | GSE222836 | GEO
Project description:Microarray transcriptomic analysis of formalin-fixed, paraffin-embedded small intestinal tumors from control (Apcmin/+;Vil-Cre-/-;RhoADN/-) and DN-RhoA (Apcmin/+;Vil-CreTG/-;RhoADN/-) mice.
2014-11-21 | E-MTAB-2981 | biostudies-arrayexpress