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Effect of E7386 on gene expression chenges in whisler follicle tissues of ApcMin/+ mice

ABSTRACT: Effect of E7386 on gene expression chenges in whisler follicle tissues of ApcMin/+ mice

PROVIDER: PRJNA665631 | ENA |

REPOSITORIES: ENA

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Effect of E7386 on gene expression chenges in whisler follicle tissues of ApcMin/+ mice

Project description:Gene expression profiling of whisker follicle tissues of ApcMin/+ mice treated with E7386

2020-12-21 | GSE158554 | GEO

Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

Project description:The transcription factor Zinc finger protein 148 (Zfp148) interacts physically with the tumor suppressor p53, but the siginficance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity. Here we hypothesized that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas. Crypt-enriched tissues were isolated by laser microdissection (PALM) from the small intestines (proximal) of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice for RNA extraction and hybridization to Affymetrix microarrays.

2016-02-10 | E-GEOD-77773 | biostudies-arrayexpress

Ablation of Lgr5-positive cells in intestinal polyps from ApcMin;Lgr5DTR mice

Project description:We performed RNAseq on intestinal polyps from diptheria toxin-treated ApcMin;Lgr5DTR mice to investigate the effect of an acute selective pressure on stem cell populations in intestinal lesions. Lgr5+ cells in the ApcMin;Lgr5DTR mice were ablated with a single intraperitoneal dose of diphtheria toxin in saline (50 μg/kg), and samples were collected after 24 hours and after 5 days. Untreated ApcMin mice were used as control. Intestinal polyps were excised and collected for RNA sequencing.

2022-06-30 | E-MTAB-10470 | biostudies-arrayexpress

Effect of dietary methyl donor depletion on gene expression in normal colons of ApcMin mice

Project description:Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls fed methyl donor sufficient diets

2012-04-30 | E-GEOD-37010 | biostudies-arrayexpress

RNA-seq of SI adenoma tissue from ApcMin and ApcMin-PCdel Mice

Project description:RNA-seq of SI adenoma tissue from ApcMin and ApcMin-PCdel Mice

| PRJNA600750 | ENA

Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

2016-02-10 | GSE77773 | GEO

Effect of dietary methyl donor depletion on gene expression in normal colons of ApcMin mice

Project description:Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls

2012-05-01 | GSE37010 | GEO

RNA-seq analyses of STAT1-delta IEC ApcMin (n=3) and STAT1-flox/flox ApcMin (n=3) mice

Project description:The interferon-inducible transcription factor STAT1 is a tumor suppressor in various malignancies. We investigated STAT1 functions in intestinal tumorigenesis of ApcMin mice. Surprisingly, loss of STAT1 in intestinal epithelial cells (STAT1ΔIEC) interfered with ApcMin induced intestinal tumor formation and tumor progression. RNASeq data demonstrated reduced expression of Indoleamine-2,3-dioxygenase-1 (IDO1) in STAT1ΔIEC ApcMin tumors. IDO1 is implicated in synthesis of kynurenine, a metabolite that induces ß-Catenin nuclear localisation and suppresses anti-tumor immune responses.

2020-04-05 | E-MTAB-5083 | biostudies-arrayexpress

Genome-wide analysis expression of ileum tumor samples from FVBN/APCmin and iPGC-1β/APCmin

Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in intestinal tumors from APCmin mice overexpressing PGC-1β specifically in the intestine. Total RNA obtained from ileum tumor samples from iPGC-1β/APCmin mice was compared to the total RNA extracted from FVBN/APCmin mice.

2015-03-01 | E-GEOD-61642 | biostudies-arrayexpress

Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

Project description:Mast cells have been suggested to either promote or suppress tumor progression but the mechanisms underlying these outcomes are unclear. Here, we show that mice with a heterozygous mutation in the adenomatous polyposis coli gene (ApcMin/+) displayed reduced intestinal tumor burden and increased survival in the background of the chemokine decoy receptor ACKR2 deficiency (ACKR2-/-). The ACKR2-/-ApcMin/+ tumors showed increased infiltration of mast cells. In mast cell-deficient Sash (c-kitW-sh/W-sh) ACKR2-/-ApcMin/+ mice the survival advantage was lost as the tumors grew rapidly and adoptive transfer of mast cells reduced the tumor burden in these mice. The tumor burden is also increased in Rag2-/-ACKR2-/-ApcMin/+ mice and the protection is reconstituted by adoptively transferred CD8+ T-lymphocytes. Mast cells from ACKR2-/- mice expressed elevated levels of chemokine receptors CCR2 and CCR5 and are also efficient in antigen presentation and activation of CD8+ T-cells. Mast cell-derived leukotriene B4 is a critical mediator of CD8+ T-lymphocyte recruitment as the BLT1-/-ACKR2-/-ApcMin/+ mice are highly susceptible to intestinal tumor induced mortality. Taken together, these data demonstrate that chemokine mediated mast cell recruitment is essential for initiating LTB4/BLT1 regulated CD8+ T-cell homing and generation of effective anti-tumor immunity against intestinal tumor development.

2017-12-31 | GSE104829 | GEO

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