Gene expression profile at single cell level of cells from the murine small intestine (SI) lacking functional Apc.
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ABSTRACT:
PROVIDER: PRJNA955216 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24154921.fastq.gz | Fastqsanger.gz | |||
| SRR24154922.fastq.gz | Fastqsanger.gz | |||
| SRR24154923.fastq.gz | Fastqsanger.gz | |||
| SRR24154924.fastq.gz | Fastqsanger.gz | |||
| SRR24154925.fastq.gz | Fastqsanger.gz |
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Project description:We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of cells within the murine small intestine in the absence of functional Apc.
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2013-04-01 | E-GEOD-40856 | biostudies-arrayexpress
Project description:Transcriptional profiling of SI adenomas in Apc floxed mice
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Project description:To analyse roles of HAI-1/Spint1 in intestinal tumorigenesis, we examined the effect of intestine-specific deletion of Spint1 gene on Apc(Min/+) mice. The loss of Hai-1/Spint1 significantly accelerated tumor formation in ApcMin/+ mice and shortened their survival periods. Mouse small intestine tumor tissue or background mucosa lacking macroscopically visible tumors were proceeded to RNA extraction and hybridization on microarrays (Affymetrix Mouse Genome 430 2.0 Array).
2013-04-01 | GSE40856 | GEO
Project description:The aim of this study was to analyze the global transcriptional profiles of small intestine (SI) Innate Lymphoid Cells (ILCs) expressing the NK cell marker NKp46. Based on differential expression of the RORgt transcription factor SI NKp46+ ILCs can be divided in NKp46+RORgt- and NKp46+RORgt+ cells. While NKp46+RORgt- cells produce IFN-g, like conventional Natural Killer (NK) cells, NKp46+RORgt+ cells secrete IL-22, like Lymphoid Tissue inducer (LTi) cells. We compared the global transcriptional profiles of both NKp46+RORgt- and NKp46+RORgt+ cells to conventional splenic NK cells and to SI NKp46-RORgt+ cells, which contain adult LTi cells. By following this approach, we showed that SI NKp46+RORγt- ILCs correspond to SI NK cells. We also identified a transcriptional program conserved in adult SI NKp46+RORγt+, NKp46-RORγt+ ILCs and fetal LTi. The various ILC cell populations analyzed in this study were isolated from C57BL/6 RORc(gt)+/GFP reporter mice. SI NKp46+RORγt- (NKp46+GFP-) cells, SI NKp46+RORγt+ cells (NKp46+GFPlow and NKp46+GFPhigh cells) and NKp46-RORγt+ ILCs, including adult LTi cells , were sorted by flow cytometry from CD3- lamina propria cells of small intestine (SI) of RORc(γt)+/GFP reporter mice . Splenic NKp46+RORγt- (NKp46+GFP-) cells were also sorted as the reference for conventional NK cells. Two replicates of each populations were produced and analyzed.
2011-06-20 | E-GEOD-29777 | biostudies-arrayexpress
Project description:Transcriptional Profiling of the Transition from Normal Intestine to Adenoma in the APC(Min/+) Mouse. Tissue was from male 91-days old APC(Min/+) mouse (an animal model for human colon cancer). RNA was purified using Trizol and labeled for hybridization to high density oligonucleotide Affymetrix MG_U74Av2 arrays, using manufacturer protocol. We measured the relative expression level of >12000 genes and ESTs. -----------------------------------------; Samples used in analysis:; * GSM12501: Normal intestine diet #1 sample C1_0112 Dnmt+/- Min/+; * GSM12502: Tumor diet #1 sample T1_0112 Dnmt+/- Min/+; * GSM12503: Normal intestine diet #1 sample C2_0112 Dnmt+/+ Min/+; * GSM12504: Tumor diet #1 sample T2_0112 Dnmt+/+ Min/+; * GSM12505: Normal intestine diet #2 sample C1_003 Dnmt+/- Min/+; * GSM12506: Tumor diet #2 sample T1_003 Dnmt+/- Min/+; * GSM12507: Normal intestine diet #2 sample C2_003 Dnmt+/+ Min/+; * GSM12508: Tumor diet #2 sample T2_003 Dnmt+/+ Min/+; * GSM12509: Normal intestine diet #3 sample C1_005 Dnmt+/- Min/+; * GSM12510: Tumor diet #3 sample T1_005 Dnmt+/- Min/+; * GSM12511: Normal intestine diet #3 sample C2_005 Dnmt+/+ Min/+; * GSM12512: Tumor diet #3 sample T2_005 Dnmt+/+ Min/+; - - - - - - - - - - - - - - - - - - - - -; Comparisons were performed as described in Chen Z, Ge B, Hudson TJ and Rozen R. Gene Expression Patterns 1, 89-93, 2002. Comparing Normal intestine vs Adenoma. - - - - - - - - - - - - - - - - - - - - -; This resulted in the identification of differentially expressed transcripts. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx WEB portal (www.Affymetrix.com) and literature.
2008-06-15 | E-GEOD-784 | biostudies-arrayexpress
Project description:Transcriptional Profiling of the Transition from Normal Intestine to Adenoma in the APC(Min/+) Mouse. Tissue was from male 91-days old APC(Min/+) mouse (an animal model for human colon cancer). RNA was purified using Trizol and labeled for hybridization to high density oligonucleotide Affymetrix MG_U74Av2 arrays, using manufacturer protocol. We measured the relative expression level of >12000 genes and ESTs. ----------------------------------------- Samples used in analysis: * GSM12501: Normal intestine diet #1 sample C1_0112 Dnmt+/- Min/+ * GSM12502: Tumor diet #1 sample T1_0112 Dnmt+/- Min/+ * GSM12503: Normal intestine diet #1 sample C2_0112 Dnmt+/+ Min/+ * GSM12504: Tumor diet #1 sample T2_0112 Dnmt+/+ Min/+ * GSM12505: Normal intestine diet #2 sample C1_003 Dnmt+/- Min/+ * GSM12506: Tumor diet #2 sample T1_003 Dnmt+/- Min/+ * GSM12507: Normal intestine diet #2 sample C2_003 Dnmt+/+ Min/+ * GSM12508: Tumor diet #2 sample T2_003 Dnmt+/+ Min/+ * GSM12509: Normal intestine diet #3 sample C1_005 Dnmt+/- Min/+ * GSM12510: Tumor diet #3 sample T1_005 Dnmt+/- Min/+ * GSM12511: Normal intestine diet #3 sample C2_005 Dnmt+/+ Min/+ * GSM12512: Tumor diet #3 sample T2_005 Dnmt+/+ Min/+ - - - - - - - - - - - - - - - - - - - - - Comparisons were performed as described in Chen Z, Ge B, Hudson TJ and Rozen R. Gene Expression Patterns 1, 89-93, 2002. Comparing Normal intestine vs Adenoma. - - - - - - - - - - - - - - - - - - - - - This resulted in the identification of differentially expressed transcripts. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx WEB portal (www.Affymetrix.com) and literature. Keywords = Mouse Keywords = Min Keywords = normal Keywords = intestine Keywords = tumor Keywords = tumour Keywords = colon cancer Keywords = gene expression Keywords = beta-catenin Keywords = high density oligonucleotide microarrays Keywords = familial adenomatous polyposis Keywords = FAP Keywords = colorectal cancer Keywords = Affymetrix MGU74Av2 GeneChip probe array Keywords = mouse model Keywords = APC Keywords = adenomatous polyposis coli Keywords: ordered
2004-10-18 | GSE784 | GEO
Project description:Nearly all colorectal cancers have dysregulated Wnt signalling, predominantly through the mutation of the Apc (Adenomatous Polyposis Coli) gene. Therefore it is of vital importance to elucidate the key Wnt target genes in intestinal cells in vivo. We have used a novel inducible cre-lox based murine system (designated ApcFlox) to investigate the consequences of perturbation of Wnt signalling following inactivation of Apc in vivo within 100% of the intestinal epithelium. We have employed microarray analysis at 3 time points within our ApcFlox system (Day 3 prior to the onset of phenotype, day 4 the establishment of the phenotype and day 5 gross phenotype of altered proliferation, differentiation and migration) and from adenomas arising in the ApcMin/+ background allowing us characterise Wnt/beta-catenin target genes based on their expression profiles during different stages of intestinal tumourigenesis. Furthermore, we have employed microarray analysis using livers from our ApcFlox system and have demonstrated that there is very little overlap in the Wnt target genes induced by Apc loss in the liver and the intestine. More importantly, we have been able to determine a novel set of putative Wnt/beta-catenin target genes which are upregulated at both early and late stages of tumourigenesis in the intestine and may represent novel therapeutic targets in colon cancer. Samples were collected from Genetcially modified mice of the genotypes indicated on the sample records. Where appropriate, gene recombination was induced using IP administration of beta-napthoflavone. Cohorts of samples were used to compare the affects of APC loss in the small intestine at three time points (and compared to matched control samples in which the gene was not recombined). Furthermore, these samples were compared to colonic polyps (and normal colon) taken from the Apcmin Mouse.
2015-01-31 | E-GEOD-65461 | biostudies-arrayexpress
Project description:The aim of this study was to analyze the global transcriptional profiles of small intestine (SI) Innate Lymphoid Cells (ILCs) expressing the NK cell marker NKp46. Based on differential expression of the RORgt transcription factor SI NKp46+ ILCs can be divided in NKp46+RORgt- and NKp46+RORgt+ cells. While NKp46+RORgt- cells produce IFN-g, like conventional Natural Killer (NK) cells, NKp46+RORgt+ cells secrete IL-22, like Lymphoid Tissue inducer (LTi) cells. We compared the global transcriptional profiles of both NKp46+RORgt- and NKp46+RORgt+ cells to conventional splenic NK cells and to SI NKp46-RORgt+ cells, which contain adult LTi cells. By following this approach, we showed that SI NKp46+RORγt- ILCs correspond to SI NK cells. We also identified a transcriptional program conserved in adult SI NKp46+RORγt+, NKp46-RORγt+ ILCs and fetal LTi.
2011-06-20 | GSE29777 | GEO
Project description:Nearly all colorectal cancers have dysregulated Wnt signalling, predominantly through the mutation of the Apc (Adenomatous Polyposis Coli) gene. Therefore it is of vital importance to elucidate the key Wnt target genes in intestinal cells in vivo. We have used a novel inducible cre-lox based murine system (designated ApcFlox) to investigate the consequences of perturbation of Wnt signalling following inactivation of Apc in vivo within 100% of the intestinal epithelium. We have employed microarray analysis at 3 time points within our ApcFlox system (Day 3 prior to the onset of phenotype, day 4 the establishment of the phenotype and day 5 gross phenotype of altered proliferation, differentiation and migration) and from adenomas arising in the ApcMin/+ background allowing us characterise Wnt/beta-catenin target genes based on their expression profiles during different stages of intestinal tumourigenesis. Furthermore, we have employed microarray analysis using livers from our ApcFlox system and have demonstrated that there is very little overlap in the Wnt target genes induced by Apc loss in the liver and the intestine. More importantly, we have been able to determine a novel set of putative Wnt/beta-catenin target genes which are upregulated at both early and late stages of tumourigenesis in the intestine and may represent novel therapeutic targets in colon cancer.
2015-01-31 | GSE65461 | GEO