Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

ABSTRACT: To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas

ORGANISM(S): Mus musculus

SUBMITTER: Huiling Xu

PROVIDER: E-GEOD-59283 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss.

2014-10-31 | GSE59283 | GEO

Transcription profiling of transition from normal intestinal epithelia to adenomas and carcinomas in the APC(Min/+) mice to identify differentially expressed transcripts.

Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis:; * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples; * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice; * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice; Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing WT vs Adenoma (n=6 x n=5; 83.3% concordance); WT vs Carcinoma (n=5 x n=5; 84% concordance); Adenoma vs Carcinoma (n=5 x n=5; 84% concordance). This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix).

2007-11-06 | E-GEOD-422 | biostudies-arrayexpress

Epithelium transition profile

Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis: * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing: * WT vs Adenoma (n=6 x n=5; 83.3% concordance) * WT vs Carcinoma (n=5 x n=5; 84% concordance) * Adenoma vs Carcinoma (n=5 x n=5; 84% concordance) This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix). Keywords = colon cancer Keywords = gene expression Keywords = DNA microarrays Keywords = beta-catenin Keywords = familial adenomatous polyposis Keywords: ordered

2003-09-12 | GSE422 | GEO

Transcript levels in the normal epithelium and adenomas of the colon of Min mice

Project description:We sought to identify gene transcripts altered in level between the normal epithelium and adenomas in colon of the Apc-Min/+ mouse. These differences in level can be compared to those observed for the colons of the Apc-Pirc/+ rat and the human.

2017-11-21 | GSE107139 | GEO

RNA-seq of intestinal crypts vs intestinal smooth muscle with a specific MMP17 deletion compared to wild-type

Project description:We wanted to assess the role of a specific smooth muscle protein (MMP17) in two different intestinal compartments, the epithelium (crypts) and the smooth muscle. To do that we isolate intestinal crypts from wild-type (WT) and knockout (KO, Mmp17-/-) mice, and obtained clean strips of smooth muscle. After muscle dissociation, we obtained RNA directly from crypts and muscle, and it was used for RNA-seq. By comparing WT and KO samples we observed a higher impact in gene expression affecting crypts, even though MMP17 is only expressed in muscle. This helped us to identify altered signaling pathways in KO crypts that linked MMP17 with SMAD4 and BMP signaling.

2021-09-27 | E-MTAB-9180 | biostudies-arrayexpress

Mus musculus

Project description:Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

| PRJNA254957 | ENA

RNA-seq of crypt cells from mouse small intestinal epithelium with an intestinal-epithelial specific deletion of LSD1 compared to wild type crypts

Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We dissociated crypts into single cells, and FACS sorted Epcam+ cells, to avoid immune-cell contamination. RNA was directly isolated from these sorted cells, and this was used for RNA seq. As KO crypts are different from WT crypts (KO crypts lack Paneth cells), identifying genes specifically regulated by LSD1 helps us to identify how LSD1 regulates intestinal crypt biology. Specifically, because we were able to combine this with ChIP-seq of the same cells, to identify where H3K4me1 levels (target of the histone demethylase LSD1) were different in the genome.

2020-11-16 | E-MTAB-7862 | biostudies-arrayexpress

Epigenomic enhancer profiling defines a signature of colon cancer [ChIP-seq]

Project description:Cancer is characterized by gene expression aberrations. Studies have largely focused on coding sequences and promoters, despite the fact that distal regulatory elements play a central role in controlling transcription patterns. Here we utilize the histone mark H3K4me1 to analyze gain and loss of enhancer activity genome wide in primary colon cancer lines relative to normal colon crypts. We identified thousands of variant enhancer loci (VELs) that comprise a signature that is robustly predictive of the in vivo colon cancer transcriptome. Furthermore, VELs are enriched in haplotype blocks containing colon cancer genetic risk variants, implicating these genomic regions in colon cancer pathogenesis. We propose that reproducible changes in the epigenome at enhancer elements drive a unique transcriptional program to promote colon carcinogenesis. Examination of 3 histone modifications and global expression data in primary colon cancer cell lines and normal colon crypt controls

2012-04-15 | E-GEOD-36204 | biostudies-arrayexpress

A gp130-induced Src/Yes-YAP Cascade Links Inflammation to Regeneration in the Mammalian Intestine

Project description:gp130Act cDNA was PCR-amplified and inserted into a plasmid containing the 12.4-kb Villin promoter. The 15.7-kb expression cassette was excised by PmeI digestion, purified, and injected into fertilized C57BL/6 oocytes to obtain founder mice, two of which transmitted the gp130Act transgene. Small intestinal crypts were isolated from WT and villin-gp130Act Tg small intestines. Total RNA was isolated from the isolated crypts using the RNeasy Mini kit (Qiagen) and used for microarray analysis.

2015-02-21 | E-MTAB-2400 | biostudies-arrayexpress

Gene expression profiling of Eed knockout and Ezh2 knockout small intestinal crypts [RNA-seq]

Project description:Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. We knocked out (using the inducible AhCre-LoxP system) Polycomb genes Eed and Ezh2 in the intestine for 6 weeks, after which crypts - the small intestinal stem cell zone - were harvested and RNA sequenced. We found Wnt, Notch and cell cycle pathways to be affected in Eed knockout (KO) but not Ezh2 KO crypts. Direct targets of Eed were determined by comparing this data with ChIP-sequencing. Small intestinal crypt mRNA profiles of 6 weeks-induced 12 weeks old Eed KO, Ezh2 KO and WT mice (all triplicates) as well as 10 days-induced Eed KO and WT organoids (duplicates) were generated by RNA sequencing over two runs and using IlluminaHiseq2000 and Hiseq2500.

2016-07-01 | E-GEOD-81576 | biostudies-arrayexpress

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