Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

ABSTRACT: Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

PROVIDER: PRJNA1123752 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29402087_1.fastq.gz	Fastqsanger.gz
	SRR29402087_2.fastq.gz	Fastqsanger.gz
	SRR29402088_1.fastq.gz	Fastqsanger.gz
	SRR29402088_2.fastq.gz	Fastqsanger.gz
	SRR29402089_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

Project description:Amidst the obesity epidemic and advancements in satiety-targeting therapies, the transcriptional control of energy metabolism is crucial for managing obesity. The transcription factor Estrogen-related receptor α (ESRRA) regulates genes involved in mitochondrial biogenesis, gluconeogenesis, oxidative phosphorylation, and fatty acid metabolism. Although not essential for basic cellular function, ESRRA is vital for energy supply during physiological and pathological challenges. Studies show Esrra mutant mice have impaired fat metabolism and absorption, with germline Esrra loss conferring resistance to high-fat diet (HFD)-induced obesity. However, these studies often overlook tissue-specific roles. Esrra knockdown in the medial pre-frontal cortex reduces feeding and HFD-induced obesity, indicating possible neurological involvement. Notably, ESRRA is highly expressed in the gastrointestinal (GI) tract, a key player in dietary lipid metabolism and target of weight loss therapies.This study aims to investigate the impact of intestinal ESRRA and determine whether it contributes to resistance to diet-induced obesity.

2024-07-10 | GSE269824 | GEO

MafB binding in P7 intestinal epithelium

Project description:MafB binding in P7 intestinal epithelium

| PRJNA862741 | ENA

Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

Project description:Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

| PRJNA1123751 | ENA

Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

2024-07-10 | GSE269825 | GEO

RIME Analysis of HNF4A binding partners in the intestinal epithelium

Project description:The mechanisms driving gene expression changes during intestinal differentiation are unclear. Our studies have shown differential recruitment and occupancy of Pol II to be a major driver of these gene expression changes. Additionally, we have identified the transcription factor HNF4 as a key player in shaping this phenomenon. To gain insights into the protein-based mechanisms underlying HNF4-mediated Pol II recruitment, we performed RIME (Rapid Immunoprecipitation Mass Spectrometry of Endogenous proteins) using anti-HNF4A antibodies in primary mouse epithelium.

2023-10-09 | MSV000093071 | MassIVE

Transformation of the intestinal epithelium by the MSI2 RNA binding protein

Project description:The MSI2 RNA binding protein has recently emerged as a potent oncogene playing key roles in hematopoietic stem cell homeostasis and malignant hematopoiesis. Here we demonstrate that MSI2 is expressed in the intestinal stem cell compartment, that its expression is elevated in colorectal adenocarcinomas, and that MSI2 loss of function abrogates colorectal cancer cell growth. We thus examined the oncogenic consequences of MSI2 gain of function in the intestinal epithelium with a drug inducible mouse model. Strikingly, MSI2 induction alone was sufficient to phenocopy the majority of morphological and molecular consequences of acute loss of the APC tumor suppressor in the intestinal epithelium. We demonstrate that this phenotype is independent of both the activation of the other oncogenic Musashi family member, Msi1, and of canonical Wnt pathway activation. Transcriptome-wide RNA-binding analysis indicates that MSI2 acts as a pleiotropic inhibitor of known intestinal tumor suppressors including Lrig1, Bmpr1a, Cdkn1a, and Pten. Finally, we demonstrate that inhibition of the PDK-AKT-mTORC1 axis downstream of Pten rescues oncogenic consequences of MSI2 induction. Taken together, our findings identify MSI2 as a central component in an unappreciated oncogenic pathway promoting intestinal transformation. 2 wild-type samples, 2 TRE-Msi2 samples

2014-12-20 | E-GEOD-64388 | biostudies-arrayexpress

ATAC-sequencing mice small intestinal epithelium with intestinal epithelium specific LSD1 knock out compared to wild type

Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.

2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress

RNAseq of small intestinal epithelium extracted from mice infected with Nippostrongylus brasiliensis

Project description:The intestinal epithelium is our first line of defense against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. Here we sequenced the small intestinal epithelium from mice infected with Nippostrongylus brasiliensis to determine how the intestinal epithelium adapts in the context of an infection. By comparing these data to small intestinal organoids treated with cytokines (see related accessions) we determine that the intestinal epithelial response to N. brasiliensis infection correspond to a type II infection driven by IL-13.

2022-05-08 | E-MTAB-9183 | biostudies-arrayexpress

MafB binding in P7 intestinal epithelium

Project description:To investigate the genetic loci bound by MafB in the intestinal epithelium, we used CUT&RUN.

2022-07-30 | GSE209867 | GEO

Expression data from heterotopically grafted mouse small intestinal epithelium and the normal colonic epithelium

Project description:Epithelia of small and large intestines differ in their structures and functions. Such heterogeneity between these two epithelial tissues might be controlled by both epithelium-intrinsic and -extrinsic programs. By employing the cell transplantation technique developed in our laboratory, we investigated how adult SI epithelial cells behave when heterotopically transplanted onto colon. Then the gene expression profiles of small intestinal epithelium heterotopically transplanted onto colon and control colonic epithelium were compared. We used laser capture microdissection and microarray analysis to compare the global gene expression profiles of small intestinal epithelium in the heterotopically grafted tissues and control colonic epithelium. Dissected epithelia obtained from serial sections (~ 30 sections) of each specimen were combined and then total RNA extraction was performed. After calculating RNA Integrity Number (RIN), we subjected one graft sample and one control colon sample, which showed the highest RIN value, for the following gene expression analysis.

2014-08-15 | E-GEOD-59410 | biostudies-arrayexpress

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