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Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

ABSTRACT: Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

PROVIDER: PRJNA1123751 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29402081_1.fastq.gz	Fastqsanger.gz
	SRR29402081_2.fastq.gz	Fastqsanger.gz
	SRR29402082_1.fastq.gz	Fastqsanger.gz
	SRR29402082_2.fastq.gz	Fastqsanger.gz
	SRR29402083_1.fastq.gz	Fastqsanger.gz

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Transcriptomic changes upon ESRRA loss 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.

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

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

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Transcription profiling by array of Apc-deficient mouse small intestinal epithelium upon Msx1 depletion.

Project description:The first step in the development of human colorectal cancer is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (Apc) gene encoding an essential tumor suppressor. The gene encoding transcriptional factor msh homeobox 1 (Msx1) displayed robust upregulation upon Apc inactivation in intestinal epithelium isolated in mice harboring the conditional allele of the Apc gene. To identify the gene signature in the small intestine upon Msx1 depletion, small intestinal epithelium from mice harboring conditional alleles of Apc and Msx1 was isolated and the gene expression profile was compared with control mice harboring the conditional allele of Apc only.

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Transcriptional changes upon Mphosph8 or Morc2a loss

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Cycling stem cells regenerate the damaged intestinal epithelium upon irradiation

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Expression profile of (inducible) homozygous Apc loss in the mouse intestinal epithelium

Project description:To asses the effect of Apc loss on the intestinal epithelium we induced homozygous VillinCreERT2 Apc flox/flox mice with tamoxifen on 3 consecutive days (day 0, 1 and 2), and harvested small intestinal epithelium on day 3.

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Transcriptional changes upon Jagn1 loss in LPS-stimulated plasmablasts.

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Transcriptional profiling of intestinal changes following APC loss

Project description:Vil-CreERT2 was used to drive loss of APC (Adenomatous polyposis coli) in the murine intestinal epithelium. 4 days post induction, mice were sampled and 1cm of tissue from the proximal intestine was collected into RNA later. This was compared to control (wild-type) intestine. This analysis allows investigation of transcriptional changes following APC loss (and therefore activation of the WNT signalling pathway).

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Expression changes in intestinal crypts upon deletion of beta-catenin

Project description:The Wnt signaling pathway is deregulated in over 90% of human colorectal cancers. β Catenin, the central signal transducer of the Wnt pathway, can directly modulate gene expression by interacting with transcription factors of the TCF/LEF-family. In the present study we investigate the role of Wnt signaling in the homeostasis of intestinal epithelium using tissue-specific, inducible beta-catenin gene ablation in adult mice. Block of Wnt/beta-catenin signaling resulted in rapid loss of transient-amplifying cells and crypt structures. Importantly, intestinal stem cells were induced to terminally differentiate upon deletion of beta-catenin resulting in a complete block of intestinal homeostasis and fatal loss of intestinal function. Transcriptional profiling of mutant crypt mRNA isolated by laser capture micro dissection confirmed those observations and allowed to identify genes potentially responsible for the functional preservation of intestinal stem cells. Keywords: genetic modification

2007-09-24 | GSE8818 | GEO

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