Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1095989 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The role of Tfr1 in non-erythroid tissues remains elusive due to the embryonic lethality of the Tfr1 global knockout mouse model. To bypass this problem, we generated a mouse model in which Tfr1 was conditionally deleted in intestinal epithelial cells (IECs). These mice developed severe IEC disruption, characterized by blunted villi, edema, loss of proliferative intervillus IECs, accumulation of lipids, and early neonatal lethality. Strikingly, a wide range of genes associated with epithelial-to-mesenchymal transition were highly upregulated in IEC lacking Tfr1. Additionally, candidate vesicular transport and sorting genes implicated in lipid absorption and trafficking were downregulated. Surprisingly, the presence of a mutant allele of Tfr1, which is unable to bind to iron-loaded transferrin, was capable of rescuing the lethality, intestinal epithelial homeostasis, and proliferation in a majority of the Tfr1 conditional knockout mice. 9 samples (3 wildtype, 3 knockout, 3 rescue) were prepared from the intestinal epithelial cells isolated from the small intestine and proximal colon.
2015-05-19 | E-GEOD-68984 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE41541: Expression data from mouse proximal intestinal epithelial Lgr5(hi) stem cells and differentiated villus cells (enterocytes from Atoh1 conditional knockout) GSE41542: H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells GSE41710: Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse Refer to individual Series
2012-10-13 | E-GEOD-41543 | biostudies-arrayexpress
Project description:Intestinal epithelial cells are covered by the brush border, which consists of densely packed microvilli. The Intermicrovillar Adhesion Complex (IMAC) connects the microvilli and is required for proper organization of the brush border. The protocadherin CDHR5 is an important member of the IMAC, but it is unclear whether CDHR5 has mainly structural functions or is also involved in cellular signaling. This issue was resolved with a CDHR5 knockout mouse model. Intestinal epithelial cells were isolated from the small intestine of four wild-type and four CDHR5 knockout mice. Bulk RNA sequencing was performed to provide insight into the functions of CDHR5 in cellular signaling and gene regulation.
2023-04-13 | E-MTAB-12525 | biostudies-arrayexpress
Project description:PRMT1 is thought to be responsible for the majority of PRMT activity in Toxoplasma gondii, but its exact function is unknown. We generated T. gondii mutants lacking PRMT1 (∆prmt1) by deletion of the PRMT1 gene. ∆prmt1 parasites exhibit morphological defects during cell division and grow slowly, and this phenotype reverses in the complemented strain ∆prmt::PRMT1mRFP. PRMT1 localizes primarily in the cytoplasm with enrichment at the centrosome, and the strain lacking PRMT1 is unable to segregate progeny accurately. Unlike wild-type and complemented parasites, ∆prmt1 parasites have abnormal daughter buds, perturbed centrosome stoichiometry, and loss of synchronous replication. Whole genome expression profiling demonstrated differences in expression of cell cycle regulated genes in ∆prmt1 relative to the complemented ∆prmt1::PRMT1mRFP and parental wild-type strains, but these changes did not correlate with a specific block in cell cycle. Although PRMT1’s primary biological function was previously proposed to be methylation of histones, our genetic studies suggest that the most critical function of PRMT1 is within the centrosome as a regulator of daughter cell counting to assure the proper replication of the parasite. RNA samples were isolated in triplicates from RH-hxgprt parent strain (W), PRMT1 knockout (K) strain and PRMT1 knockout strain complemented with RFP-tagged PRMT1 protein (C). Parasites were grown for 32h at 37C. Samples were hybridized to the Toxoplasma gondii Affymetrix microarray (ToxoGeneChip: http://ancillary.toxodb.org/docs/Array-Tutorial.html). Hybridization data was preprocessed with Robust Multi-array Average (RMA) and normalized using per chip and per gene median polishing and analyzed using the software package GeneSpring GX (Agilent Technologies).
2015-09-18 | E-GEOD-73177 | biostudies-arrayexpress
Project description:Non-muscle myosin IIA plays an important role in cell adhesion, cell migration and tissue architecture. We previously showed that low activity of the heavy chain of non-muscle myosin II Myh9 is beneficial to Lgr5+ intestinal stem cell maintenance. However, the function of Myh9 in adult mouse intestinal epithelium is largely unclear. In this study, we used the inducible Villin-creERT2 knockout approach to delete Myh9 in adult mouse intestinal epithelium and observed that homozygous deletion of Myh9 causes colitis-like morphologic changes in intestine, leads to a high sensitivity to dextran sulfate sodium and promotes the colitis related adenomas formation in colon. Myh9 deletion disturbs cell junctions and impairs intestinal lumen barrier integrity, promoting the necroptosis of epithelial cells. Consistently, these changes can be partially rescued by Ripk3 knockout. Our results indicate that Myh9 is required for the maintenance of intestinal epithelium integrity and the prevention of cell necroptosis.
2021-03-20 | GSE169225 | GEO
Project description:Gene expression was compared between E18.5 Gata4Gata6 double conditional knockout (cKO) small intestinal epithelium and E18.5 control mouse small intestinal epithleium. E18.5 mouse small intestine was collected from control and Gata4Gata6 double conditional knockout mice. Epithelial cells were isolated, and RNA was prepared. Affymetrix Mouse Gene 1.0 gene arrays were used to interrogate gene expression. Data was analyzed using dChip software.
2014-04-30 | E-GEOD-49471 | biostudies-arrayexpress
Project description:To investigate the role of Arid3a in the intestinal epithelium, we generated an inducible conditional knockout model (VillinCreERT2;Arid3afl/fl -Arid3a cKO) and we compared the gene expression analysis to WT animals (ViliinCreERT2). Animals were injected intraperitoneally with tamoxifen to induce gene deletion.
2024-07-31 | GSE212560 | GEO
Project description:The role of Tfr1 in non-erythroid tissues remains elusive due to the embryonic lethality of the Tfr1 global knockout mouse model. To bypass this problem, we generated a mouse model in which Tfr1 was conditionally deleted in intestinal epithelial cells (IECs). These mice developed severe IEC disruption, characterized by blunted villi, edema, loss of proliferative intervillus IECs, accumulation of lipids, and early neonatal lethality. Strikingly, a wide range of genes associated with epithelial-to-mesenchymal transition were highly upregulated in IEC lacking Tfr1. Additionally, candidate vesicular transport and sorting genes implicated in lipid absorption and trafficking were downregulated. Surprisingly, the presence of a mutant allele of Tfr1, which is unable to bind to iron-loaded transferrin, was capable of rescuing the lethality, intestinal epithelial homeostasis, and proliferation in a majority of the Tfr1 conditional knockout mice.
2015-05-19 | GSE68984 | GEO
Project description:Our previous studies proved that both epithelial inflammation and sub-epithelial remodeling were linked to deregulated PRMT1 expression in asthma patients. This sncRNA-seq data from the BEAS-2B cell line after over-expressed PRMT1 for 24h.
2020-10-29 | GSE147759 | GEO
Project description:Disruption of the epithelial barrier is considered a potential cause of inflammatory bowel disease (IBD). In this study, we employed the NEMOIEC-KO mouse model to study the immune mechanisms triggering chronic colitis downstream of an epithelial barrier defect. Colitis in NEMOIEC-KO mice is driven by commensal bacteria sensing through MyD88 signaling. The IL-12p40-related cytokines are induced upon microbial sensing and are known to act critically in promoting intestinal inflammation. Yet, the relative contribution of IL-12 versus IL-23 in eliciting intestinal pathology has been controversial. Using IL-12p40, IL-12p35 and IL-23p19 knockout mice we assessed the functional contribution of IL-12 and IL-23 to intestinal inflammation in the NEMOIEC-KO model.
2019-07-23 | GSE123316 | GEO