Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192945 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A non-functional myosin Vb motor in duodenal enterocytes results in disruption of epithelial cell polarity characterized by complete loss of microvilli and mislocalization of apical brush border proteins in the cytoplasm which finally cause a devastating disease in neonates with severe malabsorption defects accompanied by protracted diarrhea during infancy, classified as microvillus inclusion disease (MVID). The exact mechanisms how loss-of-function of MYO5B induces polarity loss are not completely understood in MVID pathogenesis. Obtaining better insights in cell polarity defects caused by loss of MYO5B, we performed microarray- in combination with protein expression-analysis in an inducible CaCo2 MYO5B RNAi cell system. Surprisingly, in MYO5B-depleted CaCo2 cells, CDH1 coding for the cell adhesion protein E-Cadherin and important for cell adhesion and therefore maintenance of cell polarity, was significantly downregulated. Interestingly, mesenchymal cell markers, specifically Vimentin and N-Cadherin, physiologically not expressed in differentiated epithelium, were upregulated and accompanied by increased phospho-c-jun levels in the nucleus. Importantly phospho-c-jun was also found in nuclei of duodenal enterocytes in MVID patients, indicating loss of MYO5B induces epithelial cell scattering in enterocytes. 3 Myosin 5B KD versus 3 control samples
2013-03-14 | E-GEOD-45134 | biostudies-arrayexpress
Project description:Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. The role of 15-oxo-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-oxoETE), a 15-HETE metabolite catalyzed by 15-prostaglandin dehydrogenase (15-PGDH), has been relatively unexplored in asthma. In this study, we used RNA-seq to explore the effect of 15-KETE on the transcriptome of airway epithelial cells, aiming to identify its potential downstream targets and mechanisms of action.
2026-05-21 | GSE325003 | GEO
Project description:A non-functional myosin Vb motor in duodenal enterocytes results in disruption of epithelial cell polarity characterized by complete loss of microvilli and mislocalization of apical brush border proteins in the cytoplasm which finally cause a devastating disease in neonates with severe malabsorption defects accompanied by protracted diarrhea during infancy, classified as microvillus inclusion disease (MVID). The exact mechanisms how loss-of-function of MYO5B induces polarity loss are not completely understood in MVID pathogenesis. Obtaining better insights in cell polarity defects caused by loss of MYO5B, we performed microarray- in combination with protein expression-analysis in an inducible CaCo2 MYO5B RNAi cell system. Surprisingly, in MYO5B-depleted CaCo2 cells, CDH1 coding for the cell adhesion protein E-Cadherin and important for cell adhesion and therefore maintenance of cell polarity, was significantly downregulated. Interestingly, mesenchymal cell markers, specifically Vimentin and N-Cadherin, physiologically not expressed in differentiated epithelium, were upregulated and accompanied by increased phospho-c-jun levels in the nucleus. Importantly phospho-c-jun was also found in nuclei of duodenal enterocytes in MVID patients, indicating loss of MYO5B induces epithelial cell scattering in enterocytes.
2013-03-14 | GSE45134 | GEO
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:To elucidate the epithelial cell diversity within the nasal inferior turbinates, a comprehensive investigation was conducted comparing control subjects to individuals with house dust mite-induced allergic rhinitis. This study aimed to delineate the differential expression profiles and phenotypic variations of epithelial cells in response to allergic rhinitis. This research elucidated distinct subpopulations and rare cell types of epithelial cells within the nasal turbinates, discerning alterations induced by allergic rhinitis. Furthermore, by interrogating transcriptomic signatures, the investigation provided novel insights into the cellular dynamics and immune responses underlying allergic rhinitis pathogenesis
2024-05-30 | GSE261706 | GEO
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Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes
2014-08-06 | GSE58734 | GEO
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