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Detection of Notch1-IC, Notch2-IC and EBNA2 target genes in human B cells

ABSTRACT: Notch1-IC, Notch2-IC or EBNA2 have been induced in a conditionally immortalized human B cell line (EREB2-5) in order to identify similar and unique target genes in B cells. CAT was used as a control. Keywords: time course

ORGANISM(S): Homo sapiens

PROVIDER: GSE12355 | GEO | 2009/08/06

SECONDARY ACCESSION(S): PRJNA113183

REPOSITORIES: GEO

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Transcription profiling of human time points after induction of Notch1-IC, Notch2-IC or EBNA2 in EREB2-5 cells - detection of Notch1-IC, Notch2-IC and EBNA2 target genes in human B cells

Project description:Notch1-IC, Notch2-IC or EBNA2 have been induced in a conditionally immortalized human B cell line (EREB2-5) in order to identify similar and unique target genes in B cells. CAT was used as a control. Experiment Overall Design: RNA was isolated at different time points after induction of Notch1-IC, Notch2-IC or EBNA2 in EREB2-5 cells. Three independent experiments were performed (except Notch1-IC at 3day).

2009-08-25 | E-GEOD-12355 | biostudies-arrayexpress

E-GEOD-12355

Project description:Transcription profiling by array of human B cells expressing Notch1-IC, Notch2-IC, CAT or EBNA2

2015-08-28 | E-GEOD-12355 | ExpressionAtlas

DAOY-Notch1/Notch2 knockout: transcriptome comparison

Project description:DAOY-Notch1/Notch2 knockout: transcriptome comparison

| PRJNA453919 | ENA

Homo sapiens

Project description:Detection of Notch1-IC, Notch2-IC and EBNA2 target genes in human B cells

| PRJNA113183 | ENA

Comprehensive gene expression analysis in liver tissue following forced activation of Notch1 and Notch2 signaling.

Project description:We compared the effects of Notch1 and Notch2 signaling induced by AAV8-mediated forced expression of Notch1 intracellular domain (NICD1) and Notch2 intracellular domain (NICD2), respectively, in the liver. Eight-week-old wild-type male mice were injected intraperitoneally with an NICD1- and/or NICD2-overexpressing AAV8 vector. Efficient AAV8-mediated gene transfer was confirmed by co-expressed green fluorescent protein (GFP) fluorescence in hepatocytes. A comprehensive gene expression analysis using DNA microarray indicated that the expression levels of 1704 and 1325 genes were altered by overexpressing NICD1 and NICD2, respectively, compared with the control group expressing only GFP.

2021-11-28 | GSE178886 | GEO

Notch1 and Notch2 signaling from distinct cellular sources exclusively but cooperatively regulate fetal myogenesis

Project description:During developmental myogenesis, some continuously proliferating myogenic progenitors (MPs) sustain stem/progenitor states while the rest differentiate into myocytes to form myofibers by fusion. To generate sufficient muscle, fine regulations of cell fate decision of MPs are crucial. Notch signaling has been known to regulate embryonic MPs (eMPs) that play a role in primary myogenesis by promoting cell cycle exit and suppressing premature differentiation. However, the role of Notch signaling in fetal MPs (fMPs) during secondary myogenesis is elusive because the development of fMPs already has been abrogated in Notch manipulation models. In this study, we investigated the role of Notch signaling in fMPs at an individual Notch receptor level. Surprisingly we found that Notch1 and Notch2, most similar among four Notch receptors, distinctly regulate fMPs: Notch1 induces cell cycle exit and Notch2 suppresses premature differentiation, presumably by canonical Notch signaling pathway. Additionally, we suggest that Notch1 and Notch2 signals are regulated by the ligands on myofibers and MP-lineage cells, respectively. This study will lay the groundwork for the in-depth understanding of Notch signaling in muscle formation from embryonic myogenesis to adult muscle regeneration.

2022-12-31 | GSE190521 | GEO

Transcriptional impact of conditional loss of Notch2 from adult NSCs

Project description:Adult NSCs maintenance depends on intakt Notch signaling. The role of Notch2 has only been marginally studied in adult neurogenesis. To adress the role of the Notch2 paralogue we conditionally deleted Notch2 from the adult SVZ and analysed the Notch2-deficient cells at distinct time points.

2018-01-23 | GSE99916 | GEO

Notch2 Expressed by Myofibers Influences Muscle Mass and Fiber Types

Project description:Notch receptors play crucial roles in the cell-fate decisions of tissue stem cells during development and regeneration. Notch1-3 receptors are expressed by satellite cells and their progeny. Here we found that Notch2, but not Notch1 or Notch3, was expressed in fully differentiated myofibers. Using transgenic mice that expressed a muscle-specific active form of Notch2 (N2ICD-mTG), we found that Notch2 activation remarkably reduced muscle mass and strength with a shift toward slow fibers. Transcriptome analyses revealed that growth differentiation factor 11 (GDF11) was highly up-regulated in muscles of N2ICD-mTG mice, and crucially, N2ICD-induced muscle atrophy was rescued by siRNA-mediated reduction of GDF11 expression. These data suggest that Notch2 functions in muscle to regulate muscle mass, in part, through induction of GDF11 expression, and reveal a novel aspect of Notch signaling in a terminally differentiated adult tissue.

2020-01-01 | GSE83929 | GEO

Notch2 deficiency prevents muscle atrophy induced by mechanical unloading and diabetes.

Project description:Notch signaling plays essential roles in maintenance of muscle stem cell pool. We found that Notch2, but not Notch1 and Notch3, is expressed in fully differentiated myofibers. To study the specific role of Notch2 in adult myofibers, we generated muscle-specific Notch2-knockout mice. Here, we showed that muscle-specific Notch2 deficiency prevented muscle atrophy induced by hindlimb unloading and diabetes millitus. RNA sequencing analysis revealed that the loss of Notch2 gene in myofibers inhibited gene responses to unloading and diabetes. Especially, several FoxO-target genes and atrogenes were upregulated in wildtype muscles but not in Notch2-deficient muscles by unloading and diabetes. Thus, our characterization of muscle-specific Notch2-knockout mice indicates that Notch2 acts as a regulatory factor of skeletal muscle plasticity and could be a therapeutic target of muscle atrophy.

2022-01-07 | GSE161693 | GEO

Conditional ablation of the Notch2 receptor in the ocular lens

Project description:Notch signaling is essential for proper lens development, however the specific requirements of individual Notch receptors has not been previously investigated. Here we report the lens phenotypes of Notch2 conditionally mutant mice, which exhibited severe microphthalmia, reduced pupillary openings, disrupted fiber cell morphology, eventual loss of the anterior epithelium, fiber cell dysgenesis, and cataracts. Notch2 mutants also had a persistent lens stalk phenotype at E11.5, and aberrant DNA synthesis in the fiber cell compartment by E14.5. Gene expression analyses showed elevated levels of the cell cycle regulators Cdkn1a (p21Cip1), Ccnd2 (CyclinD2) and Trp63 (p63) that negatively regulates Wnt signaling. Although removal of Notch2 phenocopied the increased proportion of fiber cells of Rbpj and Jag1 conditional mutant lenses, Notch2 is not required for AEL proliferation, suggesting that a different receptor regulates this process. Instead, we found that the Notch2 normally blocks progenitor cell death. Overall, we conclude that Notch2-mediated signaling regulates lens morphogenesis, apoptosis, cell cycle withdrawal, and secondary fiber cell differentiation. We have compared gene expression of ocular lenses of mice that are lens specific conditional mutants of Notch2 gene to that of littermate controls that had no ablation of Notch2 gene in the lens. Two lenses of each of the three conditional mutants and controls were pooled together and total RNA was harvested from embryonic day 19.5 (E19.5) lenses. Gene expression changes caused by absence of Notch2 gene in the lens were analyzed.

2011-12-31 | E-GEOD-31643 | biostudies-arrayexpress

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