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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

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. 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).

ORGANISM(S): Homo sapiens

SUBMITTER: Lothar Strobl

PROVIDER: E-GEOD-12355 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Notch1, Notch2, and Epstein-Barr virus-encoded nuclear antigen 2 signaling differentially affects proliferation and survival of Epstein-Barr virus-infected B cells.

Kohlhof Hella H Hampel Franziska F Hoffmann Reinhard R Burtscher Helmut H Weidle Ulrich H UH Hölzel Michael M Eick Dirk D Zimber-Strobl Ursula U Strobl Lothar J LJ

Blood 20090401 22

The canonical mode of transcriptional activation by both the Epstein-Barr viral protein, Epstein-Barr virus-encoded nuclear antigen 2 (EBNA2), and an activated Notch receptor (Notch-IC) requires their recruitment to RBPJ, suggesting that EBNA2 uses the Notch pathway to achieve B-cell immortalization. To gain further insight into the biologic equivalence between Notch-IC and EBNA2, we performed a genome-wide expression analysis, revealing that Notch-IC and EBNA2 exhibit profound differences in th ...[more]

PMID: 19339697

Similar Datasets

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. Keywords: time course

2009-08-06 | GSE12355 | GEO

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

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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

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

Peptidomics analysis of urine from IC/BPS patients and healthy controls

Project description:Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic and debilitating pain disorder of the bladder and urinary tract with poorly understood etiology. A definitive diagnosis of IC/BPS can be challenging because many symptoms of IC/BPS are shared with other urological disorders. An analysis of urine presents an attractive and non-invasive resource for monitoring and diagnosing IC/BPS. Here, a non-targeted LC-MS and LC-MS/MS-based peptidomics analysis of urine samples collected from IC/BPS patients were compared to urine samples from asymptomatic controls.

2022-06-06 | PXD031843 | Pride

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

Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation: MLL-AF9 transformed LGMP

Project description:To determine role of Notch signaling in AML leukemia initiating cells we used a conditional mouse knock-in model of Notch1-IC to induce Notch1-IC expression in MLL-AF9 transformed LGMP. WT and Notch1-IC+ LGMP were analyzed to determined genes controlled by Notch signaling. 12 weeks old wt lethaly irradiated mice were transplanted with 50000 cKit+ MLL-AF9-IRES-YFP infected cells from MLL-AF9 EF1 wt/wt ROSAwt/CreERT2 or MLL-AF9 EF1 wt/lsl-N1-IC ROSAwt/CreERT2 mice + 250000 support wt total bone marrow cells. 4 weeks after transplant mice were injected 2 times with tamoxifen (0.2mg/g body weight) every other day. Mice were sacrificed and analyzed 6 days after last injection. LGMP were flow purified for RNA extraction and hybridization on Affymetrix microarrays.

2013-01-18 | E-GEOD-42260 | biostudies-arrayexpress

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

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