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DAOY-Notch1/Notch2 knockout: transcriptome comparison

ABSTRACT: DAOY-Notch1/Notch2 knockout: transcriptome comparison

PROVIDER: PRJNA453919 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7073260.fastq.gz	Fastqsanger.gz
	SRR7073251.fastq.gz	Fastqsanger.gz
	SRR7073261.fastq.gz	Fastqsanger.gz
	SRR7073252.fastq.gz	Fastqsanger.gz
	SRR7073262.fastq.gz	Fastqsanger.gz

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DAOY-Notch1/Notch2 knockout: transcriptome comparison

Project description:Hyperactivation of Notch signaling and the cellular hypoxic response are frequently observed in cancers, with increasing reports of connections to tumor initiation and progression. The two signaling mechanisms are known to intersect, but while it is well established that hypoxia regulates Notch signaling, less is known about whether Notch can regulate the cellular hypoxic response. We now report that Notch signaling specifically controls expression of HIF2a, a key mediator of the cellular hypoxic response. Transcriptional upregulation of HIF2a by Notch under normoxic conditions leads to elevated HIF2a protein levels in primary breast cancer cells as well as in human breast cancer, medulloblastoma and renal cell carcinoma cell lines. The elevated level of HIF2 protein was in certain tumor cell types accompanied by down-regulation of HIF1a protein levels, indicating that high Notch signaling may drive a HIF1a-to-HIF2a switch. At the transcriptome level, the presence of HIF2a was required for approximately 21% of all Notch-induced genes: among the 1062 genes that were upregulated by Notch in medulloblastoma cells during normoxia, upregulation was abrogated in 227 genes when HIF2a expression was knocked down by HIF2a siRNA. In conclusion, our data show that Notch signaling affects the hypoxic response via regulation of HIF2a, which may be important for future cancer therapies.

2018-04-28 | GSE113753 | GEO

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

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

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

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

2009-08-06 | GSE12355 | 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 complements Notch1 to mediate inductive signaling that initiates early T cell development

Project description:Notch2 complements Notch1 to mediate inductive signaling that initiates early T cell development

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Notch2 complements Notch1 to mediate inductive signaling that initiates early T cell development

Project description:Notch signaling is the dominant intercellular signaling input during the earliest stages of T cell development in the thymus. Although Notch1 is known to be indispensable, we show that it does not mediate all Notch signaling in pre-commitment stages: Notch2 initially works in parallel to promote early murine T cell development and antagonize other fates. Notch-regulated target genes before and after T-lineage commitment change dynamically, and we show that this partially reflects shifts in genome-wide DNA binding by RBPJ, the transcription factor activated by complex formation with the Notch intracellular domain. Although Notch signaling and transcription factor PU.1 can activate some common targets in pre-commitment T progenitors, Notch signaling and PU.1 activity have functionally antagonistic effects on multiple targets, delineating separation of pro-T cells from alternative PU.1-dependent fates. These results define a distinct mechanism of Notch signal response that distinguishes the initial stages of murine T-cell development.

2020-07-12 | GSE148441 | GEO

NOTCH2 mutants

Project description:NOTCH2 mutants

| PRJNA967022 | ENA