NOTCH2 mutants
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA967022 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24423300.fastq.gz | Fastqsanger.gz | |||
| SRR24423301.fastq.gz | Fastqsanger.gz | |||
| SRR24423302.fastq.gz | Fastqsanger.gz | |||
| SRR24423303.fastq.gz | Fastqsanger.gz | |||
| SRR24423304.fastq.gz | Fastqsanger.gz |
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Project description:Assessment of the genome-wide effect of DLBCL-asscociated NOTCH2 mutants in DLBCL on RBPJ and H3K27acetylation. DLBCL cell lines U2932 cells stably expressing HA-tagged NOTCH2(WT), NOTCH2(R2400*) or NOTCH2(Q2140*) were subjected to chromatin immnunoprecipitation DNA-sequencing (ChIP-seq) for RBP-J and H3K27ac.
2024-05-03 | GSE231623 | GEO
Project description:(1) Assessment of the transcriptional changes regulated by KLHL6 upon NOTCH ligand stimulation. Bulk RNA-seq in KLHL6 WT or KO U2932 cells was performed upon incubation with stromal OP9 cells stably expressing NOTCH ligand DLL1. (2) Assessment of the transcriptional changes regulated by the KLHL6-NOTCH2 axis in a xenotransplant model of DLBCL. Bulk RNA-seq was performed in in KLHL6+/+NOTCH2+/+(WT), KLHL6-/-NOTCH2+/+(K6-KO), KLHL6+/+NOTCH2-/-(N2-KO), KLHL6-/-NOTCH2-/-(DKO) U2932 cells xenotranplanted in NSG mice trated with CHOP. (3) Assessment of the transcriptional changes regulated by the DLBCL-associated NOTCH2 mutants. Bulk RNA-seq was performed inU2932 cells stably expressing NOTCH2(WT), NOTCH2(S2156A), NOTCH2(R2400*) or NOTCH2(Q2140*).
2024-05-03 | GSE231624 | GEO
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
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.
2011-12-31 | GSE31643 | GEO
Project description:To investigate the role of Notch2 in the inflammatory response in chondrocytes, we cultured primary chondrocytes derived from wild type and Notch2 mutant mice and treated TNFalpha or vehicle. We then performed gene expression profiling analysis using data obtained from RNA-seq of wild type and Notch2 mutant chondrocytes.
2023-10-16 | GSE224255 | GEO
Project description:The Wnt-signalling pathway is one of the core de-regulated pathways in chronic lymphocytic leukemia (CLL), activated in a subset of patients by somatic coding mutations. Here we describe an alternative mechanism of Wnt-activation in malignant B cells, mediated by Notch2 activity in mesenchymal stromal cells (MSC) in the tumor microenvironment. We identified that tumor cells specifically induce and activate Notch2 in MSCs. Notch2 orchestrates the expression of target genes essential for the activation of canonical Wnt-signaling in CLL cells. Mechanistically, stromal Notch2 mediates the stabilization of â-catenin by inhibiting the activation of Gsk3-â in malignant B cells. Pharmacological inhibition of the Wnt-pathway mitigates microenvironment-mediated survival of malignant B cells in vitro. Similarly, inhibition of Notch-signaling impaired survival of CLL cells and disease engraftment in a PDX mouse model. Notch2 activation in the tumour microenvironment is a pre-requisite for the GSK3-â dependent activation of the canonical Wnt-signaling in tumor cells.
2018-09-19 | PXD010401 | Pride
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
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
Project description:Effect of DLBCL-associated NOTCH2 mutants on genomic RBP-J localization and H3K27 acetylation
| PRJNA967020 | ENA
Project description:Notch2 in promotion of bladder cancer growth and metastasis through epithelial to mesenchymal transition (EMT), cell cycle progression and maintenance of stemness. Notch2 induced gene expression in human urinary bladder cancer was measured at three independent experiments.
2014-08-21 | E-GEOD-60564 | biostudies-arrayexpress