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Notch2 over expression in urinary bladder RT4V6 cell line

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Peter Black

PROVIDER: E-GEOD-60564 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analysis of WT and Notch2-deficient classical DC subsets

Project description:Defense against attaching and effacing (A/E) bacteria requires the sequential generation of IL-23 and IL-22 to induce protective mucosal responses. While the critical source of IL-22 has been identified as CD4+ and Nkp46+ innate lymphoid cells (ILCs), the precise source of IL-23 is unclear. Here, we use genetic techniques to deplete specific classical dendritic cell (cDC) subsets and analyze immunity to the A/E pathogen Citrobacter rodentium. We find that Zbtb46+ cDCs, and specifically Notch2-dependent intestinal CD11b+ cDCs, but not Batf3-dependent CD103+ cDCs, are required for IL-23 production and immunity against C. rodentium. Notch2 controls cDC differentiation at a terminal step mediated by lymphotoxin signaling. Importantly, these results provide the first demonstration of a non-redundant function of CD11b+ cDCs in vivo. Analysis of Notch2-dependent genes in CD11b+ and DEC205+ splenic classical DC subsets. Splenocytes were harvested from littermate WT Notch2 f/f C57Bl/6 or Notch2 CD11c-cre C57Bl/6 mice and DC subsets sorted to >95% purity on the FACSAriaII.

2013-06-01 | E-GEOD-45681 | biostudies-arrayexpress

Mapping sites of O-fucose modification on mouse NOTCH2

Project description:The O-fucose modification sites on mouse NOTCH2 were determined by mass spectral glycoproteomic site mapping. The Extracellular Domain of mouse NOTCH2 was produced in HEK293T cells in the presence or absence of the three Fringe enzymes: Lunatic fringe, Manic fringe, or Radical fringe. The protein was purified from the medium, reduced and alkylated, digested with trypsin, chymotrypsin or V8 protease, and the resulting peptides were analyzed by nano-LC mass spectrometry. The majority of the sites were identified using an Agilent model 6340 Ion Trap mass spectrometer. A few sites were identified using a Q-Exactive Plus mass spectrometer.

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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.

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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

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Notch2 over expression in urinary bladder RT4V6 cell line

Project description:Notch2 in promotion of bladder cancer growth and metastasis through epithelial to mesenchymal transition (EMT), cell cycle progression and maintenance of stemness.

2014-08-21 | GSE60564 | GEO

NOTCH2 mutants

Project description:NOTCH2 mutants

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Effect of Notch2 in chondrocytes

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Notch2 controls non-autonomous Wnt-signalling in chronic lymphocytic leukaemia

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

Transcriptional impact of conditional loss of Notch2 from adult NSCs

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

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