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RNAseq of Notch signaling responsive and unresponsive thymus DN1a/b cells

ABSTRACT: RNAseq of Notch signaling responsive and unresponsive thymus DN1a/b cells

PROVIDER: PRJNA529577 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8797600_1.fastq.gz	Fastqsanger.gz
	SRR8797600_2.fastq.gz	Fastqsanger.gz
	SRR8797601_1.fastq.gz	Fastqsanger.gz
	SRR8797601_2.fastq.gz	Fastqsanger.gz
	SRR8797602_1.fastq.gz	Fastqsanger.gz

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RNAseq of Notch signaling responsive and unresponsive thymus DN1a/b cells

Project description:We report the gene expression profile of thymus DN1a/b cells that are either responsive to Notch signals, or unresponsive to Notch signals due to absence of expression of RBPJ, a key mediator of the Notch signaling pathway.

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scRNAseq of Notch signaling responsive and unresponsive bone marrow lymphoid-primed multipotent progenitors (BM LMPPs)

Project description:We report the gene expression profile of single cell BM LMPPs that are either responsive to Notch signals, or unresponsive to Notch signals due to absence of expression of RBPJ, a key mediator of the Notch signaling pathway.

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RNA-seq of Notch signaling response in RTE cells

Project description:We report the gene expression profile of recent thymic emigrant (RTE) that are either responsive to Notch signals, or unresponsive to Notch signals during their maturation process. Notch responsiveness is controled by the expression of RBPJ, a key mediator of the Notch signaling pathway.

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ATAC-seq of Notch signaling response in RTE cells

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RNA-seq of Notch signaling responsive

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scRNAseq of Notch signaling responsive and unresponsive bone marrow lymphoid-primed multipotent progenitors (BM LMPPs)

Project description:scRNAseq of Notch signaling responsive and unresponsive bone marrow lymphoid-primed multipotent progenitors (BM LMPPs)

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Notch signaling is required for induction of an innate T cell development program in human thymus

Project description:CD4 CD8 double positive (DP) thymocytes progressively shut down Notch signaling after β-selection allowing progression of the DP program and positive selection of conventional CD4 and CD8 single positive T cells. In contrast, innate CD8+ T cells are selected from DP precursors shortly after β-selection. Here, we investigated whether notch signaling is required for the initiation of the innate T cell developmental program upon TCR engagement. We show that, after β-selection, Notch activation limits progression to late DP cells and favors the development of TCRαβ/CD3 expressing CD8dim early DP progenitors. TCR engagement in these Notch dependent TCRαβ+ early DP precursors does not induce prominent apoptosis, but rather induces T-bet expression by an mTOR-dependent mechanism. Our findings indicate that Notch signaling drives the launch of an innate effector program in response to TCR agonist selection in the thymus.

2019-09-05 | GSE100519 | GEO

The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [array]

Project description:Overexpression of the oncogene MEF2C oposses NOTCH signalling in T versus B lineage decision, driving leukemia in the thymus context

2022-05-14 | GSE159506 | GEO

The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [ChIP-Seq]

Project description:Overexpression of the oncogene MEF2C opposes NOTCH signalling in T versus B lineage decision, driving leukemia in the thymus context

2022-05-14 | GSE160407 | GEO

Notch signaling suppresses the progression of colorectal tumorigenesis

Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.

2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress

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