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Homo sapiens

ABSTRACT: NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence [N1ICD]

PROVIDER: PRJNA293982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2184380.fastq.gz	Fastqsanger.gz
	SRR2184390.fastq.gz	Fastqsanger.gz
	SRR2184400.fastq.gz	Fastqsanger.gz
	SRR2184410.fastq.gz	Fastqsanger.gz
	SRR2184420.fastq.gz	Fastqsanger.gz

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NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence

Project description:NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence

| PRJNA293985 | ENA

Homo sapiens

Project description:NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence [CSM]

| PRJNA293984 | ENA

NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence

Project description:Senescence, a persistent form of cell cycle arrest, is often associated with a diverse secretome, which provides complex downstream functionality for senescent cells within the tissue microenvironment. We show that oncogene-induced senescence (OIS) is accompanied by a dynamic fluctuation of NOTCH1 activity, which drives a TGF-β-rich secretome, whilst suppressing the senescence-associated pro-inflammatory secretome through inhibition of C/EBPβ. NOTCH1 and NOTCH1-driven TGF-β contribute to ‘lateral induction of senescence’ through a juxtacrine NOTCH-JAG1 pathway. In addition, NOTCH1 inhibition during senescence facilitates upregulation of pro-inflammatory cytokines, promoting lymphocyte recruitment and senescence surveillance in vivo. Because enforced activation of NOTCH1 signalling confers a near mutually exclusive secretory profile compared to typical senescence, our data collectively indicate that the dynamic alteration of NOTCH1 activity during senescence dictates a functional balance between these two distinct secretomes: one representing TGF-β and the other pro-inflammatory cytokines, highlighting that NOTCH1 is a temporospatial controller of secretome composition.

2016-08-03 | PXD004168 | Pride

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [ATAC-Seq]

Project description:We describe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonizes the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonize the formation of RIS specific accessible regions.

2018-04-24 | GSE103588 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [RNA-Seq]

Project description:We decribe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonises the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonise the formation of RIS specific accessible regions.

2018-04-24 | GSE113060 | GEO

Whole-genome transcriptomic analysis of the cell fate switch induced by Notch activation in mouse mammary cells

Project description:Mice expressing the active form of Notch1(N1ICD) in the basal mammary epithelium (through SMAcreERT mice) were induced to express N1ICD at the onset of puberty (P24). This induces a cell fate switch that results in the acquisition of a luminal identity in the targeted cells. To understand the early signals responsible for this reprogramming of committed basal cells, we analysed by RNAseq the transcriptional changes occurring in the targeted cells after 72h of N1ICD expression. N1ICD-expressing cells express a GFP marker that was used to sort them and GFPpos cells were compared to untargeted basal cells in the same animals (GFPneg).

2018-04-30 | GSE105432 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [ChIP-Seq]

2018-04-24 | GSE103589 | GEO

Gene expression of skeletal muscles in response to overexpression of Notch1 intracellular domain (N1ICD)

Project description:Analysis of gene expression profile of Tibialis anterior (TA) skeletal muscle tissues with Notch1 intracellular domain (N1ICD) overexpression. Skeletal myogenesis involves sequential activation, proliferation, self-renewal/differentiation and fusion of myogenic stem cells (satellite cells). Notch signaling is known to be essential for the maintenance of satellite cells, but its function in late-stage myogenesis, i.e. post-differentiation myocytes and post-fusion myotubes, is unknown. Here we use muscle creatine kinase (MCK)-Cre to induce N1ICD expression in multinucleated myotubes. We found that myotube-specific Notch1 activation improved muscle regeneration and exercise performance of mdx mice, a model of Duchenne Muscular Dystrophy (DMD). Agilent microarray was performed to compare gene expression in mdx control and N1ICD-overexpressing mdx muscles. The results may provide mechanistic insights into how Notch1 activation in myotubes modulate muscle function.

2016-10-01 | GSE81242 | GEO

Aberrant activation of canonical Notch1 signaling in the mouse prostate drives epithelialcell proliferation and induces prostatic hyperplasiaby increasing androgen receptor sensitivity

Project description:To investigate the regulatory role of Notch1 signaling pathway in mouse prostate growth and development, we constructed mice with prostate-specific overactivation of Notch1 intracellular domain N1ICD, in which Notch1 signaling was overactivated in prostate epithelial cells. We then analyzed gene expression profiles in the prostates of overexpressed and normal Notch1 mice.

2023-04-11 | GSE200565 | GEO

Endothelial Jag1-RBPJK signaling promotes inflammatory leukocyte recruitment and atherosclerosis

Project description:Aim: To determine the role of NOTCH during the response-to-injury and subsequent chronic inflammatory process of the arterial wall underlying atherosclerosis. Methods and results: We have generated an endothelial-specific RBPJK depleted mice using the Cdh5 cadherin promoter (ApoE-/-;RBPJflox/flox;Cdh5- CreERT). Endothelial-specific deletion of the Notch effector RBPJK or systemic deletion of the Notch1 receptor in athero-susceptible ApoE-/- mice fed a HC diet for 6 weeks resulted in reduced atherosclerosis in the aortic arch and sinus. Intravital microscopy revealed decreased leukocyte rolling on the endothelium of ApoE-/-;RBPJflox/flox;Cdh5- CreERT, that correlated with the lesser presence of leukocyts and macrophages in the vascular wall. Consistent with this, transcriptome analysis revealed that proinflammatory and endothelial activation pathways were downregulated in atherosclerotic tissue of RBPJk-mutant mice.. Jagged1 signaling upregulation in endothelial cells promotes the physical interaction and nuclear translocation of the intracellular domain of the Notch1 receptor (N1ICD) with NF-kB,. This N1ICD and NF-kB interaction is required for reciprocal transactivation of target genes including vascular cell adhesion molecule-1 (Vcam1). Conclusions: Notch signaling pathway inactivation decreases leukocyte rolling, thereby preventing endothelial dysfunction and vascular inflammation. Thus attenuating Notch signaling may constitute a useful therapeutic strategy for atherosclerosis. Key words: atherosclerosis, endothelium, signaling pathways, Notch, NF-kB, transcriptional regulation

2017-06-30 | GSE69376 | GEO

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