Transcriptional response to Notch activation in SVG-A cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA986650 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25000100_1.fastq.gz | Fastqsanger.gz | |||
| SRR25000100_2.fastq.gz | Fastqsanger.gz | |||
| SRR25000101_1.fastq.gz | Fastqsanger.gz | |||
| SRR25000101_2.fastq.gz | Fastqsanger.gz | |||
| SRR25000102_1.fastq.gz | Fastqsanger.gz |
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Project description:SVG-A cells are immortalized fetal astrocytes that respond to Notch signaling. We characterized the transcriptional response to Notch activation in this cell line by performing RNA-seq on cells grown on tissue culture dishes coated with JAGGED1, a Notch ligand. Differential gene expression analysis shows induction of both canonical Notch responsive genes, as well as cell-type specific Notch responsive genes.
2024-02-28 | GSE235637 | GEO
Project description:The transcription factor Twist is a critical cooperating factor that confers transcriptional specificity to the Notch pathway in muscle progenitor cells (DmD8) ChIP analysis of Twi show that Twist binding is significantly enriched in Notch responsive region in DmD8 cells 3 replicates of Twist ChIP after30 min. Notch activation.
2010-07-27 | E-GEOD-22650 | biostudies-arrayexpress
Project description:Cellular responses to signalling pathways are often highly dynamic, however most analyses of developmental signalling pathways focus on a single endpoint. Here we have analyzed the temporal changes in transcription following a short Notch activation treatment and have related these to the recruitment of the Notch pathway transcription factor, CSL [Suppressor of Hairless, Su(H), in Drosophila], and to the state of RNA Polymerase II (Pol II) binding. A total of 154 genes showed significant differential expression over time and their expression profiles stratified into 14 clusters based on temporal and quantitative differences in their responses. These differences were partially reflected in the profiles of Pol II and Su(H) binding. However neither could fully account for the different response profiles. Furthermore, the timing of the different responses was unaffected by more prolonged Notch activation. Instead our data suggest that regulatory relationships between genes that segregate into different response clusters can partially account for the stratification. Thus feed-forward repression, where products of early responding Enhancer of split bHLH genes (E(spl)bHLH) inhibit expression of endogenous repressors, is one mechanism that explains the profile of genes that exhibit delayed up-regulation. E(spl)bHLH genes may therefore be responsible for co-ordinating the Notch response of a wide spectrum of other targets, explaining their critical functions in many developmental and disease contexts.
2012-12-31 | GSE35557 | GEO
Project description:Cellular responses to signalling pathways are often highly dynamic, however most analyses of developmental signalling pathways focus on a single endpoint. Here we have analyzed the temporal changes in transcription following a short Notch activation treatment and have related these to the recruitment of the Notch pathway transcription factor, CSL [Suppressor of Hairless, Su(H), in Drosophila], and to the state of RNA Polymerase II (Pol II) binding. A total of 154 genes showed significant differential expression over time and their expression profiles stratified into 14 clusters based on temporal and quantitative differences in their responses. These differences were partially reflected in the profiles of Pol II and Su(H) binding. However neither could fully account for the different response profiles. Furthermore, the timing of the different responses was unaffected by more prolonged Notch activation. Instead our data suggest that regulatory relationships between genes that segregate into different response clusters can partially account for the stratification. Thus feed-forward repression, where products of early responding Enhancer of split bHLH genes (E(spl)bHLH) inhibit expression of endogenous repressors, is one mechanism that explains the profile of genes that exhibit delayed up-regulation. E(spl)bHLH genes may therefore be responsible for co-ordinating the Notch response of a wide spectrum of other targets, explaining their critical functions in many developmental and disease contexts. DmD8 cells were cultured in Schneiders medium (Invitrogen) supplemented with 10% FBS (Sigma), 5ug/ml insulin (Sigma) and 5% penicillin / streptomycin (Sigma) according to standard protocols. Notch signalling was initiated by replacing cell media with 2mM EDTA in PBS. The cells were stimulated for 5 minutes before washing out EDTA using normal culture media. The cells were then collected at 18 time points at 0M-bM-^@M-^Y, 5M-bM-^@M-^Y, 10M-bM-^@M-^Y, 15M-bM-^@M-^Y, 20M-bM-^@M-^Y, 25M-bM-^@M-^Y, 30M-bM-^@M-^Y, 35M-bM-^@M-^Y, 40M-bM-^@M-^Y, 50M-bM-^@M-^Y, 60M-bM-^@M-^Y, 70M-bM-^@M-^Y, 80M-bM-^@M-^Y, 90M-bM-^@M-^Y, 100M-bM-^@M-^Y, 110M-bM-^@M-^Y, 120M-bM-^@M-^Y and 150M-bM-^@M-^Y after stimulation in 4 independent time trials. For control samples, for each time trial, media was replaced with fresh media to mimic the addition and removal of EDTA in corresponding experimental samples and then collected at equivalent times. For each trial 50 M-BM-5g of the untreated control RNA sample of each time point was pooled to create a trial specific reference sample. Samples from trials #1 and #3 were labelled with Cy5 and trails #2 and #4 as dye-swap with Cy3.
2012-12-31 | E-GEOD-35557 | biostudies-arrayexpress
Project description:During hematopoiesis, Notch regulates both the emergence of stem and progenitor cells and the subsequent cell fate choices and differentiation. To investigate how Notch drives cells to differentiate we have used a genome-wide approach to identify direct Notch targets in Drosophila Kc cells. These data are the results from Su(H) ChIP-Chip experiments to identify genomic regions occupied by Su(H) after Notch activation in Kc cells. 3 replicates of Su(H) ChIP after 30 min. Notch activation..
2013-03-08 | E-GEOD-43132 | biostudies-arrayexpress
Project description:Notch Activation Commits Mesoderm Cells to the Cardiac Lineage
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Project description:To identify genes upregulated in response to Notch signalling in KC cells. Keywords: Expression analysis at a single timepoint (30' after Notch activation)
2009-02-17 | GSE9965 | GEO
Project description:To identify genes upregulated in response to Notch signalling in DmD8 cells. To identify genes upregulated in response to Notch signalling in KC cells. Keywords: Expression analysis at a single timepoint (30' after Notch activation)
2009-02-17 | GSE9964 | GEO
Project description:Vasculature permeate our entire body and involved in homeostasis and progression of various disease. Endothelium is a backbone of cardiovascular system and endothelial disfunction is associated with most forms of cardiovascular disease from atherosclerosis to chronic heart failure. Decrease in shear stress, particularly due to disturbance of the blood flow by bends or vascular obstruction, lead to atherosclerosis and endothelial disfunction. Notch signaling may act as mechanosensor and assumed to be one of the central signal pathways associated with endothelial disfunction. Association of shear stress, Notch and endothelial dysfunction is well known, molecular mechanisms connected these factors still poorly understood. One might assume that long-term shear stress and dysregulation of Notch in endothelium cause changes in epigenomic profile. While epigenomic changes in shear stressed environment are known to be involved in endothelial disfunction, possible connection of Notch and epigenetic changes in endothelium has not yet been tested. Therefore, here we analyzed how activation of Notch signaling influence on histone code and secretome of endothelial cells in vitro. We found that activation of Notch increase level of N-acetylated forms of Histone 1: H1-0, H1-3, H1-4, H1-5, H1-10. These changes were also associated with changes in secretome profile of endothelium and might have broad biomedical significance in case of endothelial dysfunction.
2023-02-15 | PXD032978 | Pride
Project description:Notch signaling plays both oncogenic and tumor suppressor roles, depending on cell type. In contrast to T cell acute lymphoblastic leukemia (T-ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B-ALL leads to growth arrest and apoptosis. The Notch target Hairy/Enhancer of Split1 (HES1) is sufficient to reproduce this tumor suppressor phenotype in B-ALL, however the mechanism is not yet known. Here we report that HES1 regulates pro-apoptotic signals via the novel interacting protein Poly ADP-Ribose Polymerase1 (PARP1) in a cell type-specific manner. The interaction of HES1 with PARP1 inhibits HES1 function, induces PARP1 activation and results in PARP1 cleavage in B-ALL. HES1-induced PARP1 activation leads to self-ADP ribosylation of PARP1, consumption of NAD+, diminished ATP levels, and translocation of the Apoptosis Inducing Factor (AIF) from mitochondria to the nucleus, resulting in apoptosis in B-ALL, but not T-ALL. Importantly, induction of Notch signaling via the Notch agonist peptide DSL can reproduce these events and leads to BALL apoptosis. The novel interaction of HES1 and PARP1 in B-ALL modulates the function of the HES1 transcriptional complex and signals through PARP1 to induce apoptosis. This mechanism reveals a cell type-specific pro-apoptotic pathway which may lead to Notch agonist-based cancer therapeutics. Study involved the gene expression profiling of human acute lymphoblastic leukemia samples, and comparison of the levels of expression NOTCH1 pathway genes and targets across ALL subtypes
2011-12-12 | E-GEOD-26366 | biostudies-arrayexpress