Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339957 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Notch signaling pathway regulates several differentiation and developmental processes, and is involved in the development of a multitude of diseases. Here we investigate by ChIP-Seq the effects of overexpression of the active NOTCH1 intracellular domain (N1ICD) on H3K27ac in human adipose tissue endothelial cells.
2023-06-16 | GSE195537 | GEO
Project description:Human Notch1 intracellular domain (NICD) was overexpressed in human primary lymphatic endothelial cells (LECs) for 10 and 24 hours by adenovirus. A GFP-control adenovirus-infected cells (24hours) and uninfected cells were also analysed as controls. Total RNAs were harvested and subjected to Affymetrix U133A microarray. Human primary lymphatic endothelial cells (LECs) were isolated from human foreskin and cultured and expanded to population passages 5~6. Healthy subconfluent primary LECs were infected with adenovirus expressing human Notch1 intracellular domain (NICD) for 10 or 24 hours. In parallel, LECs were also infected with a GFP-expressing control adenovirus for 24 hours. Uninfected LECs were also used as a negative control in the same experiments
2010-03-20 | E-GEOD-20978 | biostudies-arrayexpress
Project description:Notch signaling is widely implicated in mouse mammary gland development and tumorigenesis. To investigate the effects of acute activation of Notch signaling in the mammary epithelial compartment, we generated bi-transgenic MMTV-rtTA; TetO-NICD1 (MTB/TICNX) mice that conditionally express a constitutively active NOTCH1 intracellular domain (NICD1) construct in the mammary epithelium upon doxycycline administration.
2015-05-12 | GSE51628 | GEO
Project description:Overexpression of intracellular domain(NICD) of Notch1 affected the expression level of more than 1000 genes
2016-07-01 | GSE81583 | GEO
Project description:Overexpression of intracellular domain(NICD) of Notch1 affected the expression level of more than 1000 genes 6 samples were analyzed
2016-07-01 | E-GEOD-81583 | biostudies-arrayexpress
Project description:Vascular endothelial cells upregulate the Notch ligand Jagged1 in response to inflammatory activation. Here we show that abrogation of endothelial Notch1 signaling impairs induction of key inflammatory target genes. Accordingly, inducible endothelial-targeted knockout of the canonical Notch transcription factor RBPJ reduces inflammation in a murine model of contact hypersensitivity, while overexpression of constitutive active Notch1 has the opposite effect. We show that the proinflammatory role of Notch1 can be attributed to direct genomic priming of the inflammatory landscape involving crosstalk with NF-κB/RelA and selective activation of enhancers associated with Notch-dependent inflammatory genes. This is the first evidence that canonical Notch signaling supports endothelial activation in response to inflammatory cytokines on the chromatin level.
2018-08-29 | GSE87552 | GEO
Project description:ICAP1 (also known as ITG1BP1) is a protein interaction partner of beta1-integrins and the cerebral cavernous malformation protein 1 (CCM1, also known as KRIT1). In mice Icap1 plays an important role for bone development. The function of ICAP1 in endothelial cells is poorly understood. However, the interactions with beta1-integrins and CCM1 suggest that ICAP1 should play an important role also in endothelial cells. We obtained data that ICAP1 might activate the Delta-Notch signaling cascade, a critical regulator of endothelial proliferation, migration and sprouting angiogenesis. This genome-wide expression analysis is aimed to unravelling novel mechanisms or signaling pathways how ICAP1 functions in endothelial cells. Secondly, this study aimed at defining novel target genes of Notch signaling and finally to compare the gene expression patterns of ICAP1 and NOTCH1. We used human umbilical vein endothelial cells (HUVEC) as a model system to study ICAP1 and NOTCH1 functions after adenoviral over expression in comparison to GFP over expression as control. The results of this experiment suggest that ICAP1 and NOTCH1 control a series of genes involved in cell proliferation, migration and angiogenesis. A high proportion of ICAP1-regulated genes is also regulated by NOTCH1 in a very similar manner. Human umbilical vein endothelial cells were transduced with adenovirus expressing ICAP1, NOTCH1 (only the constitutive active intracellular domain) or GFP as control. 36 hours after transduction total RNA was isolated from duplicates for genome-wide expression analysis biological replicate: GFP_1, GFP_2 biological replicate: NOTCH1_1, NOTCH1_2 biological replicate: ICAP1_1, ICAP1_2
2010-07-30 | E-GEOD-18035 | biostudies-arrayexpress
Project description:Transcriptional profiling of murine splenic mature B cells that have experienced activation-induced cytidine deaminase (Aicda) gene expression comparing control untreated B cells with B cells in which transgenic Notch1 intracellular domain (NICD1) gene, coding for an active form of Notch1, began to be expressed after Aicda promoter-driven expression of Cre recombinase. B cells that have experienced Aicda promoter activation were visualized by Cre-inducible expression of red fluorescent protein (RFP) which was inserted in the Rosa26 locus. Total RNA was extracted from splenic CD19+ RFP+ B cells isolated from mice using an RNeasy Mini kit (Qiagen, Hilden, Germany). Equal amounts of total RNA derived from 3 control mice and 3 mice with conditional activation of Notch1 signaling in mature B cells were pooled and submitted for gene expression microarray analysis. Goal was to determine the effects of conditional activation of Notch1 signaling in mature B cells.
2018-04-17 | GSE113174 | GEO
Project description:Notch signaling is critical for vascular morphogenesis by co-determining the sprouting behavior of endothelial cells. Here, we investigate the function of ubiquitin-specific peptidase 10 (USP10) in regulation of the turnover of the NOTCH1 intracellular domain. HUVEC were transfected with scrambled or USP10 targeting siRNA and then stimulated by treatment with DLL4 or control. RNA for analysis was isolated after 24 hours of DLL4 stimulation.
2019-04-26 | E-MTAB-7774 | biostudies-arrayexpress
Project description:Expression of a constitutively active Notch-1 intracellular domain (NICD) in MCF-10A cells was found to induce two distinct types of 3D structures: large, hyperproliferative structures and small, growth-arrested structures with reduced cell-to-matrix adhesion. These heterogeneous phenotypes reflect differences in Notch pathway activation levels. High Notch activity caused loss of cell adhesion and inhibition of proliferation, whereas low Notch activity maintained matrix adhesion and provoked a strong hyperproliferative response. In order to gain insight into the dosage-dependent transcriptional events triggered by Notch1 activation, gene expression profiles induced 48 hours after infection of MCF-10A cells with retroviral vectors expressing full-length Notch-1, L1601P+âP, or NICD were compared. Full-length Notch-1 induced the weakest effect, L1601P+âP induced an intermediate effect and NICD induced the strongest effect. Results provide insight into the dichotomous activites of Notch during development and tumorigenesis. Twelve samples were harvested 48 h after retroviral infection with either vector control, full-length Notch1, Notch1 L1601P+âP, or NICD. Each condition was performed in triplicate.
2010-03-23 | E-GEOD-20285 | biostudies-arrayexpress