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Next Generation Sequencing Facilitated Differential Transcriptome Study of melanoma cells transduced with Notch 1 Intracellular Domain (NICD)

ABSTRACT: Next Generation Sequencing Facilitated Differential Transcriptome Study of melanoma cells transduced with Notch 1 Intracellular Domain (NICD)

PROVIDER: PRJNA433021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6675380.fastq.gz	Fastqsanger.gz
	SRR6675390.fastq.gz	Fastqsanger.gz
	SRR6675381.fastq.gz	Fastqsanger.gz
	SRR6675391.fastq.gz	Fastqsanger.gz
	SRR6675382.fastq.gz	Fastqsanger.gz

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Similar Datasets

Next Generation Sequencing Facilitated Differential Transcriptome Study of melanoma cells transduced with Notch 1 Intracellular Domain (NICD)

Project description:Transcriptome profiling (mRNA-seq) of melanoma cells overexpressing NICD

2019-02-05 | GSE110179 | GEO

Histone variant H2A.Z deposition and acetylation directs the canonical Notch signaling response

Project description:The study deals with the elucidation of potential interaction partners of the intracellular domain of the transmembrane receptor Notch1, termed NICD. The NICD is released from the cytoplasmic tail of the Notch receptor by gamma-secretase treatment and translocated as a transcription factor to the nucleus. Here, virally transduced recombinant NICD constructs (wild-type and deltaEP hyperactive mutant) were employed for AP-MS with the aim of identifying novel NICD interactors in a murine T cell leukemia cell line.

2018-06-25 | PXD008747 | Pride

Gene expression analysis in mouse mature T-cells either upon overexpression of the NICD or knockout of H2A.Z

Project description:Genes induced by the Notch-Intracellular domain (NICD) in mouse mature T-cells (MT) are identifed. Among the induced Notch target genes we also identify those genes, which are regulated by the histone variant H2A.Z

2018-06-21 | GSE111029 | GEO

Modeling Notch-induced tumor cell survival in the Drosophila ovary identifies cellular and transcriptional response to nuclear NICD accumulation

Project description:Notch is a conserved developmental signaling pathway that is dysregulated in many cancer types, most often through constitutive activation. Tumor cells with nuclear accumulation of the active Notch receptor, NICD, generally exhibit enhanced survival while patients experience poorer outcomes. To understand the impact of NICD accumulation during tumorigenesis, we developed a tumor model using the Drosophila ovarian follicular epithelium. Using this system we demonstrated that NICD accumulation contributed to larger tumor growth, reduced apoptosis, increased nuclear size, and fewer incidents of DNA damage without altering ploidy. Using bulk RNA sequencing we identified the key Notch-induced targets involved in cell survival and DNA damage repair which were alternatively regulated prior to tumor formation. Finally, using single-cell RNA sequencing we demonstrated that genes contributing to many pathways are altered following tumor formation in a cell-type-specific manner. Ectopically expressing NICD produced dysregulated expression of genes involved in cell death regulation, immune and stress response, JAK/STAT signaling, cytoskeletal binding, adhesion, polarity, and growth regulation. This valuable tumor model for nuclear NICD accumulation in adult Drosophila follicle cells has allowed us to better understand the specific role of nuclear NICD accumulation in tumor cells in tumor cell survival and tumor progression.

2021-09-19 | GSE182505 | GEO

Expression profiling of Notch constitutive activation induced HCC in mice

2012-12-01 | GSE33486 | GEO

Expression profiling of Notch constitutive activation in the liver of mice

Project description:Notch intracellular domain (NICD) is the active form of the Notch receptor. In this mouse model, NICD is inserted in the Rosa26 locus downstream of a loxP-STOP-LoxP (lsl) sequence and therefore NICD expression is dependant on Cre recombinase expression (Mono transgenic control Rosa26-lsl-NICD) . These mice are crossed with the AFP-Cre strain that expresses Cre in hepatoblasts due to its regulation by the AFP promoter and albumin enhancer (Double transgenic mutant AFP-Cre/Rosa26-lsl-NICD). Newborn mice at day 0 and day 2 are sacrificed and liver RNA samples from control monotransgenic Rosa26-lsl-NICD and from bitransgenic AFP-Cre/Rosa26-lsl-NICD (AFP-NICD) are obtained. Whole genome expression profiling of these samples is submitted.

2012-12-01 | GSE33560 | GEO

Plasma membrane-derived extracellular microvesicles mediate non-canonical intercellular NOTCH signaling

Project description:ARMMs (arrestin domain-containing protein 1 [ARRDC1]-mediated microvesicles) are extracellular vesicles that bud directly atthe plasma membrane. However, little is known about the physiological function of these vesicles. Here we report that secreted ARMMs contain active NOTCH receptors and mediate a non-canonical intercellular NOTCH signaling. Masss pectrometry of purified ARMMs identifiedNOTCH2 as a protein component of the vesicles. The NOTCH protein in ARMMs contains the critical intracellular region (NICD) that is required for its transcriptional activity in the nucleus. ARRDC1 overexpression increased the NOTCH2 incorporation into ARMMs. Conversely, CRISPR-mediated knockout of ARRDC1 dramatically reduced the amount of NOTCH2 in secreted ARMMs. The incorporation of NOTCH2 into ARMMs is facilitated by the ITCH E3 ligase and ADAM10, which are also secreted into ARMMs. We showed NOTCH2 in ARMMs delivered into recipient cells is further activated by γ-secretase cleavage to induce NOTCH-specific signaling in recipient cells. Together, our findings revealed a role for ARMMs in a novelNOTCH signaling pathway that acts in distance beyond direct cell-cell contact.

2017-10-11 | PXD006416 | Pride

Expression profiling of Notch constitutive activation in the liver of mice

2012-12-01 | E-GEOD-33560 | biostudies-arrayexpress

Expression profiling of Notch constitutive activation induced HCC in mice

Project description:Notch intracellular domain (NICD) is the active form of the Notch receptor. In this mouse model, NICD is inserted in the Rosa26 locus downstream of a loxP-STOP-LoxP (lsl) sequence and therefore NICD expression is dependant on Cre recombinase expression. These mice are crossed with the AFP-Cre strain that expresses Cre in hepatoblasts due to its regulation by the AFP promoter and albumin enhancer. Mice from 6 to 12 months are sacrificed and liver RNA samples from control monotransgenic Rosa26-lsl-NICD and confirmed HCC lesions from bitransgenic AFP-Cre/Rosa26-lsl-NICD (AFP-NICD) are obtained. Exon expression profiling of these samples are submitted. Four liver samples from monotransgenic mice (control) and five hepatocellular carcinoma samples from bitransgenic mice are analyzed using the Affymetrix GeneChip Mouse Gene 1.0 ST Array platform. Array data was preprocessed and analyzed using GenePattern software and R.

2012-12-01 | E-GEOD-33486 | biostudies-arrayexpress

Gene expression changes in Nicd induced wing disc hyperplasia

Project description:The outcome of Notch proliferation on proliferation depends on the context. In Drosophila wing imaginal discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand te underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes during wing discs hyperplasis. these data are the results from expression profiling the RNAs from hyperplastic wing discs overexpressing Nicd. Direct comparison of third instar lavae wing imaginal disc Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) vs control (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with FRT82B ). 4 Biological replicates, the 2nd replicate was performed as a dye-swap.

2013-12-31 | E-GEOD-41428 | biostudies-arrayexpress

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