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

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

PROVIDER: PRJNA435618 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6763960.fastq.gz	Fastqsanger.gz
	SRR6763961.fastq.gz	Fastqsanger.gz
	SRR6763962.fastq.gz	Fastqsanger.gz
	SRR6763963.fastq.gz	Fastqsanger.gz
	SRR6763964.fastq.gz	Fastqsanger.gz

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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

Transformation of mature adipocytes to liposarcoma in Ad/NICD mice

Project description:Analysis of inguinal white adipose tissue (WAT) and liposarcoma (LPS) isolated from Notch1 overexpression mice (Ad/NICD). Results provide insight into molecular mechanisms underlying tumorigenic transformation of Ad/NICD mature adipocytes

2016-08-28 | GSE80433 | GEO

Gene expression profile upon TNF-a stimulation, forced expression of NICD, or TNF-a stimulation under forced expression of NICD, in human colon carcinoma-derived LS174T cells

Project description:A human colon carcinoma-derived cell line LS174T was modified to overexpress NICD, intracellular domain of Notch1, upon doxycycline addition (designated as LS174T-tetON-NICD cells), using the T-rex system (Invitrogen). We have previously shown that these cells can overexpress NICD under the control of CMV promoter (Okamoto R et al, Am J Physiol, 296(1):G23-35, 2009), and the amont of the overexpressed NICD protein reaches to the maximal level in early as 3 hours from doxycycline addition (100ng/ml), which persists for up to 24 hours. In the present experiment, LS174T-tetON-NICD cells were treated with recombinant human TNF-a (50ng/ml) alone, doxycycline alone (100ng/ml), co-treated by both TNF-a and doxycycline, or left untreated (Control) for 24 hours, and subjected for analysis. Experiment was done using a modified sub-line of LS174T cell (LS174T-tetON-NICD cells), in which overexpression of NICD can be induced by a Doxycycline dependent manner.

2018-12-31 | GSE118048 | GEO

Reprogramming of cochlear supporting cells by MYC/NICD co-activation.

Project description:Strategies to overcome irreversible cochlear hair cell (HC) damage and loss are of vital importance to develop a treatment for hearing loss. HC regeneration in adult cochlea relies on a two-phase process: 1) Reprogramming mature cochlear (SCs) to regain the properties of their younger selves; 2) Activating Atoh1, a gene responsible for HC fate-determining, in the reprogrammed adult SCs for HC regeneration. We have shown that, by transient co-activation of Myc and NICD (Notch1 intracellular domain), the adult mouse cochlea can be successfully reprogrammed to a relatively younger stage and regain progenitor capacity, with the regeneration of HCs following Atoh1 overexpression in vitro and in vivo. To identify molecules to reprogram mature cochlear SCs, we utilized single-cell RNA sequencing and uncovered the pathways and their target genes underlying MYC/NICD-mediated reprogramming. We used an in-house adult cochlea explant culture system and carried out single-cell RNA sequencing to examine the gene expression profiles of cochlear explants from a transgenic mouse model, rtTa/tet-Myc/-tet-NICD, in response to Dox-induced MYC/NICD co-activation. We have shown that a 4-day treatment by Dox in cultured adult rtTa/tetMyc/-tet-NICD cochleae was sufficient to reprogram adult SCs for HC regeneration.

2022-06-03 | GSE205187 | GEO

Gene expression analysis of SJG6 CONTROL and NICD

Project description:Mutational landscape of Oral Squamous Cell Carcinoma (OSCC) is predominated by frequent inactivating mutations in EGF- like ligand binding domain of NOTCH1. However role of NOTCH1 signalling in tumorigenesis is highly context and cell type dependent. In this study, we investigated phenotypic effect of NOTCH1 mutations in primary line derived from OSCC biopsy. Based on gain-of-function assays in NOTCH1 mutant line we demonstrated regulation of cell behaviour and morphology, by NOTCH1 intracellular domain (NICD) leading to changes in cell proliferation, migration, clonal growth and differentiation. Importantly, overexpression of NICD results in upregulation of ETV7/TEL2 which negatively regulates SERPINE1 expression and confers malignant cells with less aggressive phenotype. Further knockdown of SERPINE1 expression simulated the phenotypes observed upon rescue of NICD. In accord with our cell-based model we observed strong correlation between NOTCH1, ETV7 and SERPINE1 expression in OSCC primary tumours indicating similar deregulated mechanisms during oral carcinogenesis. Overall this study suggests a tumour suppressive role of NOTCH1 in OSCC and highlights possible mechanisms leading to changes in cell behaviour and morphology in absence of NICD potentially by regulating TEL2 and SERPINE1 expression.

2019-03-05 | GSE127770 | GEO

Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of intestinal progenitor cells in Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed midguts Methods: mRNA profiles of intestinal progenitor cells isolated from 7-day-old wild-type (Ctrl) and ttk-RNAi, dpn overexpressed(dpn OE), Nicd overexpressed(Nicd OE) and seq&Nicd overexpressed(seq&Nicd OE) Drosophila midgut were generated by deep sequencing using Illumina HiSeq 2500. Results: ttk-RNAi in intestinal progenitor cells induces the expression of many neural-specific genes, including dpn and seq. Dpn ectopic expresion explains most of the ttk-RNAi expression profile change. Seq ectopic expression explains the expression of neural-specific Notch targets in the ttk-RNAi intestinal progenitor cells.

2021-02-23 | GSE130942 | GEO

Expression analysis of KHR and KHR-NICD oral tumors

Project description:KHR-NICD oral tumors grow faster than KHR oral tumors. The hypothesis was to test for differences in gene expression between KHR and KHR-NICD oral tumors.

2015-09-09 | GSE59950 | GEO

Expression analysis of KHR and KHR-NICD oral tumors

Project description:KHR-NICD oral tumors grow faster than KHR oral tumors. The hypothesis was to test for differences in gene expression between KHR and KHR-NICD oral tumors. Total RNA was isolated for KHR (n=6) and KHR-NICD (n=6) oral tumors. Expression profiling was performed using the Illumina MouseRef-8 v2 (GPL6885) array. Studies were conducted using tumors from FVB x C57BL/6 F1 mice.

2015-09-09 | E-GEOD-59950 | 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

H2A.Z overexpression suppresses senescence and chemosensitivity in pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma is one of the most intractable and devastating of all malignant tumors. Epigenetic modifications involving both DNA methylation and histone modification have a relationship between tumor initiation and progression. However, the contribution of histone variants in the PDAC is unknown. Here, we demonstrated that the histone variant H2A.Z is highly expressed in PDAC cell lines and PDAC patients and its overexpression correlated with poor prognosis. We found that the three-histone H2A.Z isoforms (H2A.Z.1, H2A.Z.2.1 and, H2A.Z.2.2), are highly expressed in PDAC cell lines and PDAC patients. Knockdown of three H2A.Z isoforms induces a senescent phenotype, cell cycle arrest in phase G2/M, increased cyclin-dependent kinase inhibitor CDKN2A/p16, SA-β-galactosidase activity and interleukin 8 production in PDAC. Transcriptome analysis of knockdown of the H2A.Z isoforms showed altered gene expression in the fatty acid biosynthesis. As well as in the genes that control the cell cycle and DNA damage repair. Furthermore, H2A.Z isoform deficiency, reduces the tumor size in a mouse xenograft model in vivo, and sensitizes PDAC cells to gemcitabine. These results make H2A.Z a potential candidate as a diagnostic biomarker and therapeutic target for PDAC

2019-04-03 | GSE129182 | GEO

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