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Gene expression profile upon forced Notch1 activation in LS174T cells

ABSTRACT: The cell line was modified to express activated form of Notch1 (NICD1 of mouse origin) upon Doxycycline addition to the culture medium. Generation was performed by using the T-rex system (invitrogen), following manufacturer's instruction. Keywords: Genetic modification

ORGANISM(S): Homo sapiens

PROVIDER: GSE10136 | GEO | 2008/01/11

SECONDARY ACCESSION(S): PRJNA108685

REPOSITORIES: GEO

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Gene expression profile upon forced Notch1 activation in LS174T cells

Project description:The cell line was modified to express activated form of Notch1 (NICD1 of mouse origin) upon Doxycycline addition to the culture medium generated by T-rex system (invitrogen) following manufacturer's instruction. Keywords: Genetic modification Pulse-chase experiment, examining expression profile at 0h, 12h, 24h from Doxycycline addition. For details, please refer to our publication (American Journal of Physiology GI and Liver disease, e-pub at Nov 20th, 2008)

2010-05-26 | E-GEOD-10136 | biostudies-arrayexpress

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

Comprehensive gene expression analysis in liver tissue following forced activation of Notch1 and Notch2 signaling.

Project description:We compared the effects of Notch1 and Notch2 signaling induced by AAV8-mediated forced expression of Notch1 intracellular domain (NICD1) and Notch2 intracellular domain (NICD2), respectively, in the liver. Eight-week-old wild-type male mice were injected intraperitoneally with an NICD1- and/or NICD2-overexpressing AAV8 vector. Efficient AAV8-mediated gene transfer was confirmed by co-expressed green fluorescent protein (GFP) fluorescence in hepatocytes. A comprehensive gene expression analysis using DNA microarray indicated that the expression levels of 1704 and 1325 genes were altered by overexpressing NICD1 and NICD2, respectively, compared with the control group expressing only GFP.

2021-11-28 | GSE178886 | GEO

Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

Project description:A human colon carcinoma-derived cell line LS174T was modified to overexpress Hes1, a bHLH-type transcription factor, upon doxycycline addition (designated as LS174T-tetON-Hes1 cells), using the T-rex system (Invitrogen). We have previously shown that these cells can overexpress Hes1 under the control of CMV promoter (Zheng et al, Inflamm Bowel Dis, 17;2251-2260, 2011), and the amont of the overexpressed Hes1 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-Hes1 cells were treated with recombinant human IL-22 (20ng/ml) alone, doxycycline alone (100ng/ml), co-treated by both IL-22 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-Hes1 cells), in which overexpression of Hes1 can be induced by a Doxycycline dependent manner.

2013-10-01 | GSE43012 | GEO

Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

2013-10-01 | E-GEOD-43012 | biostudies-arrayexpress

Identification of Notch1 regulated genes in A549 NSCLC cell line

Project description:Notch signaling is an evolutionarily conserved signaling pathway. Notch1 signaling has been shown to potentially paly an important role in cancer development and progression. To illustrate the underlying regulating mechanisms of Notch1 activation in NSCLC, the intracellular domain of Notch1 receptor (NICD1) was overexpressed in A549 cell line and the RNA-sequences were performed.

2019-09-30 | GSE137106 | GEO

Effects of acute Notch activation on the mammary epithelial compartment in vivo

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

Transcriptomic Profiles of Immortalized Human Hepatocytes Overexpressing Intracellular Domain of NOTCH1

Project description:To investigate the effect of hyperactivation of Notch signaling in hepatocytes, an immortalized human hepatocyte cell line THLE-2 was stably transduced with control vector or plasmid harborning intracellular domain of NOTCH1 (NICD1) and the transcriptomic profiles were analyzed by RNA-seq.

2019-10-01 | GSE121170 | GEO

HEK NICD AP-MS - Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs)

Project description:Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs). Tight quantitative and temporal control of Notch activity is essential for vascular development, yet the details of Notch regulation in ECs are incompletely understood. We found that ubiquitin-specific peptidase 10 (USP10) interacted with the NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of this short-lived form of the activated NOTCH1 receptor. Accordingly, inactivation of USP10 reduced NICD1 abundance and stability, and diminished Notch-induced target gene expression in ECs. In mice, loss of endothelial Usp10 increased vessel sprouting and partially restored the patterning defects caused by ectopic expression of NICD1. Thus, USP10 functions as an NICD1 deubiquitinase, which fine-tunes endothelial Notch responses during angiogenic sprouting.

2019-04-11 | PXD013192 | Pride

Murine mature B Cells: Control vs. Notch1 Signaling Activated

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

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