Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43012 | GEO | 2013/10/01

SECONDARY ACCESSION(S): PRJNA184194

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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. Four-condition experiment, Control vs. IL-22 stimulation, Control vs Doxycycline addition (Hes1 overexpression) and Control vs IL22 stimulation+Doxycycline addition (Hes1 overexpression). Biological replicates: One for each condition, independently grown and harvested. One replicate per array.

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

Gene expression alteration in chondrocyte by HES1 overexpression

Project description:To investigate target molecules of HES1, we transduced GFP or HES1 into mouse chondrocyte cell line ATDC5, and performed the microarray analysis. HES1 overexpression increased inflammation-related genes including Il6 and Il1rl1.

2015-03-02 | GSE60737 | GEO

Hes1 and Liver Glucocorticoid Signaling

Project description:To investigate the role of HES1 during glucocorticoid signaling in the liver, we employed whole-genome microarray expressions in liver mRNA extracted from control and Hes1-liver knockout male mice (HESKOL) that had been adrenalectomized to remove endogenous glucocorticoids.

2014-01-08 | GSE52106 | GEO

Testing gene expression changes in VCaP cells following PRMT5 knockdown

Project description:VCaP cells expressing either NTC shRNA or PRMT5 shRNA 1 or shRNA 2 were treated with 100ng/ml doxycycline for 5 days This experiment is designed to see which genes and pathways are modulated by PRMT5 knockdown in VCaP cells

2015-04-15 | GSE65965 | GEO

Transcriptional responses of mantle cell lymphoma (MCL) after NIK knockdown

Project description:MCL lines were treated with or without 100ng/ml doxycycline for 7 days This experiment is designed to see if shRNA-mediated knockdown of NIK downregulates NFKB signaling in MCL lines with mutations in upstream regulators of the alternative pathway (TRAF2 & TRAF3)

2013-12-01 | GSE52435 | GEO

Effects of overexpression of Sox2 on gene expression in adult mouse intestine

Project description:In order to understand the molecular mechanisms of changes seen in the adult mouse intestine in response to Sox2 overexpression, gene expression was analyzed in the ileum upon 2-day Doxycycline (DOX) treatment of mice containing Dox-inducible Sox2 transgene. Repression of Cdx2 and of its intestinal targets was observed and confirmed by Western blotting and immunostaining. This effect of Sox2 was distinct from the effect of overexpression of Oct4. 6-8 week old TetON-Sox2, rtTA controls (no TetOP-Sox2 transgene), TetON-Oct4, and TetON-Sox2 X TetON-Oct4 mice (2 replicates) were treated for 2 days with 2 mg/ml DOX or were left untreated. Intestines (ileum part) were collected and total mRNA was extracted.

2013-05-11 | E-GEOD-28465 | biostudies-arrayexpress

Decoding the DNA binding sites associated with HES1

Project description:To investigate the DNA binding sites associated with HES1, a CUT & Tag assay was conducted utilizing an anti-flag antibody to isolate the DNA sequences that interact with HES1. Subsequently, these DNA sequences were subjected to analysis through DNA-seq. The results indicated that HES1 has the capability to bind to the promotor-transcription start sites of 1140 genes.

2024-11-13 | GSE270038 | GEO

Expression analysis of common myeloid progenitors (CMPs) expressing Hes1

Project description:High levels of Hes1 expression are frequently found in BCR-ABL-positive chronic myelogenous leukemia in blast crisis (CML-BC). In mouse bone marrow transplantation (BMT) models, co-expression of BCR-ABL and Hes1 induces CML-BC–like disease; however the underlying mechanism remained elusive. Here, based on gene expression analysis, we show that MMP-9 is upregulated by Hes1 in common myeloid progenitors (CMPs). Analysis of promoter activity demonstrated that Hes1 upregulated MMP-9 by activating NF-kB. Analysis of 20 samples from CML-BC patients showed that MMP-9 was highly expressed in three, with two exhibiting high levels of Hes1 expression. Interestingly, MMP-9 deficiency impaired the cobblestone area-forming ability of CMPs expressing BCR-ABL and Hes1 that were in conjunction with a stromal cell layer. In addition, these CMPs secreted MMP-9, promoting the release of soluble Kit-ligand (sKitL) from stromal cells, thereby enhancing proliferation of the leukemic cells. In accordance, mice transplanted with CMPs expressing BCR-ABL and Hes1 exhibited high levels of sKitL as well as MMP-9 in the serum. Importantly, MMP-9 deficiency impaired the development of CML-BC–like disease induced by BCR-ABL and Hes1 in mouse BMT models. The present results suggest that Hes1 promotes the development of CML-BC, partly through MMP-9 upregulation in leukemic cells.

2014-05-01 | GSE56921 | GEO

Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A III

Project description:The purpose of this study was to decipher the gene expression changes in the ML-DS cell line CMK upon overexpression of ARID3A. For that, we used a doxycycline-inducible gene expression system to overexpress ARID3A

2022-04-20 | GSE169740 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data