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Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA

ABSTRACT: Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA shows differential effect of Ulk1 KD on LXr responsive genes

ORGANISM(S): Mus musculus

PROVIDER: GSE74059 | GEO | 2016/03/31

SECONDARY ACCESSION(S): PRJNA298891

REPOSITORIES: GEO

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Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA

Project description:Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA shows differential effect of Ulk1 KD on LXr responsive genes AML-12 cells co-treated with 0.75mM PA+/- 10ÂµM GW3965 for 24 h +/- Ulk1 SiRNA

2016-03-31 | E-GEOD-74059 | biostudies-arrayexpress

Bulk RNA-seq of intestinal organoids upon treatment with LXR agonist GW3965

Project description:Liver X Receptor (LXR) activation in intestinal epithelial organoids promotes their growth in vitro. To investigate the downstream effect of LXR activation in intestinal epithelial cells and identify potential pathways driving regeneration, we carried out an unbiased transcriptomic analysis of intestinal epithelial organoids stimulated with the LXR agonist GW3965. In detail, wild type small intestinal crypts were seeded in vitro and stimulated with vehicle (DMSO) or GW3965. After six hours, closing crypts (organoids) were collected for RNA extraction and were analyzed by RNA sequencing.

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Intestine-specific activation of LXR via low-dose oral administration of GW3965

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RNA-seq of primary human CD4+ T cells treated with the LXR agonist GW3965, with and without TCR stimulation

Project description:We used RNA-sequencing to determine the transcriptional response to liver X receptor (LXR) activation in primary human CD4+ T cells, both at rest and under activation conditions. CD4+ T cells were isolated from 3 healthy donors and treated with the synthetic LXR agonist GW3965 (GW) for 24 hours. Gene expression was compared to control samples (CTRL) treated with the LXR antagonist GSK1440233. To activate the T cell antigen receptor (TCR), cells were pre-treated with CTRL/GW alone for 6 hours then transferred to plates containing anti-CD3 and anti-CD28 for a further 18 hours.

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Expression data from Ulk1 silencing in mouse liver and AML12 cells

Project description:Expression data from Ulk1 silencing in mouse liver and AML12 cells

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Expression data from Ulk1 silencing in mouse liver and AML12 cells

Project description:This experiments detail the differential gene expressionin hepatic cells in response to Ulk1 silencing both in vivo and in vitro We used microarrays to detail the global programme of gene expression underlying the loss of ULK1 knockdownin hepatic cells

2020-03-27 | GSE147579 | GEO

Intestine-specific activation of LXR via low-dose oral administration of GW3965

Project description:Intestine-specific activation of LXR via low-dose oral administration of GW3965

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LXR activation induces insulin resistance in primary human adipocytes

Project description:The effects of LXR stimulation by GW3965 treatment on global mRNA and miRNA expression in primary human in vitro differentiated adipocytes was investigated using microarray profiling.

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Differential translatome in the sensory neurons of the DRG treated with LXR agonist

Project description:We show differences in translatome of the sensory neurons of the DRG primary neurons treated with LXR agonist GW3965.

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Genome-wide analysis of GW3965-responsive genes in 4 different breast cancer cell lines, MCF-7, T-47D, SK-BR-3, and MDA-MB-231

Project description:Analysis of differentially expressed genes in response to the LXR agonist GW3965 in the MCF-7, T-47D, SK-BR-3, and MDA-MB-231 breast cancer cell lines. It was previously reported that GW3965 has antiproliferative effects on these 4 different breast cancer cell lines. In the present study, we additionally determine the effects of the LXR ligand on breast cancer cells and determine their mechanism of action in reducing cell proliferation.

2013-07-17 | GSE34987 | GEO

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