Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of reduced glucocorticoid receptor-RNA affinity on dexamethasone treatment

ABSTRACT: Effect of reduced glucocorticoid receptor-RNA affinity on dexamethasone treatment

PROVIDER: PRJNA893006 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22007852_1.fastq.gz	Fastqsanger.gz
	SRR22007852_2.fastq.gz	Fastqsanger.gz
	SRR22007853_1.fastq.gz	Fastqsanger.gz
	SRR22007853_2.fastq.gz	Fastqsanger.gz
	SRR22007854_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Effect of reduced glucocorticoid receptor-RNA affinity on dexamethasone treatment

Project description:The RNA binding ability of the glucocorticoid receptor (GR) remains an understudied area of GR regulation. Through in vitro binding assays, we identified a separation-of-function mutation (SoF) in the DNA-binding domain that greatly reduces RNA affinity with a slight reduction in DNA affinity. To study the effects of RNA binding on GR function, we first generated stable U2OS cells expressing wild-type GR-HaloTag, the SoF mutant, or a control (Ctrl) mutant that mimics the SoF's reduction in DNA affinity without impairing RNA affinity. We then treated the cells with dexamethsone every hour over three hours with 4-thiouridine labeling, isolated the labeled RNAs, and used deep sequencing to measure changes in the dexamethasone-driven transcriptome.

2022-12-17 | GSE216337 | GEO

RNAs bound by the glucocorticoid receptor during dexamethasone treatment

Project description:RNAs bound by the glucocorticoid receptor during dexamethasone treatment

| PRJNA901183 | ENA

Loss of Glucocorticoid Receptor Expression Mediates in Vivo Dexamethasone Resistance in T-cell Acute Lymphoblastic Leukemia

Project description:Despite decades of clinical use, mechanisms of glucocorticoid resistance are poorly understood. We treated primary murine T lineage acute lymphoblastic leukemias (T-ALLs) with the glucocorticoid dexamethasone (DEX) alone and in combination with the pan-PI3 kinase inhibitor GDC-0941 and observed a robust response to DEX that was modestly enhanced by GDC-0941. Continuous in vivo treatment invariably resulted in outgrowth of drug-resistant clones, ~30% of which showed markedly reduced glucocorticoid receptor (GR) protein expression. A similar proportion of relapsed human T-ALLs also exhibited low GR protein levels. De novo or pre-existing mutations in the gene encoding GR (Nr3c1) occurred in relapsed clones derived from multiple independent parental leukemias. CRISPR/Cas9 gene editing confirmed that loss of GR expression confers DEX resistance. Exposing drug-sensitive T-ALLs to DEX in vivo altered transcript levels of multiple genes, and this response was attenuated in relapsed T-ALLs. These data implicate reduced GR protein expression as a frequent cause of glucocorticoid resistance in T-ALL.

2019-12-13 | GSE141967 | GEO

RNAs bound by the glucocorticoid receptor during dexamethasone treatment

Project description:The RNA binding ability of the glucocorticoid receptor (GR) remains an understudied area of GR regulation. Through in vitro binding assays, we identified hairpin RNAs as GR's preferred binding motif. To study how GR-bound RNAs change with dexamethasone treatment, we first generated stable U2OS cells expressing wild-type GR-HaloTag. We then treated the cells with dexamethsone every hour over three hours, UV crosslinked, harvested, and pulled down GR using a specific and covalently-bound HaloTag ligand. GR-bound RNAs were then isolated, library prepped, and sequenced.

2022-12-17 | GSE217888 | GEO

Transcription profiling of liver from wild type and glucocorticoid receptor knock out mice after dexamethasone treatment

Project description:The aim of this study is to identify novel glucocorticoid receptor (GR) regulated hepatic target genes. In order to do so, we used microarray technology to compare the gene expression of wild type and GR-null mice after 3 hrs of dexamethasone treatment.

2009-04-30 | E-MEXP-1816 | biostudies-arrayexpress

Transcription profiling of Arabidopsis seedlings expressing LEC2-Glucocorticoid Receptor fusion protein, induced with dexamethasone for 0, 1 or 4 hours

Project description:LEAFY COTYLEDON2 activity was induced via a LEC2-Glucocorticoid Receptor fusion protein in Arabidopsis seedlings. Experiment Overall Design: Transgenic plants carrying a 35S:LEC2-Glucocorticoid Receptor transgene were used for LEC2 induction. Activity was induced in 8 day old seedlings for 1 or 4 hours with Dexamethasone application. Controls include uninduced transgenic plants and non-transgenic plants treated with Dex. Experiment Overall Design: Two biological replicates per treatment.

2007-10-03 | E-GEOD-3959 | biostudies-arrayexpress

Transcriptional profile of mouse macrophage RAW 264.7 cells upon treatment with dexamethasone or the glucocorticoid receptor modulator AZD9567 in the presence or absence of inflammatory response.

Project description:The aim of the experiment was to gain insight into the selective anti-inflammatory action of the glucocorticoid receptor modulator AZD9567 in comparison with the classical synthetic glucocorticoid dexamethasone. To this end, the transcriptional profile of macrophage RAW 264.7 cells treated with dexamethasone or AZD9567 in the presence or absence of inflammatory response (elicited by lipopolysaccharide treatment) was identified.

2023-06-30 | E-MTAB-12816 | biostudies-arrayexpress

Cryptochromes mediate rhythmic repression of the glucocorticoid receptor

Project description:The circadian transcriptional repressors cryptochromes 1 (Cry1) and 2 (Cry2) interact with the C-terminus of the glucocorticoid receptor (GR) and are required for transrepression in response to the synthetic GR ligand dexamethasone (Dex) in mouse embryonic fibroblasts. Dex induction of many genes was increased in Cry-deficient fibroblasts suggesting that cryptochromes oppose transactivation in addition to contributing to transrepression. In mice, genetic loss of Cry1 and/or Cry2 resulted in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced glucocorticoid suppression of the hypothalamic-pituitary-adrenal axis coupled with increased sensitivity to the hyperglycemic effects of glucocorticoid-mediated transactivation in the liver. Cry1 and Cry2 association with a GRE in the Pck1 promoter was stimulated by Dex, and Dex-induced transcription of pck1 was strikingly increased in Cry-deficient livers. Finally, cry1-/-;cry2-/- mice subjected to 8 weeks of chronic Dex treatment exhibited incomplete suppression of circulating corticosterone and greater glucose intolerance compared with wildtype littermates subjected to the same chronic treatment, consistent with enhanced transcriptional response to the synthetic glucocorticoid ligand. Total RNA was obtained from WT and Cry1/2 KO MEFs treated with Dexamethasone (1uM) or control EtOH for 16 hours.

2011-12-22 | E-GEOD-24469 | biostudies-arrayexpress

Transriptome responses to dexamethasone in hippocampus of pigs with different genotypes at a glucocorticoid receptor gain-of-function mutation profiled using RNA-Seq

Project description:The main aims of the experiment were to 1) chart gene networks governed by glucocorticoid receptor on a genome-wide scale, 2) to provide insights into mechanisms modulating glucocorticoid sensitivity and 3) to obtain better understanding of molecular and phenotypic consequences of the GRAla610Val substitution by examining its transcriptome signature in untreated and dexamethasone-treated animals.

2021-12-31 | E-MTAB-9098 | biostudies-arrayexpress

Insulin signaling and reduced glucocorticoid receptor activity attenuate post-prandial gene expression in liver

Project description:C57BL/6J mice were subjected to night restricted feeding (ZT12-ZT24) and livers were isolated immediate before (ZT10) and after feeding (ZT14). Combined RNA-seq, DNase-seq and H3K27Ac ChIP-seq identified hundreds of genes and enhancers regulated by acute feeding. Importantly, this feeding regulated transcriptional program follows similar rhythmic expression patterns as the intrinsic circadian transcriptional programs. ChIP-seq showed that feeding repressed enhancers were occupied by both GR and FOXO1 and occupancy of these factors were suppressed by feeding correlating with increased insulin levels and reduced corticosterone levels. Interestingly, despite considerable genome-wide overlap between GR and FOXO1, injection of dexamethasone (dex) or insulin receptor antagonist (S961) immediately before feeding, demonstrated that the glucocorticoid and insulin receptor pathways control distinct transcriptional programs. And strikingly, only combined dex and S961 treatment reversed feeding induced changes to most of the hepatic transcriptome. These corticosteroid and insulin regulated transcriptional programs are dysregulated in diet-induced obese animals.

2018-11-01 | GSE119713 | 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