Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dexamethasone responses in BRC-Abl (p210) transformed murine B-cells

ABSTRACT: For generation of pre-B cell lines, bone marrow from tibias and femurs of 4 to 8 week old C56Bl/6 mice (wt and vav-Gfi1b transgene) was infected with retroviral stocks of different BCR-Abl constructs (MSCV-GFP-IRESp210 or pSRa-p210-tkneo) and plated at a density of 5E+06 per 6 cm dish. All pre-B cells were fed twice a week and analyzed after they became stroma independent. Cells received 1E-08 M dexamethasone or vehicle for 12 hours prior to RNA extraction using TRIzol. mRNAs were converted into doublestranded cDNA using a T7-promoter tagged oligodT primer and transcribed by T7 RNA polymerase in the presence of biotinylated NTPs. Targets were hybridized to Affymetrix MOE430A arrays, washed, stained and scanned (GeneChip scanner 2500) as recommended by the manufacturer. Images were processed either by MAS5.0 (global scaling, TGT=1000) or RMAExpress (quantile normalization and background substraction) software tools. By comparing the gene expression profiles of dexamethasone and non-induced cells, dexamethasone target genes were identified Keywords: ordered

ORGANISM(S): Mus musculus

PROVIDER: GSE2342 | GEO | 2006/02/25

SECONDARY ACCESSION(S): PRJNA91567

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Dexamethasone responses in BRC-Abl (p210) transformed murine B-cells

Project description:For generation of pre-B cell lines, bone marrow from tibias and femurs of 4 to 8 week old C56Bl/6 mice (wt and vav-Gfi1b transgene) was infected with retroviral stocks of different BCR-Abl constructs (MSCV-GFP-IRESp210 or pSRa-p210-tkneo) and plated at a density of 5E+06 per 6 cm dish. All pre-B cells were fed twice a week and analyzed after they became stroma independent. Cells received 1E-08 M dexamethasone or vehicle for 12 hours prior to RNA extraction using TRIzol. mRNAs were converted into doublestranded cDNA using a T7-promoter tagged oligodT primer and transcribed by T7 RNA polymerase in the presence of biotinylated NTPs. Targets were hybridized to Affymetrix MOE430A arrays, washed, stained and scanned (GeneChip scanner 2500) as recommended by the manufacturer. Images were processed either by MAS5.0 (global scaling, TGT=1000) or RMAExpress (quantile normalization and background substraction) software tools. By comparing the gene expression profiles of dexamethasone and non-induced cells, dexamethasone target genes were identified Keywords: ordered

2006-02-25 | E-GEOD-2342 | biostudies-arrayexpress

Mus musculus

Project description:Dexamethasone responses in BRC-Abl (p210) transformed murine B-cells

| PRJNA91567 | ENA

Comparative transcriptomic profiling of overexpression of PsrA in Pseudomonas aeruginosa PAO1

Project description:PsrA, a transcription factor belonging to the TetR family, is known to participate in the regulation of fatty acid metabolism, type III secretion system, and quinolone signaling in Pseudomonas aeruginosa. Using a psrA overexpression strain, this study conducted a transcriptomic analysis to examine the role of PsrA in P. aeruginosa PAO1.

2024-07-05 | GSE249518 | GEO

Retroviral transduction of CD34+ cells with P190 and P210 BCR/ABL1 fusion genes

Project description:Expression of P190 and P210 BCR/ABL1 in normal human CD34(+) cells induces similar gene expression profiles and results in a STAT5-dependent expansion of the erythroid lineage The P190 and P210 BCR/ABL1 fusion genes are mainly associated with different types of hematologic malignancies, but it is presently unclear whether they are functionally different following expression in primitive human hematopoietic cells. We investigated and systematically compared the effects of retroviral P190 BCR/ABL1 and P210 BCR/ABL1 expression on cell proliferation, differentiation, and global gene expression in human CD34(+) cells from cord blood. Expression of either P190 BCR/ABL1 or P210 BCR/ABL1 resulted in expansion of erythroid cells and stimulated erythropoietin-independent burst-forming unit-erythroid colony formation. By using a lentiviral anti-signal transducer and activator of transcription 5 (STAT5) short-hairpin RNA, we found that both P190 BCR/ABL1- and P210 BCR/ABL1-induced erythroid cell expansion were STAT5-dependent. Under in vitro conditions favoring B-cell differentiation, neither P190 nor P210 BCR/ABL1-expressing cells formed detectable levels of CD19-positive cells. Gene expression profiling revealed that P190 BCR/ABL1 and P210 BCR/ABL1 induced almost identical gene expression profiles, and we identified a common set of 222 differentially expressed genes. Our data suggest that the early cellular and transcriptional effects of P190 BCR/ABL1 and P210 BCR/ABL1 expression are very similar when they are expressed in the same human progenitor cell population, and that STAT5 is an important regulator of BCR/ABL1-induced erythroid cell expansion. Keywords: global gene expression profiling, BCR/ABL1, CD34+ cord blood cells, CML, Ph+ ALL

2009-05-12 | GSE16042 | GEO

Transcription profiling of mouse overexpressing MHC-I after endurance training

Project description:Myosine heavy chain I was overexpressed in mouse skeletal muscle. The transgenic mice, as well as the wild type mice, were endurance trained on treadmill for 5 days/week over 8 weeks at 80% peak aerobic capacity in comparison with untrained mice. The gene expression profiles of the skeletal muscles from wild-type trained (WTT) and untrained (WTUT), and transgenic trained (TGT) and untrained (TGUT) were measured using Affymetrix Mouse430A 2.0 GeneChips. Experiment Overall Design: There were 5 WTT, 5 WTUT, 5 TGT, and 5 TGUT mice used in microarray studies.

2008-06-13 | E-GEOD-5297 | biostudies-arrayexpress

Transcription profiling of Pseudomonas aeruginosa PAO1-psrA::Tn vs. PAO1 in LB

Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Experiment Overall Design: PAO1 and PAO1-psrA::Tn cultures grown in LB and cells were harvested at mid-log phase. Total RNA was isolated from both samples, and used for cDNA synthesis. And then, the cDNA for both samples were fragmented and labeled. The cDNA of PAO1 was used for 2 GeneChips, and PAO1-psrA::Tn cDNA was used for three GeneChips.

2008-04-07 | E-GEOD-8083 | biostudies-arrayexpress

Impact of endurance training in MHC-I over-expressed Mice

2006-12-21 | GSE5297 | GEO

Proteomic study on the reproductive toxicity of Tripterygium glycosides in rats

Project description:Tripterygium glycoside tablet (TGT) is a common clinically used and effective non-steroidal immunosuppressant. However, its reproductive toxicity limits its application in pediatric immune diseases, warranting the study of the molecular mechanism behind its reproductive toxicity. In the present study, 4-week-old male SD mice were provided TGT through continuous gavage with a clinically equivalent dose of 12 mg/kg for 12 weeks. The reproductive toxicity of TGT was recorded, and its toxicity mechanism was verified through experimental validation and proteomics analyses. Our results demonstrated that TGT could significantly reduce the testosterone level in the serum as well as the concentration and survival rate of sperms. Pathological sections of the testis revealed that TGT could reduce spermatocytes at different levels and make the convoluted meridians vacuolated. Based on TMT-labeled quantitative mice testicular tissue proteomics, 34 differential proteins were screened, involving protein digestion and absorption, PPAR signaling pathway, PI3K-Akt, and other pathways, among which PI3K-Akt plays an important role in the study of reproductive injury. Western blotting results revealed that TGT could significantly downregulate the Col1A1, Col1A2, p-PI3K, and p-Akt expressions and inhibit the expression of proteins related to the PI3K-Akt signaling pathway. In summary, the clinically equivalent dose of TGT induced reproductive toxicity of 4-week-old male SD mice, possibly in relation to the inhibition of the PI3K-Akt pathway expression.

2022-03-02 | PXD031978 |

PAO1-psrA::Tn expression compared to PAO1 in LB

Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Keywords: Pseudomonas aeruginosa, wild-type PAO1 compared to PAO1-psrA::Tn

2008-02-14 | GSE8083 | GEO

Expression data from 8-10 week old WT mice maintained in room air or exposed to hyperoxia (FiO2>95%) for 48 hrs

Project description:To detect sex-specific differences in gene expression in a model of hyperoxic lung injury in adult C56BL/6J mice. In this dataset, we include the expression data obtained from lungs from 8-10 week old male and female WT C57BL/6J mice exposed to hyperoxia for 48 hours amd room air controls.These data were used to determine differences in transcriptome between male and female mice after hyperoxia exposure

2014-12-10 | GSE51039 | 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