Gene expression after felodipine
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Tushar Patel
PROVIDER: E-GEOD-23427 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Genetic association studies, pharmacological investigations and analysis of mice-lacking individual genes have made it clear that Cocaine administration and Withdrawal have a profound impact on multiple neurotransmitter systems. The GABAergic medium spiny neurons of the nucleus accumbens (NAc) exhibit changes in the expression of genes encoding receptors for glutamate and in the signaling pathways triggered by dopamine binding to G-protein-coupled dopamine receptors. Deep sequence analysis provides a sensitive, quantitative and global analysis of the effects of Cocaine on the NAc transcriptome. RNA prepared from the NAc of adult male mice receiving daily injections of Saline or Cocaine, or Cocaine followed by a period of Withdrawal, was used for high-throughput sequence analysis. Changes were validated by quantitative polymerase chain reaction or Western blot. On the basis of pathway analysis, a preponderance of the genes affected by Cocaine and Withdrawal was involved in the cadherin, heterotrimeric G-protein and Wnt signaling pathways. Distinct subsets of cadherins and protocadherins exhibited a sustained increase or decrease in expression. Sustained down-regulation of several heterotrimeric G-protein β- and γ-subunits was observed. In addition to altered expression of receptors for small molecule neurotransmitters, neuropeptides and endocannabinoids, changes in the expression of plasma membrane transporters and vesicular neurotransmitter transporters were also observed. The effects of chronic Cocaine and Withdrawal on the expression of genes essential to cholinergic, glutamatergic, GABAergic, peptidergic and endocannabinoid signaling are as profound as their effects on dopaminergic transmission. Simultaneous targeting of multiple Withdrawal-specific changes in gene expression may facilitate development of new therapeutic approaches that are better able to prevent relapse. High-throughput sequence analysis of RNA prepared from the nucleus accumbens of adult male mice receiving daily injections of Saline or Cocaine, or Cocaine followed by a period of Withdrawal. Nucleus accumbens libraries were sequenced in nine lanes (three technical replicates per sample) on an Illumina GAIIx using a 37-cycle paired-end sequencing protocol. Replicates were analyzed for intra-sample disparity and read data from all three lanes were then merged into one composite data file per sample; intra-sample coefficient of determination, R2 ≥ 0.98. The composite file was used for subsequent analyses.
2013-01-10 | E-GEOD-43410 | biostudies-arrayexpress
Project description:Effects of soy isoflavones, genistein and daidzein, on the hepatic gene expression profile and indices for lipid metabolism were compared in rats. The GeneChip data was normalized and summarized by using SuperNORM data service (Skylight Biotech Inc.). Significance of expressional change among groups was tested by 2-way ANOVA on the normalized CEL data, which was deposited in a tab-separated ASCII text format. Principal components were identified on the summarized gene data. Three groups of rats were fed with an experimental diet containing 2 g/kg of either genistein or daidzein, or a control diet free of isoflavone for 14 days. The basal composition of the experimental diet was (in g/kg): casein, 200; palm oil, 100; corn starch, 150; cellulose, 20; mineral mixture (AIN-93G), 35; vitamin mixture (AIN-93), 10; L-cystine, 3.0; choline bitartrate, 2.0 and sucrose to 1 kg.
2012-10-10 | E-GEOD-41420 | biostudies-arrayexpress
Project description:To understand how diabetes alters the protein subunits of mitochondrial Electron Transfer Chain (ETC) in the podocytes, we performed a proteomic analysis of mitochondrial proteins isolated from primary kidney podocytes of WT (C57BL/6J background) and Ins2Akita/+ diabetic (C57BL/6J background) mice.
2024-02-08 | PXD045828 | Pride
Project description:To understand how diabetes alters the protein subunits of mitochondrial Electron Transfer Chain (ETC) in the podocytes, we performed a proteomic analysis of mitochondrial proteins isolated from primary kidney podocytes of WT (C57BL/6J background) and Ins2Akita/+ diabetic (C57BL/6J background) mice.
2024-02-08 | PXD041202 | Pride
Project description:Objective: To assess the role of aldoketoreductases and other doxorubicin pharmacokinetic or pharmacogenomic genes in doxorubicin cytotoxicity, resistance, DNA binding activity, and subcellular localization, Methods: We conducted a whole genome microarray study to identify differences in between doxorubicin-sensitive MCF-7cc cells and doxorubicin-resistant MCF-7Dox2-12 cells in terms of their expression of genes related to doxorubicin pharmacokinetics or pharmacodynamics. Targets were then validated by pharmacologic inhibition in conjunction with drug metabolite profiling, drug localization, drug cytotoxicity, and drug DNA binding studies. Results: 2063 differentially expressed transcripts were identified, including 17% and 43% of genes or gene families associated with doxorubicin pharmacokinetics or pharmacodynamics (p values of significance of 0.05 and <0.0001, respectively). The largest changes in the expression of genes associated with doxorubicin pharmacokinetics and pharmacodynamics were chiefly among the aldo-keto reductases (AKRs) Akr1c2, Akr1c3 and Akr1b10 which convert doxorubicin to doxorubicinol. We observed that doxorubicinol exhibits dramatically reduced drug toxicity, reduced drug DNA-binding activity, and altered drug subcellular localization to lysosomes. Pharmacologic inhibition of these AKRs in MCF-7Dox2-12 cells restored drug cytotoxicity, and drug localization to the nucleus. Conclusion: These findings demonstrate the utility of using curated pharmacokinetic and pharmacodynamic knowledgebases to identify highly relevant genes associated with doxorubicin resistance. The products of one or more of these genes could effectively be shown to alter the drug’s properties, while inhibiting them restored drug DNA binding, cytotoxicity, and subcellular localization. Doxorubicin resistant cell lines of breast MCF-7 cells were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with four labelling replicates of both forward and reverse labellings plus another set of 8 arrays with forward labelling. Sixteen arrays were used for this experiments. The co-cultured control cells MCF-7cc12 was generated by parallel selection process in the absence of drug.
2012-11-22 | E-GEOD-27254 | biostudies-arrayexpress
Project description:In this project we used an unbiased approach to identify the proteins that interact with NDUFS4 in the mouse podocytes using the APEX2 proximity labeling system. An immortalized murine podocyte was permanently transduced with a doxycycline (DOX) inducible NDUFS4-APEX2 chimeric construct. The cells were treated with DOX for 72 h to induce NDUFS4-APEX2 expression, followed by H2O2 activation of APEX2 mediated biotinylation of neighboring proteins. Biotinylated proteins were pull down by streptavidin beads and analyzed by LC-MS/MS. Cells without DOX induction or with DOX but without H2O2 activation were used as controls
2024-02-08 | PXD041378 | Pride
Project description:Ola1 is implicated in various stress response pathways, as well as in cancer and tumor progression. However, Ola1p functions are divergent between species and still remain poorly understood. Here, we studied the role of Ola1p in the heat shock response in Saccharomyces cerevisiae. We show that deletion of OLA1 results in higher levels of proteins with protective functions for proteome stability under heat stress. We found that Ola1p enriches in detergent-resistant protein aggregates during heat stress. In heat-stressed yeast cells, it rapidly forms assemblies that localize to stress granules. In vitro, Ola1p assembly is protein autonomous and coincides with structural rearrangements that occur at similar temperatures and pH values seen in cells. We further observed that deletion of OLA1 leads to increased ubiquitination of protein aggregates formed during heat stress. Upon stress relief, central factors for protein refolding and the clearance of protein aggregates are synthesized in higher amounts in dola1 cells, whereas global translation reinitiation is decreased in these cells. Our data suggest that Ola1p is a positive factor for stabilizing the misfolded proteome that is sequestered in cytoplasmic stress granules during heat stress and, thereby, enables cells to efficiently restore a functional proteome after stress relief.
2022-02-17 | PXD025615 | Pride
Project description:The Wistar-Kyoto (WKY) rat shows marked susceptibility to crescentic glomerulonephritis, while Lewis rats are resistant. Glomerular injury and crescent formation are macrophage-dependent. The aim of this study is to use gene expression profiling to identify genetic factors that determine macrophage activation and render WKY rats susceptibile to glomerulonephritis.
2011-03-17 | E-MEXP-2624 | biostudies-arrayexpress
Project description:In the pathogenic yeast Candida albicans, the zinc cluster transcription factor Upc2p has been shown to regulate expression of ERG11 and other genes involved in ergosterol biosynthesis upon exposure to azole antifungals. ERG11 encodes lanosterol demethylase, the target enzyme of this antifungal class. Over-expression of UPC2 reduces azole susceptibility, whereas its disruption results in hypersusceptibility to azoles and reduced accumulation of exogenous sterols. Constitutive up-regulation of ERG11 is a major cause of resistance to fluconazole in clinical isolates of C. albicans, yet the mechanism for this has yet to be determined. Using genome-wide gene expression profiling, we found UPC2 and other genes involved in ergosterol biosynthesis to be coordinately up-regulated with ERG11 in a fluconazole resistant clinical isolate as compared with a matched susceptible isolate from the same patient. Sequence analysis of the UPC2 alleles of these isolates revealed that the resistant isolate contained a single nucleotide substitution in one UPC2 allele that resulted in a G648D exchange in the encoded protein. Introduction of the mutated allele into a drug susceptible strain resulted in constitutive up-regulation of ERG11 and increased resistance to fluconazole. By comparing the gene expression profiles of the fluconazole resistant isolate and of strains carrying wild-type and mutated UPC2 alleles, we identified target genes that are controlled by Upc2p. Here we show for the first time that a gain-of-function mutation in UPC2 leads to increased expression of ERG11 and imparts resistance to fluconazole in clinical isolates of C. albicans. Keywords: genome-wide expression profiling Clinical isolates S1 (susceptible) and S2 (resistant), genome strain SC5314, UPC2 disruption strains (UPC2M4A and UPC2M4B), UPC2 re-integrant strains of non-mutated UPC2 allele (UPC2M2K21A and UPC2M2K21B), and UPC2 re-integrant strains of mutated UPC2 allele (UPC2M2K31A and UPC2M2K31B) were grown for 3 hours until log phase. RNA was extracted for each isolate/strain. Experiments were performed in duplicate.
2008-11-04 | E-GEOD-11320 | biostudies-arrayexpress
Project description:HMGB2 and ER ChIPseq was investigated in the MCF-7 endocrine sensitive and LY2 endocrine resistant cell lines upon treatment with Tamoxifen.
2014-09-18 | E-MTAB-1865 | biostudies-arrayexpress