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GSE69438
Homo sapiens
39 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We identified EGF as the top candidates predicting kidney function through an intrarenal transcriptome-driven approach, and demonstrated it is an independent risk predictor of CKD progression and can significantly improve prediction of renal outcome by established clinical parameters in diverse populations with CKD from a wide spectrum of causes and stages
Publication Title
Tissue transcriptome-driven identification of epidermal growth factor as a chronic kidney disease biomarker.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 275 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
This SuperSeries is composed of the SubSeries listed below. A subset of samples profiled in this analysis were also profiled in Series GSE68127, and GSE104066. Corresponding glomerular transcriptome data can be found under GEO ID: GSE108109.
Publication Title
Metabolic pathways and immunometabolism in rare kidney diseases.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 196 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
summary : Glomerular Transcriptome from European Renal cDNA Bank subjects and living donors. Samples included in this analysis have been previously analyzed using older CDF definitions and are included under previous GEO submissions - GSE47183 (chronic kidney disease samples), and GSE32591 (IgA nephropathy samples).
Publication Title
Metabolic pathways and immunometabolism in rare kidney diseases.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 194 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
summary : Tubulointerstitial transcriptome from ERCB subjects with chronic kidney disease and living donor biopsies. Samples included in this analysis have been previously analyzed using older CDF definitions and are included under previous GEO submissions - GSE47184 (chronic kidney disease samples), and GSE32591 (IgA nephropathy samples).
Publication Title
Metabolic pathways and immunometabolism in rare kidney diseases.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 169 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
Tubulointerstitial transcriptome from human kidney biopsies in Neptune and ERCB. A number of samples profiled in this analysis were also profiled in Series GSE68127.
Publication Title
Metabolic pathways and immunometabolism in rare kidney diseases.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 106 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
Glomerular transcriptome from human kidney biopsies in Neptune and ERCB. A subset of samples profiled in this analysis were also profiled in Series GSE68127, and in GSE104066. Corresponding tubulointerstitial transcriptome data is submitted under GEO ID: GSE108113.
Publication Title
Metabolic pathways and immunometabolism in rare kidney diseases.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We hypothesize that gene expression in the cigarette smoke (CS) exposed neonatal lung and age-matched controls will be divergent. CS exposed lung will have divergence of immune response genes and structural genes. The lungs of (6) 2 week old neonatal mice exposed to 2 weeks of CS were compared to the lung of (4) 2 week old age-matched control mice. We utilized microarray analysis to examine transcriptional differences between smoke exposed neonatal lung and age-matched controls.
Publication Title
Impaired lung homeostasis in neonatal mice exposed to cigarette smoke.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 7 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Hmt1p is the predominant arginine methyltransferase in Saccharomyces cerevisiae. Its substrate proteins are involved in transcription, transcriptional regulation, nucleocytoplasmic transport and RNA splicing. Functionally, Hmt1p-catalysed methylation can also modulate protein-protein interactions. Despite Hmt1p being well-characterised, the effects of its knockout on the proteome and transcriptome have not been reported. SILAC-based analyses of the hmt1 proteome, in mid-log exponential growth, revealed a decreased abundance of phosphate-associated proteins including Pho84p (phosphate transporter), Pho8p (vacuolar alkaline phosphatase), Pho3p (acid phosphatase) along with Vtc1p, Vtc3p and Vtc4p (subunits of the vacuolar transporter chaperone complex). RNA-Seq and microarray analysis revealed a downregulation of phosphate-responsive genes in hmt1, including PHO5, PHO11 and PHO12 (acid phosphatases), PHO84 and PHO89 (phosphate transporters) and VTC3 (vacuolar transporter chaperone). Consistent with these observations, we observed a dysregulation of phosphate homeostasis in hmt1, with a general decrease in extracellular phosphatase production and a decrease in total Pi in phosphate replete medium. We show that the transcription factor Pho4p, responsible for activation of the PHO pathway, can be methylated by Hmt1p at Arg-241 and is the likely cause of phosphate dysregulation in hmt1. However, the methylation of Pho4p does not affect its nucleocytoplasmic localisation. We propose that the methylation of Pho4p may affect either its capacity to multimerise, its capacity to interact with Pho2p or target DNA, or may affect Pho4p phosphorylation at Ser-242 and/or Ser 243. Our study highlights a previously unknown function of Hmt1p in the regulation of phosphate homeostasis and suggests a means by which sensing of AdoMet may affect intracellular phosphate concentration.
Publication Title
Knockout of the Hmt1p Arginine Methyltransferase in <i>Saccharomyces cerevisiae</i> Leads to the Dysregulation of Phosphate-associated Genes and Processes.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 15 Downloadable Samples
Illumina HiSeq 2000
Description
The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages. Overall design: RNA-Seq profiles of C. elegans XO hermaphrodite and XX male L3 larvae and adults
Publication Title
Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The clinical efficacy of EGFR kinase inhibitors gefitinib and erlotinib is limited by the development of drug resistance. The most common mechanism of drug resistance is the secondary EGFR T790M mutation. Strategies to overcome EGFR T790M mediated drug resistance include the use of mutant selective EGFR inhibitors, including WZ4002, or by the use of high concentrations of irreversible quinazoline EGFR inhibitors such as PF299804. In the current study we develop drug resistant versions of the EGFR mutant PC9 cell line which reproducibly develops EGFR T790M as a mechanism of drug resistance to gefitinib. Neither PF299804 resistant (PFR) or WZ4002 resistant (WZR) clones of PC9 harbor EGFR T790M. Instead, they demonstrate activated IGF1R signaling as a result of loss of expression of IGFBP3 and the IGF1R inhibitor, BMS 536924, restores EGFR inhibitor sensitivity. Intriguingly, prolonged exposure to either PF299804 or WZ4002 results in the emergence of a more drug resistant subclone which contains ERK activation. A MEK inhibitor, CI-1040, partially restores sensitivity to EGFR/IGF1R inhibitor combination. Moreover, an IGF1R or MEK inhibitor used in combination with either PF299804 or WZ4002 completely prevents the emergence of drug resistant clones in this model system. Our studies suggest that more effective means of inhibiting EGFR T790M will prevent the emergence of this common drug resistance mechanism in EGFR mutant NSCLC. However, multiple drug resistance mechanisms can still emerge. Preventing the emergence of drug resistance, by targeting pathways activated in resistant cancers before they emerge, may be a more effective clinical strategy.
Publication Title
Resistance to irreversible EGF receptor tyrosine kinase inhibitors through a multistep mechanism involving the IGF1R pathway.
Sample Metadata Fields
Specimen part
View Samples