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GSE8322
Mus musculus
11 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We recently found that the endoplasmic reticulum (ER) stress response (ERSR) is activated in surviving cardiac myocytes in a mouse model of in vivo myocardial infarction. ATF6 is an ER stress-activated transcription factor that induces ERSR genes, some of which encode proteins that may protect against ischemic damage. However, few ERSR genes have been identified in the heart, and there have been no gene expression profiling studies of ATF6-inducible genes, in vivo. We previously generated transgenic (TG) mice that express tamoxifen-activated ATF6, ATF6-MER, in the heart; ATF6-MER conferred tamoxifen-dependent ATF6 activation and protection from ischemic damage. To understand of the mechanism of ATF6-mediated cardioprotection, gene expression profiling of ATF6-MER TG mouse hearts was performed. Activated ATF6 changed expression levels of 1,162 genes in the heart; of the 775 ATF6-inducible genes, only 23 are known ERSR genes. One of the genes not expected to be induced by ATF6 is modulatory calcinuerin-interacting protein-1 (MCIP1). MCIP1 is induced in a calcineurin/NFAT-dependent manner during myocardial hypertrophy and it can feedback inhibit cardiomyocyte growth. We found that MCIP1 expression in cultured cardiomyocytes was increased by the prototypical ER stresser, tunicamycin (TM), or by simulated ischemia. Moreover, infecting cardiomyocytes with adenovirus encoding activated ATF6 induced MCIP1 expression and inhibited myocyte growth in response to the alpha 1-adrenergic agonist, phenylephrine. These results suggest that MCIP1 can be induced in the heart by ER stresses, such as ischemia. Moreover, b integrating hypertrophy and ER stress, MCIP-modulated myocyte growth may help rejuvenate nascent ER protein folding, which could contribute to protection from ischemic damage.
Publication Title
Coordination of growth and endoplasmic reticulum stress signaling by regulator of calcineurin 1 (RCAN1), a novel ATF6-inducible gene.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Escherichia coli
- 20 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
Transcription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA.
Publication Title
Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.
Sample Metadata Fields
Compound
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Microarray expression analysis to identify global changes in transcription in response to RAF inhibition.
Publication Title
The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models harboring EGFR T790M, resistance to WZ4002 develops through aberrant activation of ERK signaling caused by either an amplification of MAPK1 or by downregulation of negative regulators of ERK signaling. Inhibition of MEK or ERK restores sensitivity to WZ4002, and the combination of WZ4002 and a MEK inhibitor prevents the emergence of drug resistance. The WZ4002 resistant MAPK1 amplified cells also demonstrate an increase both in EGFR internalization and a decrease in sensitivity to cytotoxic chemotherapy compared to the parental counterparts. Our findings provide insights into mechanisms of drug resistance to EGFR kinase inhibitors and highlight rational combination therapies that should be evaluated in clinical trials.
Publication Title
Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The conducting airway epithelium of the rodent and human lung is made up of about equal proportions of ciliated and secretory cells. In addition, in regions where the epithelium is pseudostratfied, ~30% of the epithelium consists of undifferentiated basal cells (BCs). Evidence suggests that these BCs are multipotent stem cells that can self renew over the long term and give rise to both ciliated and secretory lineages. The goal of this project is to identify cellular and molecular mechanisms by which the basal cells normally maintain the epithelium and repair it after injury.
Publication Title
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The conducting airway epithelium of the rodent and human lung is underlaid by mesenchymal cells that include vasculature, smooth muscle, fibroblasts and cartilage. The goal of this project is to identify cellular and molecular changes in the mesenchyme after injury to the epithelium by exposure to SO2 and which may participate in repair of the epithelium
Publication Title
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
Illumina HiSeq 2000
Description
To study the transcriptome of human prostate cancer cells, RNA-seq experiments were performed. Overall design: RNA was harvested after 72h of steroid deprivation to study the basal transcriptome of LNCaP and 22rv1 cells, two human AR-positive prostate cancer cell lines,
Publication Title
Reprogramming of Isocitrate Dehydrogenases Expression and Activity by the Androgen Receptor in Prostate Cancer.
Sample Metadata Fields
Subject
View Samples- Arabidopsis thaliana
- 22 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Identification of TBF1-dependent and SA, elf18-responsive genes in Arabidopsis
Publication Title
The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition.
Sample Metadata Fields
Specimen part, Treatment
View Samples