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accession-icon GSE106710
An analysis of the effect of indacaterol and GSK 256066 alone and in combination on gene expression changes in the BEAS-2B human airway epithelial cell line.
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray analysis was performed on RNA extracted from BEAS-2B cells treated with indacaterol, GSK 256066 and indacaterol and GSK 256066 in combination to identify differentially expressed genes that may contribute to the beneficial and deleterious effects of 2-adrenoceptor agonists and phosphodiesterase 4 inhibitors in obstructive lung diseases.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE84880
A comparison of GS-5759, a bifunctional 2-adrenoceptor agonist and PDE4 inhibitor, and indacaterol and GSK 256066 in combination on gene expression changes in the BEAS-2B human airway epithelial cell line
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

GS-5759 is a bifunctional ligand composed of a quinolinone-containing pharmacophore found in several 2-adrenoceptor agonists linked covalently to a phosphodiesterase 4 inhibitor (PDE4) related to GSK 256066 by a pent-1-yn-1-ylbenzene spacer. The object of the study was to detemine if gene expression changes induced by GS-5759 were replicated by a 2-adrenoceptor agonist (indacaterol; Ind) and a PDE4 inhibitor (GSK 256066; GSK) in combination.

Publication Title

GS-5759, a Bifunctional β2-Adrenoceptor Agonist and Phosphodiesterase 4 Inhibitor for Chronic Obstructive Pulmonary Disease with a Unique Mode of Action: Effects on Gene Expression in Human Airway Epithelial Cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE84645
Expression analysis of transgenic mice with a cardiac specific overexpression of DSC2.
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene expression data indicate an early up-regulation of inflammatory and fibrotic remodeling pathways in DSC2 transgenic mice vs. non-transgenic control mice. The mice were analyzed at the age of 3.5 and 13 weeks.

Publication Title

Transgenic mice overexpressing desmocollin-2 (DSC2) develop cardiomyopathy associated with myocardial inflammation and fibrotic remodeling.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE27973
Human airway epithelial responses to rhinovirus infection and cigarette smoke extract alone and in combination
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16.

Publication Title

Cigarette smoke modulates expression of human rhinovirus-induced airway epithelial host defense genes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE60058
Tfap2a dependnt cha
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Neo/null loss of Tfap2a in E10.5 mouse facial prominences

Publication Title

Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage.

Sample Metadata Fields

Specimen part

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accession-icon GSE23559
The role of dietary leucine and dairy protein on hepatic gene expression
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

We used microarray to determine the differences in hepatic gene expression for diet-induced obese Sprague-Dawley rats consuming different dietary proteins. Proteins of interest included skim milk powder (dairy), casein, and the branched-chain amino acid, leucine.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE61092
Expression data from the commensal bacteria Escherchia coli strain HB101 interacting with Caenorhabditis elegans and/or Giardia duodenalis
  • organism-icon Escherichia coli
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Homeostatic interactions between the host and its resident microbiota is important for normal physiological functions and if altered, it could lead to dysbiosis, a change in the structure and function of the microbiota, and as a result to various pathophysiologies. Altered structure in bacterial community is associated with various pathophysiologies, but we are just beginning to understand how these structural changes translate into functional changes. Environmental factors including pathogenic infections can lead to altered interactions between the host and its resident microbiota.

Publication Title

Giardia duodenalis-induced alterations of commensal bacteria kill Caenorhabditis elegans: a new model to study microbial-microbial interactions in the gut.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56819
Effects of knockdown of ROCK1 and ZIPK on gene expression in cultured human vascular smooth muscle cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Rho-associated kinase (ROCK) and zipper-interacting protein kinase (ZIPK) have been implicated in diverse physiological functions, including smooth muscle contraction, cell proliferation, cell adhesion, apoptosis, cell migration and inflammation. Many aspects of regulation via ROCK and ZIPK, however, remain unclear. In this study, we utilized an siRNA approach to knock down ROCK1 and ZIPK in cultured human arterial smooth muscle cells. Microarray analysis was performed, using a whole-transcript expression chip, to identify changes in gene expression profiles induced by ROCK1 and ZIPK knockdown. ROCK1 knockdown affected the expression of 553 genes (355 down-regulated and 198 up-regulated), while ZIPK knockdown affected the expression of 390 genes (219 down-regulated and 171 up-regulated). A high incidence of up- and down-regulation of transcription regulator genes was observed in both ROCK1 and ZIPK knockdowns. Other markedly affected groups included transporters, kinases, peptidases, transmembrane and G protein-coupled receptors, growth factors, phosphatases and ion channels. Three microRNAs (mir-145, mir-199 and mir-622) were up-regulated by ROCK1 knockdown, whereas ZIPK knockdown had no effect on microRNA expression. 76 differentially expressed genes were common to ROCK1 and ZIPK knockdown, of which 41 were down-regulated and 26 up-regulated by both treatments, while the other 9 genes were differentially up/down-regulated. Ingenuity Pathway Analysis identified five pathways shared between the two knockdowns, which are mainly involved in cell cycle regulation. Marked differences in the effects of ROCK1 and ZIPK knockdown on the genes involved in cell cycle regulation suggested that ROCK1 and ZIPK regulate the cell cycle by different mechanisms. ROCK1, but not ZIPK knockdown significantly reduced the viability of vascular SMC. ROCK1 knockdown also affected several cytokine signaling pathways with up-regulation of 5 and down-regulation of 4 cytokine genes, in contrast to ZIPK knockdown, which affected the expression of only two cytokine genes (both down-regulated). IL-6 gene expression and secretion of IL-6 protein were up-regulated by ROCK1 knockdown, whereas ZIPK knockdown reduced IL-6 mRNA expression and IL-6 protein secretion and ROCK1 protein expression, suggesting that ROCK1 may inhibit IL-6 secretion. IL-1 mRNA and protein levels were increased in response to ROCK1 knockdown. Finally, ROCK1 but not ZIPK knockdown inhibited proliferation of vascular smooth muscle cells. We conclude that ROCK1 and ZIPK have diverse, but predominantly distinct regulatory functions in vascular smooth muscle cells.

Publication Title

The effects of knockdown of rho-associated kinase 1 and zipper-interacting protein kinase on gene expression and function in cultured human arterial smooth muscle cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE21514
The mRNA and microRNA expression profile of the RNA-induced silencing complex in human U-87 astrocytoma cells and primary human astrocytes
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

mRNA and microRNA expression was examined in global cellular fractions and in RNA-induced silencing complex (RISC)-immunoprecipitated cell fractions in cultured primary human astrocytes (ScienCell) and in cultured human U-87 MG astrocytoma cells (ATCC). ABSTRACT: Background: GW/P bodies are cytoplasmic ribonucleoprotein-rich foci that are involved in microRNA (miRNA)-mediated messenger RNA (mRNA) silencing and degradation. These mRNA regulatory functions within GW/P bodies are mediated by GW182 and its binding partner hAgo2 when bound to miRNA within the RNA-induced silencing complex (RISC). Although miRNAs and mRNAs are known to be localized to RISC in a variety of cells, to date no published study has examined the profile of specific miRNA and mRNA targeted to the RISC. Methodology/Principle Findings: In this study, RISC mRNA and miRNA components were profiled by microarray analysis of human U-87 astrocytoma cells and primary human astrocytes with total RNA extracted from the RISC as well as the global cellular fractions. The novel findings of this study were fourfold: (1) miRNAs are highly enriched in primary astrocyte RISC compared to U-87 astrocytoma RISC, (2) astrocytoma cells and primary astrocytes each contain unique RISC miRNA profiles as compared to their respective cellular miRNA profiles, (3) miR-195, 10b, 29b, 19b, 34a and 455-3p were upregulated and miR-181b was downregulated in U-87 astrocytoma RISC as compared to primary astrocyte RISC, and (4) RISC contain mostly downregulated mRNAs in primary astrocytes and U-87 astrocytoma cells. Conclusions/Significance: We show that in U-87 astrocytoma cells, miR-34a and miR-195 were upregulated in RISC suggesting an oncogenic role for these miRNAs. Three miR34a-targeted mRNAs and two miR-195-targeted mRNAs were downregulated. One miR-195-targeted mRNA was upregulated. Biological pathway analysis of RISC mRNA components suggests that the RISC plays a pivotal role in cancer, inflammatory disease, immunological disease, the cell cycle, cellular movement and numerous cell signaling pathways. This study points to the importance of the RISC and ultimately GW/P body composition and function and in miRNA and mRNA deregulation in astrocytoma cells and possibly for other brain tumors.

Publication Title

The microRNA and messengerRNA profile of the RNA-induced silencing complex in human primary astrocyte and astrocytoma cells.

Sample Metadata Fields

Cell line

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accession-icon GSE52127
Brain tumor initiating cell response to microglia
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis.

Publication Title

Therapeutic activation of macrophages and microglia to suppress brain tumor-initiating cells.

Sample Metadata Fields

Cell line

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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