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accession-icon GSE74817
Time Course of Adults Vaccinated with Influenza TIV Vaccine 2009-2012
  • organism-icon Homo sapiens
  • sample-icon 615 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Systems Analysis of Immunity to Influenza Vaccination across Multiple Years and in Diverse Populations Reveals Shared Molecular Signatures.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE74813
Time Course of Adults Vaccinated with Influenza TIV Vaccine during 2010/11 Flu Season (HIPC cohort)
  • organism-icon Homo sapiens
  • sample-icon 284 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Systems approaches have been used to describe molecular signatures driving immunity to influenza vaccination in humans.

Publication Title

Systems Analysis of Immunity to Influenza Vaccination across Multiple Years and in Diverse Populations Reveals Shared Molecular Signatures.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE74816
Time Course of Adults Vaccinated with Influenza TIV Vaccine during 2011/12 Flu Season
  • organism-icon Homo sapiens
  • sample-icon 177 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Systems approaches have been used to describe molecular signatures driving immunity to influenza vaccination in humans.

Publication Title

Systems Analysis of Immunity to Influenza Vaccination across Multiple Years and in Diverse Populations Reveals Shared Molecular Signatures.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE74815
Time Course of Adults Vaccinated with Influenza TIV Vaccine during 2010/11 Flu Season (FluCenter cohort)
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Systems approaches have been used to describe molecular signatures driving immunity to influenza vaccination in humans.

Publication Title

Systems Analysis of Immunity to Influenza Vaccination across Multiple Years and in Diverse Populations Reveals Shared Molecular Signatures.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE74811
Time Course of Adults Vaccinated with Influenza TIV Vaccine during 2009/10 Flu Season
  • organism-icon Homo sapiens
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Systems approaches have been used to describe molecular signatures driving immunity to influenza vaccination in humans.

Publication Title

Systems Analysis of Immunity to Influenza Vaccination across Multiple Years and in Diverse Populations Reveals Shared Molecular Signatures.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE107865
PBMC gene expression from Crohn's disease patients before Infliximab therapy.
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

About 40% IBD patients treated with anti-TNF antibodies do not respond to therapy. Baseline biomarkers of response are therefore of interest. By combining computational deconvolution of gene expression and meta-analysis approaches we identified cellular biomarkers in tissue (validated in 2 cohorts by IHC of biopsies), and investigated associated gene biomarkers in blood. This dataset provides data from the validation cohort III (blood).

Publication Title

Cell-centred meta-analysis reveals baseline predictors of anti-TNFα non-response in biopsy and blood of patients with IBD.

Sample Metadata Fields

Disease, Disease stage, Treatment, Subject, Time

View Samples
accession-icon SRP052229
Improved transcription and translation with L-leucine stimulation of mTORC1
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2. We previously reported that mTORC1 was inhibited and overall translation was reduced in RBS cells. Treatment of RBS cells with L-leucine partially rescued mTOR function and protein synthesis, correlating with increased cell division. In this study, we use RBS as a model for mTOR inhibition and analyze transcription and translation with ribosome profiling to determine genome-wide effects of L-leucine. The translational efficiency of many genes is increased with Lleucine in RBS cells including genes involved in ribosome biogenesis, translation, and mitochondrial function. snoRNAs are strongly upregulated in RBS cells, but decreased with L-leucine. Imprinted genes, including H19 and GTL2, are differentially expressed in RBS cells consistent with contribution to mTORC1 control. This study reveals dramatic effects of L-leucine stimulation of mTORC1 and supports that ESCO2 function is required for normal gene expression and translation. Overall design: 42 samples of human fibroblast cell lines with various genotypes (wt, corrected, and esco2 mutants) are treated with l-leucine or d-leucine (control) for 3 or 24 hours. Biological replicates are present.

Publication Title

Improved transcription and translation with L-leucine stimulation of mTORC1 in Roberts syndrome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP131067
Roles of the Brca2 and Wapl complexes with Pds5 in sister chromatid cohesion, cohesin localization, and gene expression [RNA-seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA expression was measured by RNA-seq in Drosophila ML-DmBG3-c2 cells depleted for proteins involved in sister chromatid cohesion, and in developing third instar wing discs with or withough brca2 gene mutations Overall design: RNA expression in depleted cells was compared to mock treated cells and RNA expression in wing discs from brca2 mutant Drosophila was compared to expression in wing discs without brca2 mutations This series includes mock RNAi treated samples re-used from GSE100547.

Publication Title

Brca2, Pds5 and Wapl differentially control cohesin chromosome association and function.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE11887
Differential Cardiac Gene Regulation by Arg- and Gly389 Polymorphic Forms of the beta1-adrenergic Receptor
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The beta1-adrenergic receptor (beta1AR; ADRB1) polymorphism Arg 389Gly is located in an intracellular loop and is associated with distinct human and mouse cardiovascular phenotypes. To test the hypothesis that beta1-Arg389 and beta1-Gly389 alleles could differentially couple to pathways beyond that of classic Gs-adenylyl cyclase (AC)/cAMP signaling, we performed comparative gene expression profile analyses on hearts from wildtype and transgenic mice that expressed either human beta1-Arg389 and beta1-Gly389 receptors, or AC5 adenyl cyclase, sampling at an early age and stage, prior to the onset of pathologic features. We observed substantial overlap of dysregulated genes across all three transgenic heart models, consistent with a shared coupling to cAMP-dependent regulation of cardiac processes and adaptive responses. All three models up-regulated genes associated with RNA metabolism and translation, and down-regulated genes associated with mitochondria and energy metabolism, consistent with cAMP-driven increase in cardiac contractility, protein synthesis, and compensatory down-regulation of mitochondrial energy production. Both beta1AR transgenics activated additional genes associated with kinase-dependent pathways, and uniquely, beta1-Arg389 hearts caused up-regulation of genes associated with inflammation, programmed cell death, and extracellular matrix. These results substantially expand the scope of 7-transmembrane domain receptor signaling propagation beyond known cognate G-protein couplings. Moreover, they implicate alterations of a repertoire of processes evoked by a single amino acid variation in the cardiac beta1AR that might be exploited for genotype-specific heart failure diagnostics and therapeutics.

Publication Title

Differential coupling of Arg- and Gly389 polymorphic forms of the beta1-adrenergic receptor leads to pathogenic cardiac gene regulatory programs.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE21517
ADAM13 knockdown in Xenopus laevis cranial neural crest
  • organism-icon Xenopus laevis
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

ADAMs are transmembrane metalloproteases that control cell behavior by cleaving both cell adhesion and signaling molecules. The cytoplasmic domain of ADAMs can regulate the proteolytic activity by controlling the subcellular localization and/or the activation of the protease domain. Here we show that the cytoplasmic domain of ADAM13 is cleaved and translocates into the nucleus. Preventing this translocation renders the protein incapable of promoting cranial neural crest (CNC) cell migration in vivo, without affecting its proteolytic activity. In addition, the cytoplasmic domain of ADAM13 regulates the expression of multiple genes in the CNC. This study shows that the cytoplasmic domain of ADAM metalloproteases can perform essential functions in the nucleus of cells and may contribute substantially to the overall function of the protein.

Publication Title

Translocation of the cytoplasmic domain of ADAM13 to the nucleus is essential for Calpain8-a expression and cranial neural crest cell migration.

Sample Metadata Fields

Specimen part

View Samples
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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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