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accession-icon GSE9600
Insulin-like growth factor-1 receptor inhibitor, AMG-479, in cetuximab-refractory head and neck squamous cell carcinoma
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Recurrent and/or metastatic head and neck squamous cell carcinoma (HNSCC) remains one of the most difficult cancers to treat with limited chemotherapeutic options. Here, we describe a patient with HNSCC who had complete response to methotrexate (MTX) after progressing on multiple cytotoxic agents; cetuximab, a monoclonal antibody (mAb) against Epidermal Growth Factor Receptor (EGFR), and AMG 479, a mAb against Insulin-like Growth Factor-1 Receptor (IGF-1R).

Publication Title

Insulin-like growth factor-1 receptor inhibitor, AMG-479, in cetuximab-refractory head and neck squamous cell carcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE81189
Expression data from Tbet+ and Tbet- Memory B cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was important even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages.

Publication Title

Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.

Sample Metadata Fields

Specimen part

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accession-icon SRP162257
Cortisol acting through the glucocorticoid receptor is not responsible for exercise-enhanced growth but does affect the white skeletal muscle transcriptome in zebrafish (Danio rerio)
  • organism-icon Danio rerio
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Forced sustained swimming exercise at optimal speed enhances growth in many fish species, particularly through hypertrophy of the white skeletal muscle. The exact mechanism of this effect has not been resolved yet. To explore the mechanism, we first subjected wild-type zebrafish to an exercise protocol validated for exercise-enhanced growth, and showed that exercised zebrafish, which indeed showed enhanced growth, had higher cortisol levels than the non-exercised controls. A central role was therefore hypothesized for the steroid hormone cortisol acting through the Glucocorticoid receptor (Gr). Second, we subjected wild-type zebrafish and zebrafish with a mutant Gr to exercise at optimal, suboptimal and super-optimal speeds and compared them with non-exercised controls. Exercised zebrafish showed growth enhancement at all speeds, with highest growth at optimal speeds. In the Gr mutant fish, exercise resulted in growth enhancement similar to wild-type zebrafish, indicating that cortisol cannot be considered as a main determinant of exercise-enhanced growth. Finally, the transcriptome of white skeletal muscle tissue was analysed by RNA sequencing. The results of this analysis showed that in the muscle tissue of Gr mutant fish a lower number of genes is regulated by exercise than in wild-type fish (183 versus 351). A cluster of 36 genes was regulated by exercise in both wild-type and mutant fish. In this cluster, genes involved in transcriptional regulation and protein ubiquitination were overrepresented. Since growth was enhanced similarly in both wild-type fish and mutants, these processes may play an important role in exercise-enhanced growth. Overall design: Deep-sequencing transcriptome analysis of white muscle samples derived from wild-type (++) or glucocorticoid receptor (Gr) mutant (--) Danio rerio specimens that were exposed to either a resting (REST) or a swimming (UOPT) regimen: wild-type resting (REST++; n=3), Gr mutant resting (REST--; n=3), wild-type swimming (UOPT++; n=3), Gr mutant swimming (UOPT--; n=3).

Publication Title

Cortisol Acting Through the Glucocorticoid Receptor Is Not Involved in Exercise-Enhanced Growth, But Does Affect the White Skeletal Muscle Transcriptome in Zebrafish (<i>Danio rerio</i>).

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE78227
The maleless gene mitigates global aneuploid effect and evolutionary shift from X to autosomes
  • organism-icon Drosophila melanogaster
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

During sexual dimorphism, the loss of one entire X chromosome in Drosophila males is achieved largely via a broad genome-wide aneuploid effect. Exploring how MSL proteins and two large non coding RNAs (roX1 and roX2) modulate trans-acting aneuploid effect for equality to females, we employ a system biology approach (microarray) to investigate the global aneuploid effect of maleless(mle) mutation by disrupting MSL binding. A large number of the genes (144) that encode a broad spectrum of cellular transport proteins and transcription factors are located in the autosomes of Drosophila melanogaster.

Publication Title

Drosophila maleless gene counteracts X global aneuploid effects in males.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21839
Transcriptome analysis of wild type E. coli (K-12 MG1655) comparing to mutant E. coli strain (ECOM4) under aerobic and anaerobic conditions
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Cytochrome oxydases and quinol monooxygenase were removed from the E. coli genome resulting in oxygen-independent physiology

Publication Title

Deletion of genes encoding cytochrome oxidases and quinol monooxygenase blocks the aerobic-anaerobic shift in Escherichia coli K-12 MG1655.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26591
Genome-scale reconstruction of the PurR regulon reveals its role in the adenine stimulon of Escherichia coli K-12 MG1655
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The PurR regulon in Escherichia coli K-12 MG1655.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26588
Transcriptome analysis of E. coli MG1655
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Expression profiling of wild type and purR deletion strains of E. coli K-12 MG1655 under both M9 minimal media and addition of adenine.

Publication Title

The PurR regulon in Escherichia coli K-12 MG1655.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4133
The Genome Wide Distribution of Acetylated Histone H4 Remodelled through Human Primary Myoblast Differentiation
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a), Affymetrix Human Genome U133B Array (hgu133b)

Description

The simultaneous genotyping of tens of thousands of SNP using SNP microarrays is a very important tool that is revolutionizing genetics and molecular biology. In this work, we present a new application of this technique by using it to assess chromatin immunoprecipitation (CHIP) as a means to assess the multiple genomic locations bound by a protein complex recognized by an antibody. We illustrate the use of this technique with an analysis of the change in histone H4 acetylation, a marker of open chromatin and transcriptionally active genomic regions, which occur during the differentiation of human myoblasts into myotubes. Our results are validated by the observation of a significant correlation between the histone modifications detected and the expression of the nearby genes, as measured by DNA microarrays.

Publication Title

ChIP on SNP-chip for genome-wide analysis of human histone H4 hyperacetylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4131
Determination of myotube and myoblast expression levels
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene expression was determined for both myotubes and myoblasts using Affymetrix HG-U133 A/B arrays.

Publication Title

ChIP on SNP-chip for genome-wide analysis of human histone H4 hyperacetylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE34631
Transcriptome analysis of E. coli in M9 minimal media supplemented with propylene glycol or glycerol
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

The aim of this study is to investigate the changes of global gene expression in E. coli during a carbon source shift.

Publication Title

Network context and selection in the evolution to enzyme specificity.

Sample Metadata Fields

No sample metadata fields

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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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Developed by the Childhood Cancer Data Lab

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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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