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accession-icon E-MEXP-347
Transcription profiling of long-lived Ames dwarf mice investigating the loss of liver sexual dimorphism
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Gender-specific alterations in gene expression and loss of liver sexual dimorphism in the long-lived Ames dwarf mice.

Publication Title

Gender-specific alterations in gene expression and loss of liver sexual dimorphism in the long-lived Ames dwarf mice.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE54169
Differential regulation patterns of anti-CD20 mAbs in MCL
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We investigated the differential regulation patterns of type I anti-CD20 monoclonal antibody (mAb) rituximab and type II obinutuzumab on a transcriptional level. Using a panel of MCL cell lines, we determined the effects of obinutuzumab and rituximab as monotherapies as well as in combination on cell viability and proliferation.

Publication Title

Differential regulation patterns of the anti-CD20 antibodies obinutuzumab and rituximab in mantle cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE26936
Expression data from rat urinary bladder and non-glandular stomach tissue samples
  • organism-icon Rattus norvegicus
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Seven novel and potent Raf small molecule kinase inhibitors were evaluated in 7-day oral repeat-dose rat toxicity studies. All compounds tested induced hyperplasia in multiple tissues. Microarrays were used to investigate transciptional changes associated by treatment with a single compound to gain insight into the cellular changes that may contribute to the tissue hyperplasia.

Publication Title

Raf inhibition causes extensive multiple tissue hyperplasia and urinary bladder neoplasia in the rat.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE42676
Functional genomics in perinatal asphyxia and fetal asphyctic preconditioning in the brain
  • organism-icon Rattus norvegicus
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Fetal asphyctic (FA) preconditioning is effective in attenuating brain damage incurred by a subsequent perinatal asphyctic insult. Unraveling mechanisms of this endogenous neuroprotection, activated by FA preconditioning, is an important step towards new clinical strategies for asphyctic neonates. Genomic reprogramming is thought to be, at least in part, responsible for the protective effect of preconditioning. Therefore, we investigated whole genome differential expression in the preconditioned rat brain.

Publication Title

Fetal asphyctic preconditioning alters the transcriptional response to perinatal asphyxia.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE7760
Exon Level Expression Profiling: a Novel Unbiased Transcriptome Analysis for Body Fluids
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Transcriptome analysis of partially degraded and fragmented RNA samples from body fluids

Publication Title

Exon-level expression profiling: a comprehensive transcriptome analysis of oral fluids.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57757
Expression profiles of sorted murine lung Eosinophils following allergen challenge
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The eosinophil transcriptome analysis indicated a robust transcription change in eosinophils following allergen challenge in the lung.

Publication Title

Carbonic anhydrase IV is expressed on IL-5-activated murine eosinophils.

Sample Metadata Fields

Specimen part

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accession-icon GSE36091
Gene Expression profiles of colon from VhlF/F, VhlIE, VhlF/F/Apcmin/+, VhlIE/Apcmin/+
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify the precise molecular mechanisms that could contribute to the increase in colon carcinogenesis, microarray gene expression analysis was performed on colon RNA isolated from 5-week-old VhlF/F and VhlIE, VhlIE/Apcmin/+ and VhlF/F/Apcmin/+ mice.

Publication Title

Hypoxia-inducible factor-2α activation promotes colorectal cancer progression by dysregulating iron homeostasis.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE26101
Histone acetylation and DNA demethylation of T-cells result in an anaplastic large cell lymphoma-like phenotype.
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A characteristic feature of anaplastic large cell lymphoma (ALCL) is the significant reduction of the T-cell expression program despite its T-cell origin, a finding very similar to the loss of B-cell identity of classical Hodgkin lymphoma (cHL). Previously we demonstrated that epigenetic mechanisms are active in cHL to induce this peculiar phenotype. The results show that combined DNA demethylation and histone acetylation of T-cell lines induce an almost complete extinction of the T-cell phenotype, including the down-regulation of essential T-cell receptor signalling pathway genes such as CD3, LCK and ZAP70, as well as an up-regulation of ALCL-characteristic genes. In contrast, combined DNA demethylation and histone acetylation of ALCL cells is not able to reconstitute their T-cell phenotype. This clearly demonstrates that similar epigenetic mechanisms are active in ALCL and cHL which are responsible for the extinction of their cell type characteristic phenotype.

Publication Title

Histone acetylation and DNA demethylation of T cells result in an anaplastic large cell lymphoma-like phenotype.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE32885
Loss of heat shock protein HSPA4 aggravates pressure overload-induced myocardial damage
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Failure of molecular chaperones to direct the correct folding of newly synthesized proteins leads to the accumulation of misfolded proteins in cells. HSPA4 is a member of the heat shock protein 110 family (HSP110) that acts as a nucleotide exchange factor of HSP70 chaperones. We found that the expression of HSPA4 is upregulated in murine hearts subjected to pressure overload and in failing human hearts. To investigate the cardiac function of HSPA4, Hspa4 knockout (KO) mice were generated and exhibited cardiac hypertrophy and fibrosis. Hspa4 KO hearts were characterized by a significant increase in heart weight/body weight ratio, elevated expression of hypertrophic and fibrotic gene markers, and concentric hypertrophy with preserved contractile functions. Cardiac hypertrophy in Hspa4 KO hearts was associated with enhanced activation of gp130-STAT3, CaMKII, and calcineurin-NFAT signaling. Further analyses revealed a significant increase in cross sectional area of cardiomyocytes, and in expression levels of hypertrophic markers in cultured neonatal Hspa4 KO cardiomyocytes suggesting that the hypertrophy of mutant mice was a result of primary defects in cardiomyocytes. Gene expression profile in hearts of 3.5-week-old mice revealed a differentially expressed gene sets related to ion channels and stress response. Taken together, these results reveal that HSPA4 is implicated in protection against pressure overload-induced heart failure.

Publication Title

Targeted disruption of Hspa4 gene leads to cardiac hypertrophy and fibrosis.

Sample Metadata Fields

Sex

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accession-icon SRP123229
Characterization of DCL4 missense alleles provides novel insights into its ability to process distinct classes of dsRNA substrates
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In the model plant Arabidopsis thaliana, four Dicer-like proteins (DCL1-4) mediate the production of various classes of small RNAs (sRNAs). Among these four proteins, DCL4 is by far the most versatile RNaseIII-like enzyme and previously identified dcl4 missense alleles were shown to uncouple the production of the various classes of DCL4-dependent sRNAs. Yet, little is known about the molecular mechanism pertaining this uncoupled production. Here, by studying the subcellular localization, interactome and binding to the sRNA precursors of three distinct dcl4 missense alleles, we simultaneously highlight the absolute requirement of its helicase domain for efficient production of all DCL4-dependent sRNAs, and identify an important determinant of DCL4 versatility within its PAZ domain that is mandatory for efficient processing of intramolecular foldback dsRNA precursors but dispensable for the production of siRNAs from RDR-dependent dsRNA susbtrates. This study not only provides novel insights into DCL4 mode of action in plants but also delineates interesting tools to further study the complexity of plant RNA silencing pathways. Overall design: RNA library of immunoprecipitated RNA from Col-0 (WT), pDCL4-DCL4-6:FHA/dcl4-2 and pDCL4-DCL4-8:FHA/dcl4-2 Arabidopsis flowers or seedlings were generated by deep sequencing, using Illumina HiSeq 2500 v4.

Publication Title

Characterization of DCL4 missense alleles provides insights into its ability to process distinct classes of dsRNA substrates.

Sample Metadata Fields

Specimen part, Subject

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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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