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accession-icon GSE3467
The role of micro-RNA genes in papillary thyroid carcinoma
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We show that numerous miRNAs are transcriptionally up-regulated in papillary thyroid carcinoma (PTC) tumors compared with unaffected thyroid tissue. Among the predicted target genes of the three most upregulated miRNAs (miRs 221, 222 and 146b), only less than 15% showed significant downexpression in transcript level between tumor and unaffected tissue. The KIT gene which is known to be downregulated by miRNAs 221 and 222 displayed dramatic loss of transcript and protein in those tumors that had abundant mir-221, mir-222, and mir-146b transcript.

Publication Title

The role of microRNA genes in papillary thyroid carcinoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE25436
Expression data from melanoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Differential gene expression analysis of parental and sub-lines of melanoma cell line resistant to F5 CTL lymphocyte

Publication Title

Molecular mechanism of MART-1+/A*0201+ human melanoma resistance to specific CTL-killing despite functional tumor-CTL interaction.

Sample Metadata Fields

Cell line

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accession-icon GSE33607
Expression data from mouse B16-F10 cells exposed to hypoxic conditions in vitro.
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Analysis of gene expression profile of B16-F10 murine melanoma cells exposed to hypoxic conditions (1% oxygen) or hypoxia mimicry (cobalt chloride) for 24 hours. Gene expression profiles were analyzed using MG-U74Av2 oligonucleotide microarrays. Data analysis revealed 2541 probesets (FDR<5%) for 1% oxygen experiment and 364 probesets (FDR<5%) for cobalt chloride, that showed differences in expression levels. Analysis of hypoxia-regulated genes (1% O2) by stringent Family-Wise Error Rate estimation indicated 454 significantly changed transcripts (p<0.05). The most upregulated genes were Lgals3, Selenbp1, Nppb (more than ten-fold increase). Both hypoxia and hypoxia-mimicry induced HIF-1 regulated genes. However, unsupervised analysis (Singular Value Decomposition) revealed distinct differences between gene expression induced by these two experimental conditions.

Publication Title

Gene expression profile of B 16(F10) murine melanoma cells exposed to hypoxic conditions in vitro.

Sample Metadata Fields

Cell line

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accession-icon GSE37590
Natural genetic variation in yeast longevity
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

A quantitative genetic analysis of the yeast replicative life span was carried out by sampling the natural genetic variation

Publication Title

Natural genetic variation in yeast longevity.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP118922
Comprehensive Analysis of Gene Expression Patterns in Friedreich's Ataxia Fibroblasts by RNA Sequencing Reveals Altered Levels of Protein Synthesis Factors and Solute Carriers
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease usually caused by large homozygous expansions of GAA repeat sequences in intron 1 of the frataxin (FXN) gene. FRDA patients have low FXN mRNA and frataxin protein levels when compared with heterozygous carriers or healthy controls. Presently, there is no effective treatment for FRDA, and biomarkers to measure therapeutic trial outcomes and/or to gauge disease progression are lacking. Peripheral tissues, including blood cells, buccal cells, and skin fibroblasts, can readily be isolated from FRDA patients and used to define molecular hallmarks of disease pathogenesis. However, because these tissues are not directly involved in disease pathogenesis, their relevance as models of the molecular aspects of the disease is yet to be decided. Transcriptome profiling of FRDA skin fibroblasts revealed significantly upregulated expression of genes encoding plasma membrane solute carrier proteins. Conversely, the expression of genes encoding accessory factors and enzymes involved in cytoplasmic and mitochondrial protein synthesis was consistently decreased in the FRDA cells. Finally, comparison of genes differentially expressed in FRDA fibroblasts to 3 previously published gene expression signatures defined for FRDA blood cells showed substantial overlap between the independent datasets, including correspondingly deficient expression of antioxidant defense genes. Together, these results indicate that gene expression profiling of cells derived from peripheral tissues can, in fact, consistently reveal novel molecular pathways of the disease. Overall design: We used RNA sequencing to profile the transcriptomes of primary fibroblast cell lines derived from 18 FRDA patients and 17 unaffected control individuals.

Publication Title

A Comprehensive Transcriptome Analysis Identifies FXN and BDNF as Novel Targets of miRNAs in Friedreich's Ataxia Patients.

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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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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