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accession-icon SRP058313
RNA sequencing of ILK-deficient hair follicle bulge stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We sequenced mRNA from FACS purified hair follicle bulge stem cells from 21 d old control and ILK-deficient mice, 3 biological replicates each Overall design: Examination of mRNA levels in control and ILK-deficient hair follicle bulge stem cells

Publication Title

Integrin-linked kinase regulates the niche of quiescent epidermal stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28160
Significant Effects of Antiretroviral Therapy on Global Gene Expression in Brain Tissues of Patients with HIV-Associated Neurocognitive Disorders
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Antiretroviral therapy (ART) has reduced morbidity and mortality in HIV infection; however HIV-1-associated neurocognitive disorders (HAND) persist despite treatment. We used microarray analysis in post-mortem brain tissues to determine ART effectiveness in the brain and to identify molecular signatures of HAND under ART.

Publication Title

Significant effects of antiretroviral therapy on global gene expression in brain tissues of patients with HIV-1-associated neurocognitive disorders.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

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accession-icon SRP101636
Quantitative Analysis of Wild Type and miR-203 KO transcriptomes in the rat endometrial adenocarcinoma cell line RUCA-I
  • organism-icon Rattus norvegicus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: identification of mRNAs that are potential targets of miR-203 in the endometrium and endometrial carcinoma Methods: mRNA profiles of three batches of wild-type (WT) and three independently generated miR-203 knockout (miR-203 KO) RUCA-I cells were produced by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped between 30 and 50 million sequence reads per sample to the rat genome (build rn6) and identified 26751 transcripts of which 1591 are differentially expressed in WT and miR-203 KO cells (p<0.05). Overall design: mRNA profiles of three WT batches and three independently generated miR-203 KO RUCA-I rat endometrial adenocarcinoma cell lines were produced by deep sequencing, using Illumina HiSeq2500.

Publication Title

Role of miR-203 in estrogen receptor-mediated signaling in the rat uterus and endometrial carcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26682
MRE11 Deficiency Increases Sensitivity to Poly(ADP-ribose) Polymerase Inhibition in Microsatellite Unstable Colorectal Cancers.
  • organism-icon Homo sapiens
  • sample-icon 331 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We have performed bioinformatic approaches to identify the level of enrichment between gene expression profiles characterizing MSI tumors and gene changes induced in vitro by the PARP-1 inhibitor Phenanthridinone and others using the Connectivity Map tool. In a first step, we have anyzed the expression of 300 colorectal cancers from the MECC study and generated a gene expression signature by microsatellite status. The criteria followed for selection of probe sets and detailed lists to be submitted subsequently to the Connectivity Map have been published previously by us in Clinical Cancer Research in 2009. In a second step, once we observed that deficiency in MRE11 exist among MSI tumors, our interest was focused on assessing if the homologous recombination pathway showed evidence of deregulation in MSI tumors. Therefore, we examined the expression levels of those genes integrated in the KEGG pathway hsa03440 using the previously generated gene expression data set.

Publication Title

MRE11 deficiency increases sensitivity to poly(ADP-ribose) polymerase inhibition in microsatellite unstable colorectal cancers.

Sample Metadata Fields

Sex, Age

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accession-icon SRP174478
Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis. Overall design: Total RNA was extracted from the nontumor and tumor tissue of an Alb-Cre/Fbxl5F/F male mouse (nontumor, n = 5; tumor, n = 5) or two littermate control Fbxl5F/F mice (nontumor, n = 6; tumor, n = 6) at 45 weeks of age.

Publication Title

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE48459
Sarcoptes scabiei Mites Modulate Gene Expression In Human Skin Equivalents
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents that changed expression in response to the burrowing of live scabies mites.

Publication Title

Sarcoptes scabiei mites modulate gene expression in human skin equivalents.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE4135
Wild type yeast and H3del(1-28) and H4del(2-26) yeast grown in complete synthetic media
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Yeast lacking the H3 or H4 amino termini, and corresponding wild type strains, were grown in synthetic media. These conditions induce Gcn4-activated transcription.

Publication Title

Contribution of the histone H3 and H4 amino termini to Gcn4p- and Gcn5p-mediated transcription in yeast.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6073
Rap1 and Abf1 DNA-binding ts mutants and wild type after 1 hr at 37 C
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Abf1 and Rap1 are General Regulatory Factors that contribute to transcriptional activation of a large number of genes, as well as to replication, silencing, and telomere structure in yeast. In spite of their widespread roles in transcription, the scope of their functional targets genome-wide has not been previously determined. We have used microarrays to examine the contribution of these essential GRFs to transcription genome-wide, by using ts mutants that dissociate from their binding sites at 37 C. We combined this data with published ChIP-chip studies and motif analysis to identify probable direct targets for Abf1 and Rap1. We also identified a substantial number of genes likely to bind Rap1 or Abf1, but not affected by loss of GRF binding. Interestingly, the results strongly suggest that Rap1 can contribute to gene activation from farther upstream than can Abf1. Also, consistent with previous work, more genes that bind Abf1 are unaffected by loss of binding than those that bind Rap1. Finally, we showed for several such genes that the Abf1 C-terminal region, which contains the putative activation domain, is not needed to confer this peculiar "memory effect" that allows continued transcription after loss of Abf1 binding.

Publication Title

Genome-wide analysis of transcriptional dependence and probable target sites for Abf1 and Rap1 in Saccharomyces cerevisiae.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5404
Expression data from Drosophila subjected to artificial selection on aggression
  • organism-icon Drosophila melanogaster
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Genes relevant to manifestion of and variation in aggression behavior might be differentially expressed in lines selected for divergent levels of aggression.

Publication Title

Quantitative genomics of aggressive behavior in Drosophila melanogaster.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1639
Rpd3 and histone H3 and H4 deletions/mutations
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Signal intensity data for rpd3 delete, H3delta(1-28), H3(K4,9,14,18,23,27Q), H4delta(2-26), H4(K5,8,12,16Q), rpd3 delete H3delta(1-28), and rpd3 delete H4(K5,8,12,16Q) yeast grown in rich (YPD) media

Publication Title

Genome-wide analysis of the relationship between transcriptional regulation by Rpd3p and the histone H3 and H4 amino termini in budding yeast.

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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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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