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accession-icon SRP067963
Transcriptome profiling of post-mature green seeds from Arabidopsis ddcc mutant and wild-type
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The role of on-CG methylation in seed development and dormancy remains unknown. There are four genes in charge of non-CG methylation in Arabidopsis: drm1, drm2, cmt2 and cmt3. The majority of non-CG methylation in vegetative tissues, leaf, is gone in homozygous ddcc mutant line (Hume et al., 2014). To uncover the possible role of non-CG DNA methylation in seed development and dormancy, we characterized the transcriptome of ddcc mutant in Arabidopsis post-mature green seeds using Illumina sequencing. Meanwhile, post-mature green seeds from wild type were used as control. Overall design: Illumina sequencing of transcripts from post-mature green seeds of ddcc mutant and wild type. Two biological replicates were collected.

Publication Title

Similarity between soybean and <i>Arabidopsis</i> seed methylomes and loss of non-CG methylation does not affect seed development.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP067454
Myc-dependent gene activation and repression in oncogene-addicted liver tumors (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Tumors driven by activation of the transcription factor Myc generally show oncogene addiction. However, the gene-expression programs that depend upon sustained Myc activity in those tumors remain unknown. We have addressed this issue in a model of liver carcinoma driven by a reversible tet-Myc transgene, combining gene expression profiling with the mapping of Myc and RNA Polymerase II on chromatin. Switching off the oncogene in advanced carcinomas revealed that Myc is required for the continuous activation and repression of distinct sets of genes, constituting no more than half of those deregulated during tumor progression, and an even smaller subset of all Myc-bound genes. We further showed that a Myc mutant unable to associate with the co-repressor protein Miz1 is defective in the initiation of liver tumorigenesis. Altogether, our data provide the first detailed analysis of a Myc-dependent transcriptional program in a fully developed carcinoma, revealing that the critical effectors of Myc in tumor maintenance must be included within defined subsets (ca. 1,300 each) of activated and repressed genes. Overall design: RNAseq samples of control liver (n=11), tet-Myc tumors (n=16), tet-Myc tumors with short-term Myc inactivation (n=8), tet-MycVD tumors (n=11)

Publication Title

Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE22392
Expression data from hESCs, hiPSCs and human fibroblasts.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Detailed analysis comparing hiPSC lines that were newly generated and compared them to already established hiPSC lines

Publication Title

Molecular analyses of human induced pluripotent stem cells and embryonic stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE76765
Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach.

Publication Title

Tumor cell survival dependence on the DHX9 DExH-box helicase.

Sample Metadata Fields

Specimen part

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accession-icon GSE49009
A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE49161
A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 1)
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

SUMMARY Despite numerous genome-wide association studies involving glioblastoma (GBM), few therapeutic targets have been identified for this disease. Using patient derived glioma sphere cultures (GSCs), we have found that a subset of the proneural (PN) GSCs undergo transition to a mesenchymal (MES) state in a TNFa/NFkB dependent manner with an associated enrichment of CD44 sub-populations and radio-resistant phenotypes. To the contrary, MES GSCs exhibit constitutive NFkB activation, CD44 enrichment and radio-resistance. Patients whose tumors exhibit a higher MES metagene, increased expression of CD44, or activated NFkB were associated with poor radiation response and shorter survival. Our results indicate that NFkB activation mediated MES differentiation and radiation resistance presents an attractive therapeutic target for GBM.

Publication Title

Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE49162
A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 2)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

SUMMARY Despite numerous genome-wide association studies involving glioblastoma (GBM), few therapeutic targets have been identified for this disease. Using patient derived glioma sphere cultures (GSCs), we have found that a subset of the proneural (PN) GSCs undergo transition to a mesenchymal (MES) state in a TNFa/NFkB dependent manner with an associated enrichment of CD44 sub-populations and radio-resistant phenotypes. To the contrary, MES GSCs exhibit constitutive NFkB activation, CD44 enrichment and radio-resistance. Patients whose tumors exhibit a higher MES metagene, increased expression of CD44, or activated NFkB were associated with poor radiation response and shorter survival. Our results indicate that NFkB activation mediated MES differentiation and radiation resistance presents an attractive therapeutic target for GBM.

Publication Title

Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP131037
Using Next-Generation Sequencing Transcriptomics to Determine Markers of Post-traumatic Symptoms - preliminary findings from a post-deployment cohort
  • organism-icon Homo sapiens
  • sample-icon 78 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Post-traumatic stress disorder is a concerning psycho behavioral disorder thought to emerge from the complex interaction between genetic and environmental factors. For soldiers exposed to combat, the risk of developing this disorder is two-fold and diagnosis is often late, when much sequela has set in. To be able to identify and diagnose in advance those at “risk” of developing PTSD, would greatly taper the gap between late sequelae and treatment. Therefore, this study sought to test the hypothesis that the transcriptome can be used to track the development of PTSD in this unique and susceptible cohort of individuals. Gene expression levels in peripheral blood samples from 85 Canadian infantry soldiers (n = 58 subjects negative for PTSD symptoms and n = 27 subjects with PTSD symptoms) were determined by RNA sequencing technology following their return from deployment to Afghanistan. Count-based gene expression quantification, normalization and differential analysis (with thorough correction for confounders) revealed significant differences in two genes, LRP8 and GOLM1 . These preliminary results provide a proof-of-principle for the diagnostic utility of blood-based gene expression profiles for tracking symptoms of post-traumatic stress disorder in soldiers returning from tour. It is also the first to report transcriptome-wide expression profiles alongside a post-traumatic symptom checklist. Overall design: Peripheral blood samples from 85 Canadian infantry soldiers (n = 58 subjects negative for PTSD symptoms and n = 27 subjects with PTSD symptoms)

Publication Title

Using Next-Generation Sequencing Transcriptomics To Determine Markers of Post-traumatic Symptoms: Preliminary Findings from a Post-deployment Cohort of Soldiers.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE27927
Post-fasting olfactory, transcriptional, and feeding responses in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

The sensation of hunger after a period of fasting and the sensation of satiety after eating is crucial to behavioral regulation of food intake, but the biological mechanisms regulating these sensations are incompletely understood. We studied the behavioral and physiological adaptation to fasting in the vinegar fly (Drosophila melanogaster). Here we show that flies demonstrated increased behavioral attraction to food odor when food-deprived with no corresponding increase in sensitivity in the peripheral olfactory system. Flies increased their food intake transiently in the post-fasted state, but returned to a stable baseline feeding level within 24 hr after return to food. This modulation in feeding was accompanied by a significant increase in the size of the crop organ of the digestive system, suggesting that fasted flies responded both by increasing their food intake and storing reserve food in their crop. The post-fasting feeding response was observed in both male and female flies of diverse genetic backgrounds. Expression profiling of head, body, and chemosensory tissues by microarray analysis revealed several hundred genes that are regulated by feeding state, including 247 genes in the fly head. We performed RNA interference-mediated knockdown of, takeout, one of the genes strongly downregulated by fasting in multiple tissues. When takeout was knocked down in all neurons the post-fasting feeding response was abolished. These observations suggest that a coordinated transcriptional response to internal physiological state may regulate both ingestive behaviors and chemosensory perception of food

Publication Title

Post-fasting olfactory, transcriptional, and feeding responses in Drosophila.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE58149
Expression analysis in hipsc-derived neurons exposed to botulinum neurotoxin A subtype 1 and a type A atoxic derivative
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcriptome analysis of RNA extracted from human induced pluripotent stem cell (hipsc)-derived neurons exposed to botulinum neurotoxin type A1 (BoNT/A1) and an atoxic derivative, BoNT/A ad.

Publication Title

Analysis of gene expression in induced pluripotent stem cell-derived human neurons exposed to botulinum neurotoxin A subtype 1 and a type A atoxic derivative.

Sample Metadata Fields

Specimen part

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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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