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accession-icon SRP162816
RNA sequencing of CFU-GM derived from CD34+ cells expressing PRR14L shRNA or a scramble control
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Here we are using RNA-Seq to study the effect of PRR14L knockdown on transcriptome of hematopoietic cells differentiated towards the granulomonocytic lineage. Overall design: RNAseq was performed on individual CFU-GM with shRNA-mediated PRR14L knockdown and scramble control to study the effects of PRR14L knockdown on the transcriptome of hematopoietic cells differentiated towards the granulomonocytic lineage.

Publication Title

PRR14L mutations are associated with chromosome 22 acquired uniparental disomy, age-related clonal hematopoiesis and myeloid neoplasia.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE25632
Surgical specimens of primary glioblastoma multiform: mRNA and miRNA profiling
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

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accession-icon GSE25630
Genome-wide analysis of gene expression in surgical specimens of primary glioblastoma multiform
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

We used a genome-wide coding gene expression profiling to identify a gene signature for the molecular classification or prognostic prediction of primary GBMs.

Publication Title

miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE115577
Tumor & Tumor-Adj Gene Expression in the Nurses' Health Study Cohorts
  • organism-icon Homo sapiens
  • sample-icon 434 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Gene expression data from the Nurses' Health Study

Publication Title

PAM50 Molecular Intrinsic Subtypes in the Nurses' Health Study Cohorts.

Sample Metadata Fields

Disease stage, Treatment

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accession-icon SRP032280
MDA-MB-231 cell line transcriptome
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

RNAseq to determine baseline expression of kinome in MDA-MB-231 claudin-low breast cancer cell line

Publication Title

Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP032344
SUM159PT cell line transcriptome
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

RNAseq of SUM159PT claudin-low breast cancer cell line to determine baseline kinome expression

Publication Title

Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE87304
Impact of molecular subtypes in muscle-invasive bladder cancer on predicting response and survival outcome to neoadjuvant chemotherapy: results from a multi-institutional validation study
  • organism-icon Homo sapiens
  • sample-icon 298 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version, custom CDF (huex10st)

Description

Four different molecular classifications of muscle-invasive bladder cancer (MIBC) based on gene expression have been proposed. With the ultimate goal of utilizing these molecular subtypes for personalized treatment, we investigated their significance in the context of neoadjuvant cisplatin-based chemotherapy (NAC).

Publication Title

Impact of Molecular Subtypes in Muscle-invasive Bladder Cancer on Predicting Response and Survival after Neoadjuvant Chemotherapy.

Sample Metadata Fields

Age, Disease, Disease stage, Treatment

View Samples
accession-icon GSE8083
PAO1-psrA::Tn expression compared to PAO1 in LB
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa.

Publication Title

The Pseudomonas aeruginosa PsrA responds to long-chain fatty acid signals to regulate the fadBA5 beta-oxidation operon.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP049069
A spinal opsin controls early neural activity and drives a behavioral light response
  • organism-icon Danio rerio
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Purpose: using RNA-seq as a screening tool to determine candidate genes of interest within a genetically defined neural subpopulation in the zebrafish embryonic spinal cord. Results: The early embryonic spinal cord displays patterns of spontaneous activity that generate the earliest motor behavior in the zebrafish. We show the behavior and the neural activity to be inhibited by environmental levels of light. Since at these young ages the fish is blind, and since restricted illumination patterns on the trunk of the fish can elicit a photo-response, we hypothesized that the photo-inhibition is an intrinsic property of the active central pattern generator network within the spinal cord. We FACS-isolated cells from this network as well as those from a panneuronal population and sequenced mRNAs. Through differential expression analysis we identified vertebrate ancient long opsin a as a candidate and then further validated its function in the circuit through knockdown and rescue experiments. Overall design: RNA sequencing of 2 FACS purified neural populations from zebrafish spinal cord.

Publication Title

A spinal opsin controls early neural activity and drives a behavioral light response.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7704
In vivo evidence of Pseudomonas aeruignosa nutrient acquisition and pathogenesis in the cystic fibrosis lung
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

One of the hallmarks of Pseudomonas aeruginosa cystic fibrosis (CF) infection is very high-cell-density (HCD) replication in the lung, allowing this bacterium to induce virulence controlled by HCD quorum-sensing systems. However, the nutrient sources sustaining HCD replication in this chronic infection is largely unknown. Hence, understanding the nutrient factors contributing to HCD in the CF lung will yield new insights into the 'metabolic pathogenicity' and potential treatment of CF infections caused by P. aeruginosa. Herein, we performed microarray studies of P. aeruginosa directly isolated from the CF lung to demonstrate its metabolic capability and virulence in vivo. Our in vivo microarray data, confirmed by real-time reverse-transcription-PCR, indicated P. aeruginosa expressed several genes for virulence, drug-resistance, and utilization of multiple nutrient sources (lung surfactant lipids and amino acids) contributing to HCD replication. The data also indicates deregulation of several pathways, suggesting in vivo evolution by deregulation of a large portion of the transcriptome during chronic CF infection. To our knowledge, this is the first in vivo transcriptome of P. aeruginosa in a natural CF infection, and it indicates several important aspects of pathogenesis, drug-resistance, and nutrient-utilization never before observed in vivo.

Publication Title

In vivo evidence of Pseudomonas aeruginosa nutrient acquisition and pathogenesis in the lungs of cystic fibrosis patients.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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