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accession-icon SRP056237
Analysis of bone marrow derived mast cell transcriptomes in presence or absence of SialostatinL
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Goal of this study was to compare transcriptional changes in stimulated mast cells in the absence or presence of sialostatinL Overall design: mRNA profiles of 4 weeks old mast cells (BMMC derived from C57BL/6 mice ) stimulated for 24h with ionomycin in absence or presence of tick derived sialostatinL were generated by deep sequencing using Illumina HiSeq2000

Publication Title

Tick Salivary Sialostatin L Represses the Initiation of Immune Responses by Targeting IRF4-Dependent Transcription in Murine Mast Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE75808
Differential Ly6C Expression after Renal Ischemia-Reperfusion Identifies Unique Macrophage Populations
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI.

Publication Title

Differential Ly6C Expression after Renal Ischemia-Reperfusion Identifies Unique Macrophage Populations.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP059039
Elucidating the etiology and molecular pathogenicity of infectious diarrhea by high throughput RNA sequencing
  • organism-icon Homo sapiens
  • sample-icon 206 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Diarrhea remains a major cause of death in children. Current diagnostic methods largely rely on stool culture and suffer from low sensitivity and inadequate specificity, often leading to inappropriate treatment. The objective of the present study was to use RNA sequencing (RNAseq) analysis to determine blood transcriptional profiles specific for several common pathogenic bacteria and viruses that cause diarrhea in children. We collected whole blood samples from children in Mexico having diarrhea associated with a single pathogen and without systemic complications. Our RNAseq data suggested that the blood signatures can differentiate children with diarrhea from healthy children either with or without bacterial colonization. Moreover, we detected different expression profiles from bacterial and viral infection, demonstrating for the first time the use of RNAseq to identify the etiology of infectious diarrhea. Overall design: 255 whole blood samples from 246 children including children with diarrhea caused by rotavirus (n=60 total; 5 repeated; 55 unique), E.coli (n=55), Salmonella (n=36), Shigella (n=37), adenovirus (n=8), norovirus (n=7), and control children (n=52 total; 4 repeated; 48 unique).

Publication Title

Shared and organism-specific host responses to childhood diarrheal diseases revealed by whole blood transcript profiling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37484
The effect of sucrose and sulfamethoxazole on the Arabidopsis transcriptome
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

A chemical screen was performed in search of compounds that modify plant responses to sucrose. This screen uncovered that sulfamethoxazole (SMX), a folate biosynthesis inhibitor, acted synergistically with sucrose to inhibit hypocotyl elongation, suggesting interaction between these two pathways. Transcriptome analysis was performed to identify changes in transcript abundance that may underpin crosstalk between sucrose and SMX. Three-day-old dark-grown seedlings were treated to sucrose and SMX at concentrations that induced no change in hypocotyl elongation when administered independently, yet restricted elongation when both were present in the growth media (10mM and 0.2M, respectively). This analysis uncovered multiple core auxin signalling components that exhibit altered transcript abundance in response to co-treatment with sucrose and SMX, suggesting that auxin signalling mediates crosstalk between these two pathways. This study highlights an input through which metabolic status can shape plant growth and development through hormone signalling.

Publication Title

Interplay between sucrose and folate modulates auxin signaling in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE30339
IDH1 Mutation is a Master Regulator of Epigenomic Remodeling and is Sufficient to Establish the Glioma Hypermethylator Phenotype
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype.

Sample Metadata Fields

Specimen part

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accession-icon GSE30336
Expression analysis of 52 glioma clinical samples (36 CIMP+ and 16 CIMP-) and 6 cell line samples
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Glioma CIMP (G-CIMP) is a powerful determinant of tumor pathogenicity but the molecular cause of G-CIMP is a fundamental question that is unresolved. Here, we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), directly causes the G-CIMP in gliomas by remodeling the methylome.

Publication Title

IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype.

Sample Metadata Fields

Specimen part

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accession-icon GSE98905
The BET bromodomain inhibitor CPI203 overcomes resistance to ABT-199 (venetoclax) by downregulation of BFL-1/A1 in in vitro and in vivo models of MYC+/BCL2+ double hit lymphoma
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Double Hit Lymphoma (DHL) were treated with the BRD4 inhibitor 100 nM CPI203 for 6h

Publication Title

The BET bromodomain inhibitor CPI203 overcomes resistance to ABT-199 (venetoclax) by downregulation of BFL-1/A1 in in vitro and in vivo models of MYC+/BCL2+ double hit lymphoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP049203
RNA-Seq Analysis in purified iPS cell-derived neuronal samples
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We characterized the gene expression differences in mDA neurons from all PD (Parkinson''s disease) cases (6 independent samples) and controls (8 independent samples), identifying 1,028 differentially expressed genes making up the PD expression signature. Strikingly, MAOB gene was identified as significantly differentially expressed (p = 0.046). The heat map clearly differentiates cases from controls, where interestingly most differentially expressed genes had lower expression in PD cases compared to controls. In the clustering, the RNA expression pattern of the control (C2) with a family history of PD located close to the PD expression signature suggested a susceptibility to PD. Overall design: RNA was isolated from FAC-sorted cells of 14 samples (biological duplicates for each cell line, 7 cell lines in total) using RNeasy Micro Kit (QIAGEN). Quality control of the RNA was carried out with the Agilent Bio-analyzer, Qubit 2.0 at the MPSR of Columbia University. 100 ng of RNA with RIN = 9 were used for generating mRNA-focused libraries using TruSeq RNA Sample Preparation Kit v2 and sequencing on an Illumina 2000/2500 V3 Instrument offered by the Columbia Genome Center.

Publication Title

iPSC-derived dopamine neurons reveal differences between monozygotic twins discordant for Parkinson's disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28260
Renal cortex and medulla microRNA and mRNA expression differences between hypertensive and normotensive patients
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Gene expression profiling reveals renin mRNA overexpression in human hypertensive kidneys and a role for microRNAs.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP169631
REV-ERBa regulates TH17 cell development and autoimmunity
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

ROR?t is well recognized as the lineage defining transcription factor for TH17 cell development. However, the cell-intrinsic mechanisms that negatively regulate TH17 cell development and autoimmunity remain poorly understood. Here we demonstrate that the transcriptional repressor REV-ERBa is exclusively expressed in TH17 cells, competes with ROR?t for their shared DNA consensus sequence, and negatively regulates TH17 cell development via repression of genes traditionally characterized as ROR?t-dependent, including Il17a. Deletion of REV-ERBa enhanced TH17-mediated pro-inflammatory cytokine expression, exacerbating experimental autoimmune encephalomyelitis (EAE) and colitis. Treatment with REV-ERB-specific synthetic ligands, which have similar phenotypic properties as ROR? modulators, suppressed TH17 cell development, was effective in colitis intervention studies, and significantly decreased the onset, severity, and relapse rate in several models of EAE without affecting thymic cellularity. Our results establish that REV-ERBa negatively regulates pro-inflammatory TH17 responses in vivo and identifies the REV-ERBs as potential targets for the treatment of TH17-mediated autoimmune diseases. Overall design: 10 samples; 5 conditions with 2 replicates per condition

Publication Title

REV-ERBα Regulates T<sub>H</sub>17 Cell Development and Autoimmunity.

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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