refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 84 results
Sort by

Filters

Technology

Platform

accession-icon SRP176670
G1E cells infected with control (HMD empty vector), human GATA1, or human GATA1 mutant cDNA
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

G1E cells infected with control (HMD empty vector), human GATA1, or human GATA1 mutant cDNA Overall design: 3 Biological replicates per condition for RNA-seq

Publication Title

Impaired human hematopoiesis due to a cryptic intronic <i>GATA1</i> splicing mutation.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP007885
CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. Overall design: CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.

Publication Title

CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP051765
Therapy induced tumour secretomes promote resistance and tumour progression
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Drug resistance invariably limits the clinical efficacy of targeted therapy with kinase inhibitors against cancer. We found that targeted therapy with BRAF, ALK, or EGFR inhibitors induces a complex network of secreted signals in drug-stressed melanoma and lung adenocarcinoma cells. This therapy-induced secretome (TIS) stimulates the outgrowth, infiltration and metastasis of drug-resistant cancer clones in the tumour. Additionally, the TIS supports the survival of drug-sensitive cells, contributing to incomplete tumour regression. We used transcriptomic analysis of sensitive tumour cells and xenograft tumours treated with vehicle, vemurafenib, or crizotinib to identify the transcriptional drivers and to dissect the TIS in melanoma (A375, Colo800, UACC62) and lung adenocarcinoma (H3122). In addition, we utilize cell type–specific mRNA purification by translating ribosome affinity purification (TRAP) to identify pathways that are up-regulated in resistant cells (A375R) in response to the regressing tumour microenvironment. Overall design: Analysis of the response of drug sensitive melanoma and lung adenocarcinoma cells to pharmacological inhibition of their driver oncogene and gene expression analysis of drug resistant cancer cells responding to different tumor microenvironments.

Publication Title

Therapy-induced tumour secretomes promote resistance and tumour progression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP126511
Global transcriptional changes in U87MG glioblastoma cells upon shRNA-mediated TRIM52 knockdown
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

shRNA-mediated ablation of the RING-finger protein TRIM52 from multiple glioblastoma cell lines reduces proliferation and tumorigenesis. To identify gene signatures underlying this phenomenon, transcritional profile of TRIM52 knockdown cells was compared to control cells. Upon TRIM52 ablation, we find 278 differentially regulated genes. Gene ontology analysis reveals that many of the upregulated genes are associated with glycolysis and biosynthetic processes. Overall design: U87MG glioblastoma cells were stably transduced with doxycycline-inducible shRNA constructs targeting TRIM52 (two different shRNAs) or controls (two different non-targeting shRNAs). Knockdown was induced for five days using 2µg/ml doxycycline. shRNA expressing cells were sorted based on shRNA-coupled GFP expression via flow cytometry. mRNA sequening was performed in duplicate per shRNA cell line.

Publication Title

Human tripartite motif protein 52 is required for cell context-dependent proliferation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP075880
Effect of SF3B1 suppression in cancer cells with different SF3B1 copy-number levels
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Breast cancer cell lines containing stable dox inducible shRNAs targeting SF3B1 were profiled by RNA sequencing. We determined the effect of gene expression and splicing changes before and after knocking down SF3B1 in cell lines with normal copy number (SF3B1neutral) or partial copy loss (SF3B1loss) cell lines Overall design: RNA profiles for SF3B1 suppression were generated from 8 breast cancer cell line pairs (-/+ dox) with no techincal replicates.

Publication Title

Copy-number and gene dependency analysis reveals partial copy loss of wild-type SF3B1 as a novel cancer vulnerability.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE65624
Hepatic Gene Expression in LIRKO Mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Control and Liver Insulin Receptor KO mice (LIRKO) were sacrificed in the non-fasted state. RNA was prepared from liver samples and subjected to expression microarray analysis

Publication Title

Flavin-containing monooxygenase 3 as a potential player in diabetes-associated atherosclerosis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP169553
A genetic murine model of CLL based on B cell-restricted expression of Sf3b1 mutation and Atm deletion
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

The RNA splicing factor SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its functional role in the pathogenesis of this disease has not been firmly established. Here, we show that conditional expression of heterozygous Sf3b1-K700E mutation in mouse B lineage cells disrupts pre-mRNA splicing, alters B-cell development and function, and induces a state of cellular senescence. B-cell restricted expression of this mutation combined with Atm deletion led to the overcoming of cellular senescence, together with enhanced genome instability and the development of clonal B220+CD5+ CLL cells in elderly mice at low penetrance. Mice with CLL-like disease were found to have amplifications of chromosomes 15 and 17. Integrated transcriptome and proteome analysis of the CLL-like cells revealed coordinated dysregulation of multiple CLL-associated cellular processes. This included an unexpected signature of deregulated B-cell receptor (BCR) signaling, which we could also identify in SF3B1-mutated CLL samples from two independent patient cohorts. Notably, human CLLs harboring SF3B1 mutations exhibited greater sensitivity and altered response kinetics to BTK kinase ibrutinib. Our genetically faithful murine model of CLL thus reveals fresh insights regarding the impact of SF3B1 mutation on CLL pathogenesis and suggests a system for identifying vulnerabilities related to this mutation that can be further exploited for the treatment of CLLs with this common mutation. Overall design: RNA-seq of B cells from WT, Sf3b1 MT, Atm MT, DM and DM-CLL mice

Publication Title

A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE147197
Expression data from patients that has received grass pollen sublingual immunotherapy treatment for two years.
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Prevalence and severity of allergic diseases have increased worldwide. To date, respiratory allergy phenotypes are not fully characterized and, in addition, the mechanisms underlying sublingual immunotherapy (SLIT) are still unknown.

Publication Title

Exploring novel systemic biomarker approaches in grass-pollen sublingual immunotherapy using omics.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE114707
Expression data from allergic patients to profilin
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Prevalence and severity of allergic diseases have increased worldwide. To date, respiratory allergy phenotypes are not fully characterized and, along with inflammation progression, treatment is increasingly complex and expensive. Profilin sensitization constitutes a good model to study the progression of allergic inflammation.

Publication Title

Multi-omics analysis points to altered platelet functions in severe food-associated respiratory allergy.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE26212
The effects of EBV transformation on gene expression and methylation levels
  • organism-icon Homo sapiens
  • sample-icon 82 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The effects of EBV transformation on gene expression levels and methylation profiles.

Sample Metadata Fields

Sex, Specimen part, Subject

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact