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accession-icon SRP062126
RNA-Seq: assessment of transcript level analysis tools [seq]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

This study uses spiked-in transcript in order to compares various bioinformatics approaches and tools to assemble, quantify abundance and detect differentially expressed transcripts using RNA-Seq data. Mouse total RNA seq was extracted from embryonic stem cells (ES) before (designated as day 0) and four days after the addition of retinoic acid. 48 spikes were made in vitro from plasmid constructs and added to the total RNA in different concentrations (each mix has a set of different spike concentrations, see paper''s method). We found that detection of differential expression at the gene level is acceptable, yet on the transcript-isofom level all tools tested were lacking accuracy and precision. Overall design: Mouse total RNA was extracted from embryonic stem cells (ES) before (designated as day 0) and four days after the addition of retinoic acid (RA) (designated as day 4). Mouse spike-ins consisting of 48 different mouse RNA transcripts were generated in vitro from plasmid constructs and added to the total RNA. 23 of the spike-ins originate from 10 different locus regions, so that each locus is represented by at least two different transcripts. The remaining 25 spike-ins represent different loci.

Publication Title

Using Synthetic Mouse Spike-In Transcripts to Evaluate RNA-Seq Analysis Tools.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE75138
RNA-Seq: assessment of transcript level analysis tools [array]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study uses spiked-in transcript in order to compare various bioinformatics approaches and tools to assemble, quantify abundance and detect differentially expressed transcripts using RNA-Seq data. Mouse total RNA seq was extracted from embryonic stem cells (ES) before (designated as day 0) and four days after the addition of retinoic acid. 48 spikes were made in vitro from plasmid constructs and added to the total RNA in different concentrations (each mix has a set of different spike concentrations, see paper's method). We found that detection of differential expression at the gene level is acceptable, yet on the transcript-isofom level all tools tested were lacking accuracy and precision.

Publication Title

Using Synthetic Mouse Spike-In Transcripts to Evaluate RNA-Seq Analysis Tools.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon SRP073613
Identification of mRNAs with reduced ribosomal loading upon knock-down of translation factor DAP5 from hESCs.
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We have generated stable human ESCs (H9) expressing control or DAP5-targeting shRNA. Polysome profiles reveal no major changes in overall translation. PolyA+ RNA and RNA accociated with heavy polysomal fractions were purified in biological duplicates and sequenced using Illumina HiSeq 2000 instrument. We identified 122 potential mRNA targets of DAP5 translation that display reduced ribosomal loading, and hence reduced translation, in the absence of DAP5. Overall design: Total mRNA and heavy polylsomal fractions from shNT and shDAP5 expressing hESCs, each in duplicate, was deep sequenced.

Publication Title

Cap-independent translation by DAP5 controls cell fate decisions in human embryonic stem cells.

Sample Metadata Fields

Subject

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accession-icon SRP152871
LATS1 and LATS2 suppress breast cancer progression by maintaining cell identity and metabolic state [mouse]
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Deregulated activity of the LATS tumor suppressors has broad implications on cellular and tissue homeostasis. We examined the consequences of downregulation of either LATS1 or LATS2 in breast cancer. Consistent with their proposed tumor suppressive roles, expression of both paralogs is significantly downregulated in human breast cancer, and loss of either paralog accelerated mammary tumorigenesis in mice. However, each paralog had a distinct impact on breast cancer. Thus, LATS2 depletion in luminal B tumors resulted in metabolic rewiring, with increased glycolysis and reduced PPARg signaling. Furthermore, pharmacological activation of PPARg elicited LATS2-dependent death in luminal B-derived cells. In contrast, LATS1 depletion augmented cancer cell plasticity, skewing luminal B tumors towards increased expression of basal-like features, in association with increased resistance to hormone therapy. Hence, these two closely related paralogs play distinct roles in protection against breast cancer; tumors with reduced expression of either LATS1 or LATS2 may rewire signaling networks differently and thus respond differently to anti-cancer treatments. Overall design: RNA was isolated from Lats1-CKO and Lats2-CKO PyMT tumors (4 samples from each). For each genotype, the corresponding wt littermate controls were used (3 samples in each batch).

Publication Title

LATS1 and LATS2 suppress breast cancer progression by maintaining cell identity and metabolic state.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP128580
PEST-domain-enriched tyrosine phosphatase and glucocorticoids as regulators of mast cell signalling
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

PEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFa, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs. Overall design: Biological replicates are sequenced and analyzed. The samples are either wild-type or mutant for PEP and cells were sensitized with Ig-E, activated with Dinitrophenol and glucocorticoid treatment done with Dexamethasone.

Publication Title

Transcriptomic data on the role of PEST-domain-enriched tyrosine phosphatase in the regulation of antigen-mediated activation and antiallergic action of glucocorticoids in mast cells.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE15852
Expression data from human breast tumors and their paired normal tissues
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.

Publication Title

Gene expression patterns distinguish breast carcinomas from normal breast tissues: the Malaysian context.

Sample Metadata Fields

Specimen part, Disease stage, Race

View Samples
accession-icon GSE59874
PIK3CA(H1047R)-evoked breast tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 49 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE40875
Early parity-induced gene expression in mouse mammary cell subtypes
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the effect of early pregnancy on the gene expression profiles of stromal and various epithelial mammary cell subpopulations in mice.

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59872
Gene expression profiling of Lgr5-creERT2/PIK3CA H1047R and K8-creERT2/PIK3CA H1047R-evoked mammary tumors
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the gene expression profile of mammary tumors derived from Lgr5- and K8-positive cell-of-origins

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59870
Gene expression profiling of preneoplastic Lgr5-creERT2/PIK3CAH1047R mammary subsets
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from Lgr5-creERT2/PIK3CA H1047R mice

Publication Title

PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.

Sample Metadata Fields

Specimen part, Treatment

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

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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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