refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 101 results
Sort by

Filters

Technology

Platform

accession-icon GSE60932
Gene expression changes in limb buds of Nipbl-haploinsufficient mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Multiple genes are dysregulated in hindlimb buds of Nipbl-deficient embryos. In all, more than 1000 limb bud genes were found to be significantly altered in expression by microarray analysis of E10.5 mouse hindlimb buds.

Publication Title

Nipbl and mediator cooperatively regulate gene expression to control limb development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP212125
A conditionally immortalized Gli1-positive kidney mesenchymal cell line models myofibroblast transition
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Glioma-associated oncogene homolog-1 (Gli1)-positive resident mesenchymal stem cell-like cells are the predominant source of kidney myofibroblasts in fibrosis, but investigating Gli1-positive myofibroblast progenitor activation is hampered by the difficulty of isolating and propagating primary cultures of these cells. Using a genetic strategy with positive and negative selection, we isolated Kidney-Gli1 (KGli1) cells that maintain expression of appropriate mesenchymal stem cell-like cell markers, respond to hedgehog pathway activation, and display robust myofibroblast differentiation upon treatment with transforming growth factor-ß (TGF-ß). Coculture of KGli1 cells with endothelium stabilizes capillary formation. Single-cell RNA sequencing (scRNA-seq) analysis during differentiation identified autocrine ligand-receptor pair upregulation and a strong focal adhesion pathway signal. This led us to test the serum response factor inhibitor CCG-203971 that potently inhibited TGF-ß-induced pericyte-to-myofibroblast transition. scRNA-seq also identified the unexpected upregulation of nerve growth factor (NGF), which we confirmed in two mouse kidney fibrosis models. The Ngf receptor Ntrk1 is expressed in tubular epithelium in vivo, suggesting a novel interstitial-to-tubule paracrine signaling axis. Thus, KGli1 cells accurately model myofibroblast activation in vitro, and the development of this cell line provides a new tool to study resident mesenchymal stem cell-like progenitors in health and disease. Overall design: DropSeq on primary culture kidney Gli1+ cells harvasted from 0, 6, 12, and 24 hrs after TGF-beta treatment

Publication Title

A conditionally immortalized Gli1-positive kidney mesenchymal cell line models myofibroblast transition.

Sample Metadata Fields

Sex, Treatment, Subject

View Samples
accession-icon SRP049988
Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor, though its targets in lung epithelial cells are largely uncharacterized. RNA-seq after EHF depletion or overexpression showed significant alterations in the expression of genes involved in response to wounding. EHF knockdown also targeted genes in pathways of epithelial development and differentiation and locomotory behavior. Overall design: mRNA profiles from Calu-3 cells treated with negative control (NC) or EHF siRNA, in quintuplicate. mRNA profiles from 3 pcDNA (empty vector control) clones and 3 pcDNA-EHF overexpression A549 clones, 3-4 replicates each.

Publication Title

Ets homologous factor regulates pathways controlling response to injury in airway epithelial cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP124606
Transcriptome change caused by lowered intracellular S-adenosylmethionine level in the X63/0 mouse plasma cell line.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

We aimed to examine the gene expression changes responding to a depletion of intracellular S-adenosylmethionine (SAM). The mouse plasma cell line X63/0 was treated with the SAM-synthetase inhibitor cycloleucine (cLEU), and the total RNA was isolated and analyzed by RNA-sequencing. As a result, we idntified 27 genes, including the ubiquitous SAM-synthetase MAT2A, whose expssions were up-regulated by two-fold or more. Overall design: Total RNA was extracted from the mouse plasma cell line X63/0 before/after a three-hour treatment with 30 mM cycloleucine. This experiment was triplicated, and the resulting six samples were applied to RNA-sequencing.

Publication Title

S-Adenosylmethionine Synthesis Is Regulated by Selective N<sup>6</sup>-Adenosine Methylation and mRNA Degradation Involving METTL16 and YTHDC1.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP174478
Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis. Overall design: Total RNA was extracted from the nontumor and tumor tissue of an Alb-Cre/Fbxl5F/F male mouse (nontumor, n = 5; tumor, n = 5) or two littermate control Fbxl5F/F mice (nontumor, n = 6; tumor, n = 6) at 45 weeks of age.

Publication Title

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP076488
RNA-seq analyses of ID4-EGFP+ undifferentiated spermatogonia and sorted subpopulations.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

P6 ID4-EGFP+ undifferentiated spermatogonia, including those stained robustly (high) or weakly (low) for TSPAN8 were isolated by FACS. Overall design: Three replicate preparations of each population were used for independent RNA-seq using SMART-seq v4, Nextera XT libraries, Hiseq2500 sequencing, and TopHat/Bowtie/Cufflinks analyses.

Publication Title

TSPAN8 Expression Distinguishes Spermatogonial Stem Cells in the Prepubertal Mouse Testis.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE38742
Modeling tumor subtypes in vivo using lineage restricted transgenic shRNA
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Expression analysis from two genetically engineered mouse models of osteosarcoma determine the expression profile of mouse osteosarcoma Human osteosarcoma (OS) is comprised of three different subtypes: fibroblastic, chondroblastic and osteoblastic. We previously generated a mouse model of fibroblastic OS by conditional deletion of p53 and Rb in osteoblasts. Here we report an accurate mouse model of the osteoblastic subtype using shRNA-based suppression of p53. Like human OS, tumors frequently present in the long bones and preferentially disseminate to the lungs; features less consistently modeled using Cre:lox approaches. Our approach allowed direct comparison of the in vivo consequences of targeting the same genetic drivers using different technology. This demonstrated that the effects of Cre:lox and shRNA mediated knock-down are qualitatively different, at least in the context of osteosarcoma. Through the use of complementary genetic modification strategies we have established a model of a distinct clinical subtype of OS that was not previously represented and more fully recapitulated the clinical spectrum of this human tumor.

Publication Title

Modeling distinct osteosarcoma subtypes in vivo using Cre:lox and lineage-restricted transgenic shRNA.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE145367
GeneChip Expression Array
  • organism-icon Rattus norvegicus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression analysis to compare control cells and sorted cells

Publication Title

Identification of two major autoantigens negatively regulating endothelial activation in Takayasu arteritis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE22954
Artificially induced epithelial-mesenchymal transition in surgical subjects: its implications in clinical and basic cancer research
  • organism-icon Homo sapiens
  • sample-icon 144 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Artificially induced epithelial-mesenchymal transition in surgical subjects: its implications in clinical and basic cancer research.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

View Samples
accession-icon GSE33103
Overall aiEMT in surgical samples of esophageal cancer patients
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

Surgical samples have long been used as important subjects for cancer research. In accordance with an increase of neoadjuvant therapy, biopsy samples have recently become imperative for cancer transcriptome. On the other hand, both biopsy and surgical samples are available for expression profiling for predicting clinical outcome by adjuvant therapy; however, it is still unclear whether surgical sample expression profiles are useful for the prediction by the use of biopsy samples because little has been done about comparative gene expression profiling between the two kinds of samples.

Publication Title

Artificially induced epithelial-mesenchymal transition in surgical subjects: its implications in clinical and basic cancer research.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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