refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 237 results
Sort by

Filters

Technology

Platform

accession-icon SRP118618
Defining transcription factor networks that govers SCC growth [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Differential gene expression analysis were performed between Pitx1 silenced SCC cells and controls in two independent SCC lines Overall design: Compared control and Pitx1 deficient cells to define gene sets control by Pitx1 in SCCs.

Publication Title

De Novo PITX1 Expression Controls Bi-Stable Transcriptional Circuits to Govern Self-Renewal and Differentiation in Squamous Cell Carcinoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE98062
Gene expression in non-adherent MDA-MB-468 subpopulation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Plasticity between adhesive and less-adhesive states is important for mammalian cell behaviour. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of MDA-MB-468 breast carcinoma cells which grows in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices.

Publication Title

A dual phenotype of MDA-MB-468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE76811
Identification of MMP12 as a potential new target for prevention and treatment of cardiometabolic disease
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Obesity is strongly associated with the metabolic syndrome, a compilation of risk factors that predispose individuals to the development of cardiometabolic disease (CMD), i.e. cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Controlling or preventing the worldwide epidemic of metabolic syndrome requires novel interventions to address this substantial health challenge. The objective of this study was the identification of potential new targets for the simultaneous prevention and treatment of insulin resistance and atherosclerosis, conditions that underlie T2DM and CVD, respectively. Therefore, we used an unbiased bioinformatics approach to identify molecules that are upregulated in both conditions by combining data from two microarray experiments and two meta-analyses. In the microarray experiments we compared gene expression in white adipose tissue (WAT) of obese mice as well as aortae of obese and atherosclerotic mice to respective lean controls. Furthermore, we performed a meta-analysis of published microarrays investigating atherosclerotic vessels and included a published meta-analysis on T2DM into our analyses. We obtained a pool of thirty-four genes that were upregulated in 3 out of the 4 underlying databases. These included well-known as well as novel crucial molecules for treatment of T2DM and CVD. Macrophage metalloelastase 12 (MMP12) was found highly ranked in all analyses and, therefore, chosen for further validation. Analyses of visceral and subcutaneous white adipose tissue from obese compared to lean mice and humans convincingly confirmed the up-regulation of MMP12 in obesity at mRNA, protein and, of note, activity levels. In conclusion, by this unbiased approach an interesting pool of potential molecular targets or biomarkers for treatment and prevention of CMD was identified with MMP12 being confirmed on multiple levels.

Publication Title

Identification of matrix metalloproteinase-12 as a candidate molecule for prevention and treatment of cardiometabolic disease.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP090187
Transcriptional profiling of Regulatory T-cells isolated from neonatal skin and skin draining lymph nodes (SDLNs)
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to Tregs in neonatal skin relative to peripheral Tregs Methods: Tregs from telogen skin and SDLNs were purified by cell sorting (using the Treg GFP reporter mouse line Foxp3-DTR/GFP) to generate mRNA transcription profiles. Results: Transcriptional profiling revealed a unique neonatal skin Treg signature relative to SDLN Tregs Conclusion: Our study represents the first detailed analysis of the neonatal skin Treg transcriptome. Overall design: mRNA profiles of skin and SDLN Tregs isolated from 13 day old Foxp3-DTR/GFP mice.

Publication Title

Commensal Microbes and Hair Follicle Morphogenesis Coordinately Drive Treg Migration into Neonatal Skin.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE35340
Notch is active in Langerhans Cell Histiocytosis and confers pathognomonic features on dendritic cells.
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Langerhans cell histiocytosis (LCH) is a disease characterized by the accumulation of eponymous CD1a+ Langerin+ Langerhans-cell (LC)-like dendritic cells (DC) of largely unknown origin. Here we have performed comparative transcriptome analysis of highly purified CD207+/CD1a+ Langerhans cell histiocytosis (LCH) cells derived from different locations and disease courses and three major human dendritic cell lineages: epidermal Langerhans cells, myeloid dendritic cells (mDC1) and plasmacytoid dendritic cells (pDC) in order to investigate the relationship between LCH cells and naturally occurring dendritic cells. Data obtained indicate that LCH cells form a distinct DC entity. Furthermore, we have identified transcripts that are uniquely expressed by LCH cells in comparison to LC, mDC1, and pDC, and induce LCH-specific features in human DC.

Publication Title

Notch is active in Langerhans cell histiocytosis and confers pathognomonic features on dendritic cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE48970
Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor STAT1 is essential for interferon- (IFN) mediated protective immunity in humans and mice. Two splice isoforms of STAT1, STAT1 and STAT1, differ with regard to a C-terminal transactivation domain, which is absent in STAT1. Dimers of STAT1 are therefore considered transcriptionally inactive and potential competitive inhibitors of STAT1. Contrasting this view, generation and analysis of mice deficient for either STAT1 or STAT1 demonstrated transcriptional activity of the STAT1 isoform and its enhancement of innate immunity. Gene expression profiling in primary cells revealed overlapping, but also non-redundant and gene-specific activities of STAT1 and STAT1 in response to IFN. Consistently, both isoforms mediated protective, IFN-dependent immunity against the bacterium Listeria monocytogenes, although with remarkably different efficiency. In contrast, STAT1 and STAT1 were largely redundant for transcriptional responses to IFN/ and for IFN/-dependent antiviral activity. Collectively, our data shed new light on how STAT1 isoforms contribute to antimicrobial immunity.

Publication Title

STAT1β is not dominant negative and is capable of contributing to gamma interferon-dependent innate immunity.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE24744
The interferon induced transmembrane protein 1 (Ifitm1): detailed analysis on its assumed functions
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Several functions have been suggested for the interferon induced transmembrane protein 1 (Iftitm1) gene in mammals. Originally it was identified as a member of a gene family that is highly inducible by type I and type II inteferons. Based on its expression during primordial germ CELl (PGC) specification it was suggested to be required for normal PGC migration. Ifitm1 targeted knockdown experiments in mouse embryos provided evidence that the gene might be necessary for normal somitogenesis. Finally, the complete deletion of the Ifitm gene cluster on mouse chromosome 7 revealed that the five deleted Ifitm1 genes are not essential for PCG migration and fertility. Here, we generated a novel targeted knockin allele of the Ifitm1 gene by replacing its coding region with a lacZ reporter gene to systematically reassess the suggested functions of this gene.

Publication Title

In vivo functional requirement of the mouse Ifitm1 gene for germ cell development, interferon mediated immune response and somitogenesis.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE43658
Transcriptional co-factor TBLR1 controls lipid mobilization in white adipose tissue
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Lipid mobilization (lipolysis) in white adipose tissue (WAT) critically controls lipid turnover and adiposity in humans. While the acute regulation of lipolysis has been studied in detail, the transcriptional determinants of WAT lipolytic activity remain still largely unexplored. Here we show that the genetic inactivation of transcriptional co-factor transducin beta-like-related (TBLR) 1 blunts the lipolytic response of white adipocytes through the impairment of cAMP-dependent signal transduction. Indeed, mice lacking TBLR1 in adipocytes are defective in fasting-induced lipid mobilization and when placed on a high fat diet show aggravated adiposity, glucose intolerance and insulin resistance. TBLR1 levels are found to increase under lipolytic conditions in WAT of both human patients and mice, correlating with serum free fatty acids (FFA). As a critical regulator of WAT cAMP signaling and lipid mobilization, proper activity of TBLR1 in adipocytes may thus represent a critical molecular checkpoint for the prevention of metabolic dysfunction in subjects with obesity-related disorders.

Publication Title

Transcriptional cofactor TBLR1 controls lipid mobilization in white adipose tissue.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP050365
A common cell state in Triple Negative Breast Cancers represents a druggable vulnerability
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

A basal (MDAMB468) and luminal (ZR75-1) cell line were treated with DMSO or PKC412 for 6h Overall design: 2 DMSO and 3 PKC412 treated samples for each cell line

Publication Title

Targeting a cell state common to triple-negative breast cancers.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE53157
Gene expression profiling associated with the progression to poorly differentiated thyroid carcinomas
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Poorly differentiated thyroid carcinomas (PDTC) represent a heterogeneous, aggressive entity, presenting features that suggest a progression from well-differentiated carcinomas.

Publication Title

Gene expression profiling associated with the progression to poorly differentiated thyroid carcinomas.

Sample Metadata Fields

Sex, Age, Specimen part

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