refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 166 results
Sort by

Filters

Technology

Platform

accession-icon GSE5789
Effect of 13 weeks of subchronic exposure to TCDD, PeCDF, PCB126, PCB153 and PCB126/PCB153 on hepatic gene expression
  • organism-icon Rattus norvegicus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

This study investigates the effects of the aryl hydrocarbon receptor (AhR) ligands TCDD, PCB126 and PeCDF; the non-AhR ligand PCB153 and the binary mixture PCB126/PCB153 on hepatic gene expression in female sprague dawley rats. Rats were treated with toxicological equivalent doses of TCDD (100ng/kg), PeCDF (200ng/kg), PCB126 (1000ng/kg) and PCB153 (1000ug/kg) 5 days a week for 13 weeks.

Publication Title

Hepatic gene downregulation following acute and subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE40220
INTESTINAL FILTER FOR USE IN OESOPHAGEAL CANCER RESEARCH
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This study utilise the examination of normal gastro-intestinal tissues to determine a tissue specific signal for use in deriving the intestinal signature of intestinal metaplasias of the oesophagus. Normal oesophageal, colonic and duodenal tissue biopsies were taken after informed consent and RNA was extracted following histological examination of adjacent tissues for normal aperaing mucosa.

Publication Title

The characterization of an intestine-like genomic signature maintained during Barrett's-associated adenocarcinogenesis reveals an NR5A2-mediated promotion of cancer cell survival.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE85543
Transcriptional effects of soluble CD40 ligand on human nave B cells
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

We performed microarray analysis to derive gene signatures down-stream of soluble CD40 ligand stimulation in human naive B cells. Nave B cells were purified from healthy donor PBMC using negative selection beads (Miltenyi) and cultured with sCD40L at 2.5ug/ml for 6hr before microarray analysis. In the same study, cells were also harvested at day 5 post-stimulation to confirm sCD40L-induced B cell activation and proliferation. FACS analysis confirmed soluble CD40L induced up-regulation of CD86 and CD69 at 24hr. B cell proliferation was measured at day 4 post-stimulation by EdU incorporation.

Publication Title

CD40L-Dependent Pathway Is Active at Various Stages of Rheumatoid Arthritis Disease Progression.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE85544
Transcriptional effects of soluble CD40 ligand on human immature dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

We performed microarray analysis of sCD40L-stimulated iDC to derive a signature of CD40 activation. Human monocytes from normal healthy donors were differentiated to iDCs with GM-CSF and IL4. FACS analysis demonstrated the immature status of these cells, illustrated by low expression of CD80, CD40, and CD86. We confirmed that sCD40L induces the maturation of DCs, characterized by higher expression of CD80, HLA-DR, CD86, CD83 and CD40 and secretion of pro-inflammatory cytokines at 24hr post-stimulation. Cells were harvested at 1, 3 and 24hr post-stimulation for microarray analysis.

Publication Title

CD40L-Dependent Pathway Is Active at Various Stages of Rheumatoid Arthritis Disease Progression.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE67358
Promotion of pancreatic cancer metastasis by mutant p53
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The TP53 transcription factor is frequently mutated at later stages of epithelial cancers, indicating a possible role in their invasion and metastasis. Importantly, in most cases rather than a simple loss of function p53 mutation, point mutations of p53 accumulate at the protein level and may have dominant negative functions. This study analyses gene expression differences between mice harbouring p53 mutation who do and do not develop metastasis.

Publication Title

Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE27171
Migrating Schistosoma japonicum schistosomula induce type-2 inflammation in the murine lung
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Migrating schistosomula are an important stage of the schistosome lifecycle and represent a key target for elimination of infection by natural and vaccine induced host immune responses. To gain a better understanding of how these parasites initiate a primary host immune response we have characterised the host lung response to migrating Schistosoma japonicum schistosomula using a combination of histochemistry, microarrays and quantitative cytokine analysis. Our data suggest that, during a S. japonicum infection, actively migrating schistosomula induce a Type-2 cytokine response in the lung that may support the subsequent development of a CD4+ T helper 2 (Th2) response against egg antigens. This hypothesis is supported by the fact that schistosomula and schistosome eggs are known to express important Th2-inducing antigens such as omega-1, peroxiredoxin, kappa-5 and IPSE/alpha1. The host lung response to migrating schistosomula was associated with increased numbers of macrophages and expression of markers for alternatively activated macrophages (AAM) in the lung. Activation of AAM in the lung and at the systemic level could lead to the modulation of the host immune response to favour parasite survival. Induction of these cells could also contribute to diminished inflammatory responses to, for example, allergy and asthma that are known to be associated with helminth infections. These data enhance our understanding of the mechanisms whereby schistosomes may evade the immune response and the mechanisms by which schistosome infection can help influence the host response following exposure to allergenic stimuli.

Publication Title

Migrating Schistosoma japonicum schistosomula induce an innate immune response and wound healing in the murine lung.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon SRP060598
Mitotic stress is an integral part of the oncogene-induced senescence program that promotes multinucleation and cell cycle arrest
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signalling. OIS is frequently accompanied by multinucleation; however, the origin of this is unknown. Here we show that multinucleate OIS cells originated mostly from failed mitosis. Prior to senescence, mutant RasV12 activation in primary human fibroblasts compromised mitosis, associated with abnormal expression of mitotic genes that enter M-phase. Simultaneously, RasV12 activation enhanced survival of damaged mitoses, culminating in extended mitotic arrest and aberrant exit from mitosis via mitotic slippage. ERK-dependent transcriptional up-regulation of Mcl1 was responsible for enhanced slippage of cells with mitotic defects and subsequent cell survival. Importantly, mitotic slippage and oncogene signalling synergistically induced senescence and key senescence regulators p21 and p16. We propose that activated Ras induces transcriptional changes that predispose cells undergoing OIS to mitotic stress and multinucleation. Overall design: We used RNA-seq of IMR90 cells with inducible expression of oncogenic RasV12 that were synchronised in mitosis, to characterise the nature of mitotic defects that lead to multinucleation of oncogene-induced senescent cells

Publication Title

Mitotic Stress Is an Integral Part of the Oncogene-Induced Senescence Program that Promotes Multinucleation and Cell Cycle Arrest.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE20948
The Effect of Hepatitis C Virus Infection on Host Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatitis C Virus is a leading cause of chronic liver disease. The identification and characterisation of key host cellular factors that play a role in the HCV replication cycle is important for the understanding of disease pathogenesis and the identification of novel anti-viral therapeutic targets. Gene expression profiling of HCV infected Huh7 cells by microarray analysis was performed to identify host cellular genes that are transcriptionally regulated by infection. The expression of host genes involved in cellular defence mechanisms (apoptosis, proliferation and anti-oxidant responses), cellular metabolism (lipid and protein metabolism) and intracellular transport (vesicle trafficking and cytoskeleton regulation) was significantly altered by HCV infection. The gene expression patterns identified provide insight into the potential mechanisms that contribute to HCV associated pathogenesis. These include an increase in pro-inflammatory and pro-apoptotic signalling and a decrease in the anti-oxidant response pathways of the infected cell.

Publication Title

Gene expression profiling indicates the roles of host oxidative stress, apoptosis, lipid metabolism, and intracellular transport genes in the replication of hepatitis C virus.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP115897
A molecular roadmap of the aorta-gonad-mesonephros region reveals BMPER as a novel regulator of HSC maturation [AGM]
  • organism-icon Mus musculus
  • sample-icon 75 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In the developing embryo, haematopoietic stem cells (HSCs) emerge from the aorta-gonad-mesonephros (AGM) region but the molecular regulation of this process is poorly understood. Recently, the progression from E9.5 to E10.5 and polarity along the dorso-ventral axis have been identified as clear demarcations of the supportive HSC niche. To identify novel secreted regulators of HSC maturation, we performed RNA-sequencing over these spatio-temporal transitions in the AGM region, and supportive OP9 cell line. Overall design: RNA-sequencing profiles of the aorta-gonad-mesonephros region from E9.5 embryos and E10.5 embryos sub-dissected into dorsal (AoD), ventral (AoV) and urogenital ridges (UGR) and pooled from between 15 and 34 embryos in three separate experiments.

Publication Title

A molecular roadmap of the AGM region reveals BMPER as a novel regulator of HSC maturation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP115898
A molecular roadmap of the aorta-gonad-mesonephros region reveals BMPER as a novel regulator of HSC maturation [OP9]
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In the developing embryo, haematopoietic stem cells (HSCs) emerge from the aorta-gonad-mesonephros (AGM) region but the molecular regulation of this process is poorly understood. Recently, the progression from E9.5 to E10.5 and polarity along the dorso-ventral axis have been identified as clear demarcations of the supportive HSC niche. To identify novel secreted regulators of HSC maturation, we performed RNA-sequencing over these spatio-temporal transitions in the AGM region, and supportive OP9 cell line. Overall design: RNA-sequencing profiles of OP9 cells grown in flat, submersed culture or reaggregate and cultured at the liquid-gas interface were compared.

Publication Title

A molecular roadmap of the AGM region reveals BMPER as a novel regulator of HSC maturation.

Sample Metadata Fields

Specimen part, Cell line, 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