refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 99 results
Sort by

Filters

Technology

Platform

accession-icon GSE39291
Expression Profiles of HepG2 cells treated with following oxidants: 100M menadione, 200M TBH or 50M H2O2
  • organism-icon Homo sapiens
  • sample-icon 124 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

The transcriptomic changes induced in the human liver cell line HepG2 by 100M menadione, 200M TBH or 50M H2O2 after treatment for 0.5, 1, 2, 4, 6, 8 and 24h.

Publication Title

Time series analysis of oxidative stress response patterns in HepG2: a toxicogenomics approach.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE63580
Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE63552
Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells (Affymetrix)
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Understanding toxicity pathways of engineered nanomaterials (ENM) has recently been brought forward as a key step in 21st century ENM risk assessment. Molecular mechanisms linked to phenotypic end points is a step towards the development of toxicity tests based on key events, which may allow for grouping of ENM according to their mechanisms of action. This study identified molecular mechanisms underlying mitochondrial dysfunction in human bronchial epithelial BEAS 2B cells following exposure to one of the most studied multi-walled carbon nanotubes (MWCNTs; Mitsui-7). Asbestos was used as a positive control and a non-carcinogenic glass wool material was included as a negative fibre control. Decreased mitochondrial membrane potential (MMP) was observed for MWCNTs at a biologically relevant dose (0.25 g/cm2) and for asbestos at 2 g/cm2, but not for glass wool. Extensive temporal transcriptomic and microRNA expression analyses identified a 330-gene signature related to MWCNT- and asbestos-induced MMP. Fourty-nine of the MMP-associated genes showed highly similar expression patterns over time (six time points) and the majority was found to be regulated by two transcription factors strongly involved in mitochondrial homeostasis, APP and NRF1. In addition, four miRNAs were associated with MMP and one of them, miR-1275, was found to negatively correlate with a large part of the MMP-associated genes. Cellular processes such as gluconeogenesis, glucose metabolism, mitochondrial LC-fatty acid -oxidation and spindle microtubule function were enriched among the MMP-associated genes and miRNAs. These results are expected to be useful in the identification of key events in ENM-related toxicity pathways for the development of molecular screening techniques.

Publication Title

Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE12836
PDGF-B induces a homogeneous class of oligodendrogliomas from embryonic neural progenitors
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas.

Publication Title

PDGF-B induces a homogeneous class of oligodendrogliomas from embryonic neural progenitors.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP076340
Single-Cell RNAseq Reveals That Pancreatic ß-Cells From Very Old Male Mice Have a Young Gene Signature
  • organism-icon Mus musculus
  • sample-icon 207 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Aging improves pancreatic ß-cell function in mice. This is a surprising finding since aging is typically associated with functional decline. We performed single-cell RNA sequencing of ß-cells from 3 and 26 month old mice to explore how changes in gene expression contribute to improved function with age. The old mice were healthy, had reduced blood glucose levels and increased ß-cell mass, which correlated to their body weight. ß-cells from young and old mice had similar transcriptome profiles. In fact, only 193 genes (0.89% of all detected genes) were significantly regulated (= 2-fold; false discovery rate < 0.01; normalized counts > 5). Of these, 183 were downregulated and mainly associated with pathways regulating gene expression, cell cycle, cell death and survival as well as cellular movement, function and maintenance. Collectively, our data show that ß-cells from very old mice have transcriptome profiles similar to those of young mice. These data support previous findings that aging is not associated with reduced ß-cell mass or functional ß-cell decline in mice. Overall design: Single-cell RNA sequencing of mouse pancreatic islet beta cells

Publication Title

Single-Cell RNAseq Reveals That Pancreatic β-Cells From Very Old Male Mice Have a Young Gene Signature.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

View Samples
accession-icon SRP070425
Use of the Fluidigm C1 platform for RNA sequencing of single mouse pancreatic islet cells
  • organism-icon Mus musculus
  • sample-icon 622 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

This study provides an assessment of the Fluidigm C1 platform for RNA sequencing of single mouse pancreatic islet cells. The system combines microfluidic technology and nanoliter-scale reactions. We sequenced 622 cells allowing identification of 341 islet cells with high-quality gene expression profiles. The cells clustered into populations of alpha-cells (5%), beta-cells (92%), delta-cells (1%) and PP-cells (2%). We identified cell-type specific transcription factors and pathways primarily involved in nutrient sensing and oxidation and cell signaling. Unexpectedly, 281 cells had to be removed from the analysis due to low viability (23%), low sequencing quality (13%) or contamination resulting in the detection of more than one islet hormone (64%). Collectively, we provide a resource for identification of high-quality gene expression datasets to help expand insights into genes and pathways characterizing islet cell types. We reveal limitations in the C1 Fluidigm cell capture process resulting in contaminated cells with altered gene expression patterns. This calls for caution when interpreting single-cell transcriptomics data using the C1 Fluidigm system. Overall design: Single-cell RNA sequencing of mouse C57BL/6 pancreatic islet cells

Publication Title

Use of the Fluidigm C1 platform for RNA sequencing of single mouse pancreatic islet cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE2852
Ochratoxin A study on rat liver and kidney gene expression
  • organism-icon Rattus norvegicus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Ochratoxin A gene expression profiling in liver and kidney, with time points of exposure from 7 days to 12 motnhs

Publication Title

A toxicogenomics approach to identify new plausible epigenetic mechanisms of ochratoxin a carcinogenicity in rat.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP092805
Amino Acid Transporter Slc38a5 Mediates Glucagon Receptor Inhibition-Induced Pancreatic a-Cell Hyperplasia in Mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Glucagon supports glucose homeostasis by stimulating hepatic gluconeogenesis, in part by promoting the uptake and conversion of amino acids into gluconeogenic precursors. Genetic disruption or pharmacologic inhibition of glucagon signaling results in elevated plasma amino acids, and compensatory glucagon hypersecretion involving expansion of pancreatic a-cell mass. Regulation of pancreatic a- and ß-cell growth has drawn a lot of attention because of potential therapeutic implications. Recent findings indicate that hyperaminoacidemia triggers pancreatic a-cell proliferation via an mTOR-dependent pathway. We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative a-cells, and that Slc38a5 is critical for the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased a-cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. These results show that Slc38a5 is a key component of the feedback circuit between glucagon receptor signaling in the liver and amino acid-dependent regulation of pancreatic a-cell mass in mice. Overall design: Examination of the transcriptomes of pancreatic islets of mice treated with GCGR-antibody and an isotype control antibody.

Publication Title

Amino Acid Transporter Slc38a5 Controls Glucagon Receptor Inhibition-Induced Pancreatic α Cell Hyperplasia in Mice.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP093627
Transcriptomes of enriched mouse islet alpha cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Glucagon supports glucose homeostasis by stimulating hepatic gluconeogenesis, in part by promoting the uptake and conversion of amino acids into gluconeogenic precursors. Genetic disruption or pharmacologic inhibition of glucagon signaling results in elevated plasma amino acids and compensatory glucagon hypersecretion involving expansion of pancreatic a cell mass. Recent findings indicate that hyperaminoacidemia triggers pancreatic a cell proliferation via an mTOR-dependent pathway. We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative a cells and that Slc38a5 controls the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased a cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. These results show that Slc38a5 is a key component of the feedback circuit between glucagon receptor signaling in the liver and amino-acid-dependent regulation of pancreatic a cell mass in mice. Overall design: Examination of the transcriptomes of islet non-beta-cells of GcgR knock out mice.

Publication Title

Amino Acid Transporter Slc38a5 Controls Glucagon Receptor Inhibition-Induced Pancreatic α Cell Hyperplasia in Mice.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE29532
Exon-array profiling of peripheral blood cells in the first hours of acute coronary syndrome patients
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Identifying novel candidate biomarker gene differentially expressed in the peripheral blood cells of patients with early stage acute myocardial infarction using microarray as a high throughput screening technology.

Publication Title

Novel genes detected by transcriptional profiling from whole-blood cells in patients with early onset of acute coronary syndrome.

Sample Metadata Fields

Specimen part, Disease, Time

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