refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 196 results
Sort by

Filters

Technology

Platform

accession-icon GSE103899
Expression data from mouse adrenal glands extracted from wild-type (WT) and Cyp11b2tm1.1(cre)Brlt;Prkar1afl/fl(KO) adrenals
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

We demonstrate that PKA signalling drives zonal conversion within adult adrenocortical lineage in a sexually dimorphic manner. Our data establish that Prkar1a genetic ablation (leading to constitutive PKA activation) in the adult adrenocortical lineage leads to endocrine hyperactivity and accelerates adrenal cortex renewal. This results in increased zona fasciculata differentiation and final conversion into reticularis-like zone. This phenomenon relies partly on sex-dependent mechanisms of cortical renewal, on which the male androgenic milieu exerts a repressive action through induction of WNT signalling, which in turn antagonizes PKA signalling and cortical cell turnover.

Publication Title

PKA signaling drives reticularis differentiation and sexually dimorphic adrenal cortex renewal.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP074846
Next generation sequencing analysis of soy glyceollins and 17-ß estradiol: Effects on transcript abundance in the female mouse brain
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Purpose: The goal of this study was to compare and contrast the next generation sequencing data to data obtained from a whole brain microarray study Overall design: Examination of the effects of Glyceollin alone, 17ß Estradiol alone or in combination on gene expression in the adult female mouse brain

Publication Title

Next generation sequencing analysis of soy glyceollins and 17-β estradiol: Effects on transcript abundance in the female mouse brain.

Sample Metadata Fields

Sex, Cell line, Subject

View Samples
accession-icon GSE54356
Gene regulation in denervated hairy skin of the adult rat
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This study aimed to quantify the regulation of transcripts in the hairy skin of the back of adult rats in the condition of loss of sensory and autonomic (sympathetic) innervation (i.e., denervated). Denervated skin has reduced wound healing capacity, reduced proliferation of epidermal progenitor cells, and also expresses factors that regulate ingrowth of sensory and sympathetic axons from neighboring regions of innervated skin. It was expected that this quantification f transcript regulation would offer insight into the general and specific mechanisms that may contribute to these important biological processes.

Publication Title

categoryCompare, an analytical tool based on feature annotations.

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
accession-icon GSE60760
Gene expression responses to chronic low dose arsenite exposure
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation.

Publication Title

Inorganic Arsenic-induced cellular transformation is coupled with genome wide changes in chromatin structure, transcriptome and splicing patterns.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE64375
Immediate Transcriptional Changes in Response to High Dose Radiation Exposure
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

One of the most likely risks astronauts on long duration space missions face is exposure to ionizing radiation associated with highly energetic and charged heavy (HZE) particles. Since access to medical expertise on such a mission is limited at best, early diagnosis and mitigation of such exposure is critical. In order to accurately determine the dosage within 1 hour post-exposure, dose-dependent biomarkers are needed. Therefore, we performed a dose-course transcriptional analysis for radiation exposure at 0, 0.3, 1.5, and 3.0 Gy with corresponding time point at 1 hour (hr) post-exposure using Affymetrix GeneChip Human Gene 1.0 ST v1 Array chips. The analysis of our data suggests a set of sensitive genetic biomarkers specific to each radiation level as well as generic radiation response biomarkers. Upregulated biomarkers can then be used within lab-on-a-chip (LOC) systems to detect exposure to ionizing radiation.

Publication Title

Transcriptional profile of immediate response to ionizing radiation exposure.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE72551
Transcriptional changes in sensory ganglion associated with primary afferent collateral sprouting in spared dermatome model
  • organism-icon Rattus norvegicus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Primary afferent collateral sprouting (PACS) is a process whereby non-injured primary afferent neurons respond to some stimulus by extending new branches from existing axons. In the model used here (spared dermatome), the intact sensory neurons respond to the denervation of adjacent areas of skin by sprouting new axon branches into that adjacent denervated territory. Neurons of both the central and peripheral nervous systems undergo this process, which contributes to both adaptive and maladaptive plasticity. Investigations of gene expression changes associated with PACS can provide a better understanding of the molecular mechanisms controlling this process. Consequently, it can be used to develop treatment for spinal cord injury to promote functional recovery.

Publication Title

Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
accession-icon SRP070673
Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers Elovl2 as a novel regulator of glucose-induced insulin secretion
  • organism-icon Mus musculus
  • sample-icon 383 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Defective insulin secretion by pancreatic ß cells underlies the development of type 2 diabetes (T2D). High fat diet-fed mice are commonly used to study diabetes progression, but studies are usually limited to a single strain, such as C57Bl/6J. Here, we use a systems biology approach to integrate large phenotypic and islet transcriptomic data sets from six commonly used strains fed a high fat or regular chow diet to identify genes associated with glucose intolerance and insulin secretion. One of these genes is Elovl2, encoding very long chain fatty acid elongase 2. ELOVL2 is responsible for the synthesis of the polyunsaturated fatty acid, docosahexaenoic acid (DHA). We show that DHA rescues glucose-induced insulin secretion and cytosolic Ca2+ influx impaired by glucolipotoxicity, and that Elovl2 over-expression is able to restore the insulin secretion defect under these conditions. We propose that increased endogenous DHA levels resulting from Elovl2 up-regulation counteracts the insulin secretion defect associated with glucolipotoxicity. Although we focus our experimental validation on Elovl2, the comprehensive data set and integrative network model we used to identify this candidate gene represents an important novel resource to dissect the molecular aetiology of ß cell failure in murine models. Overall design: 6 mouse strains, 4 time points, 2 diets

Publication Title

Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers a role for <i>Elovl2</i> in glucose-induced insulin secretion.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

View Samples
accession-icon GSE72754
Down-regulation of Interferon signature in systemic lupus erythematosus patients by active immunization with Interferon alpha-Kinoid extended follow-up
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Interferon-alpha Kinoid (IFN-K) is a therapeutic vaccine composed of IFN-alpha2b coupled to a carrier protein. In a phase I/II placebo-controlled trial, we observed that IFN-K significantly decreases the IFN gene signature in whole blood RNA samples from SLE patients (see GSE39088). Here, we analyzed extended follow-up data from IFN-K-treated patients, in terms of persistence of neutralizing anti-IFN Abs, gene expression profiling and safety.

Publication Title

Interferon α kinoid induces neutralizing anti-interferon α antibodies that decrease the expression of interferon-induced and B cell activation associated transcripts: analysis of extended follow-up data from the interferon α kinoid phase I/II study.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Subject, Time

View Samples
accession-icon GSE72747
Global gene expression profiles in whole blood total RNA from patients with lupus nephritis, before and after initiation of therapy
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Patients with systemic lupus erythematosus are characterized by the spontaneous over-expression of interferon(IFN)-induced genes in peripheral blood RNA samples. In the present study, we wanted to study the evolution of the IFN gene signature in the peripheral blood of patients with lupus nephritis, before and after initiation of immunosuppressive therapy.

Publication Title

Interferon α kinoid induces neutralizing anti-interferon α antibodies that decrease the expression of interferon-induced and B cell activation associated transcripts: analysis of extended follow-up data from the interferon α kinoid phase I/II study.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Treatment, Subject, Time

View Samples
accession-icon SRP066356
Characterization of macrophage - cancer cell crosstalk in estrogen receptor positive and triple-negative breast cancer
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both cell types to understand how different cancer cells educate host cells to support tumor growth Overall design: To characterize the differences in macrophage activation under the influence of either ER+ or TNBC breast cancer cells, we cultured freshly isolated human peripheral monocytes with two breast cancer cell lines (T47D, ER+ and MDA-MB-231, TNBC) in an in vitro transwell co-culture assay. The transwell setting allowed us to investigate the effect of soluble mediators on macrophage activation since direct cell contact of these cells was inhibited by a (PET) membrane (pore size 0.4 µm).

Publication Title

Transcriptional profiling of macrophage and tumor cell interactions in vitro.

Sample Metadata Fields

No sample metadata fields

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