refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 194 results
Sort by

Filters

Technology

Platform

accession-icon GSE38573
Expression data from cerebrum in a spontaneous mutant mouse, laggard.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found a new spontaneous mutant mouse, laggard, characterized by general weakness in movements and retardation in growth.

Publication Title

Kif14 mutation causes severe brain malformation and hypomyelination.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE21572
Expression data from human stomach cell lines (MKN45 and MKN45P)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Analysis to find splicing variants that are differentially expressed in a highly metastatic stomach cancer cell line, MKN45P, versus its parental cell line, MKN45

Publication Title

Identification of a novel protein isoform derived from cancer-related splicing variants using combined analysis of transcriptome and proteome.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE148350
Microglia transcriptome in a rat model of ischemic stroke
  • organism-icon Rattus norvegicus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Microglia are key regulators of inflammatory response after stroke and brain injury. Here we profiled the microglia transcriptome isolated from a spontaneously hypertensive rat model of focal cerebral ischemia.

Publication Title

Transcriptomic characterization of microglia activation in a rat model of ischemic stroke.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE64907
NSCLC Driven by DDR2 Mutation is Sensitive to JQ1 and Dasatinib Combination Therapy
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Genetically engineered mouse models of lung cancer have demonstrated an important role in understanding the function of novel lung cancer oncogenes and tumor suppressor genes identified in genomic studies of human lung cancer. Further, these models are important platforms for pre-clinical therapeutic studies. Here, we generated a mouse model of lung adenocarcinoma driven by mutation of the Discoidin Domain Receptor 2 (DDR2) gene combined with loss of TP53. DDR2L63V;TP53L/L mice developed poorly differentiated lung adenocarcinomas in all transgenic animals analyzed with a latency of 40-50 weeks and a median survival of 67.5 weeks. Mice expressing wild-type DDR2 with combined TP53 loss did not form lung cancers. DDR2L63V; TP53L/L tumors displayed robust expression of DDR2 and immunohistochemical markers of lung adenocarcinoma comparable to previously generated models of lung adenocarcinoma though also displayed concomitant expression of the squamous cell markers p63 and SOX2. Tumor-derived cell lines were not solely DDR2 dependent and displayed up-regulation of and partial dependence on MYCN. Combined treatment with the BET inhibitor JQ1 and the mutltitargeted DDR2 inhibitor dasatinib inhibited tumor growth in vitro and in vivo. Together, these results suggest that DDR2 mutation can drive lung cancer initiation in vivo and provide a novel mouse model for lung cancer therapeutics studies.

Publication Title

NSCLC Driven by DDR2 Mutation Is Sensitive to Dasatinib and JQ1 Combination Therapy.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE97287
Acute v. baseline PBMC gene expression in patients with Systemic Capillary Leak Syndrome
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The Systemic Capillary Leak Syndrome (SCLS) is an extremely rare and potentially life-treating vascular disorder of unknown etiology. SCLS is characterized by dramatic and transient episodes of hypotensive shock and edema due to plasma leakage into peripheral tissues. The disorder has garnered increased attention during the last several years because of the resemblance of its initial presentation to more common disorders such as systemic anaphylaxis, sepsis, and acute infections with the Ebola/Marburg family of filoviruses. Although approximately 70-80% of patients with SCLS have a concurrent monoclonal gammopathy of unknown significance (MGUS), any contribution of the paraprotein to acute flares is unknown. To identify circulating factors that contribute to the onset of acute SCLS crises, we performed transcriptomic profiling of paired peripheral blood mononuclear cell fractions obtained from patients during acute attacks and convalescent intervals using microarray. 61 genes were significantly up- or downregulated more than 2.5 fold in acute samples relative to baseline. One of the most upregulated genes was ADM, which encodes the vasoactive peptide adrenomedullin. The ADM surrogate pro-ADM was markedly elevated in SCLS acute sera compared to remission samples or sera from healthy controls. Monocytes and endothelial cells (ECs) from SCLS subjects expressed significantly more ADM in response to proinflammatory stimuli compared to healthy control cells. Application of ADM to ECs exerted protective effects on vascular barrier function. These results suggest a pathogenic contribution of ADM to the profound pressor-resistant hypotension that characterizes the initial stages of SCLS.

Publication Title

Adrenomedullin surges are linked to acute episodes of the systemic capillary leak syndrome (Clarkson disease).

Sample Metadata Fields

Specimen part, Disease, Subject

View Samples
accession-icon GSE33372
Hypothalamic gene expression profile indicates a reduction in G-protein signaling in the wfs1 mutant mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

WFS1 gene is coding protein with unknown function but its functional deficiency causes different neuropsychiatric and neuroendocrine syndromes. In the present study we aimed to find the functional networks influenced by the Wfs1 deficiency in the hypothalamus. We performed gene expression profiling (Mouse Gene 1.0 ST Arrays) in Wfs1 deficient mice (ko). Modified t-statistics was used for comparison of groups (wt vs ko). Functional annotation of the alterations in RNA levels was performed with Ingenuity Pathway Analysis. 305 genes were differentially expressed with nominal p-value less than 0.01. FDR adjusted p-values were significant (0.007) only for two genes C4b (t=9.66) and Wfs1 (t=-9.03). However, several genes related to the G-protein signalling were very close to the FDR adjusted significance. For instance, Rgs4 (regulator of G-protein signalling 4) was down-regulated (-0.34, t=-5.4) in Wfs1 deficient mice. Changes in Rgs4 and C4B expression were confirmed by QRT-PCR. In humans, Rgs4 is in the locus for bipolar disease (BPD) and its expression is down-regulated in BPD. C4b is the gene related to the neurodegenerative diseases. In conclusion, hypothalamic gene expression profiling indicates alterations in some functionally relevant molecular pathways explaining the clinical syndrome in the Wolfram syndrome patients.

Publication Title

Hypothalamic gene expression profile indicates a reduction in G protein signaling in the Wfs1 mutant mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE15914
Interleukin-7 promotes monocyte/macrophage arrest on endothelial cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: It is recognized that atherosclerosis can regresses at least in animal models. However, little is known about the mechanisms. We induced regression of advanced atherosclerosis in apolipoprotein E deficient (APOE/) mice and studied underlying mechanisms. Unexpectedly, our study led to the role of interleukin-7 (IL-7) in atherogenesis.

Publication Title

Interleukin-7 induces recruitment of monocytes/macrophages to endothelium.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE15385
Transwell-cultured and miRNAs-transfected T84 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MicroRNAs are small non-coding RNA species, some of which are playing important roles in cell differentiation. However, the level of participations of microRNAs in epithelial cell differentiation is largely unknown. Here, we found that expression levels of four microRNAs (miR-210, miR-338-3p, miR-33a and miR-451) were significantly increased in differentiated stage of T84 cells, compared with undifferentiated stage. Additionally, we demonstrate that miR-338-3p and miR-451 contribute to the formation of epithelial basolateral polarity by facilitating translocalization of beta1 integrin to the basolateral membrane. However, candidate target mRNAs of miR-338-3p and miR-451 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms.

Publication Title

MicroRNA-338-3p and microRNA-451 contribute to the formation of basolateral polarity in epithelial cells.

Sample Metadata Fields

Cell line, Treatment, Time

View Samples
accession-icon SRP156398
The Effect of PRMT5 deficiency on thymic iNKT cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Protein arginine methylation is a post-translational modification catalyzed by protein arginine methyltransferase (PRMT). To elucidate the role of PRMT5 in T cells, we generated T-cell specific PRMT5-deficient mice (Prmt5 flox/d Cd4-Cre mice) and found a severe loss of thymic iNKT cells as well as a reduced number in peripheral CD4+ and CD8+ T cells. As iNKT cells were significantly decreased in the stage 1, 2 and 3 of developmental stages, RNA-seq was performed using stage 1 iNKT cells of control and PRMT5-deficient mice. This transcriptome analysis will provide mechanistic insight into how PRMT5 contributes to thymic iNKT cell development. Overall design: Stage 1 iNKT cells were sorted from thymus of control and Prmt5 flox/D Cd4-Cre mice. Total RNA was extracted and RNA-seq was performed by Ion Proton.

Publication Title

Arginine methylation controls the strength of γc-family cytokine signaling in T cell maintenance.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE55143
Effect of chronic valproic acid treatment on hepatic gene expression profile in Wfs1 knockout mouse.
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Aim of the present study was to compare the effect of chronic VPA treatment in wild type and Wfs1 knockout mice on hepatic gene expression profile.

Publication Title

Effect of chronic valproic Acid treatment on hepatic gene expression profile in wfs1 knockout mouse.

Sample Metadata Fields

Sex, 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