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accession-icon GSE60620
Reduction of DNA methylation suppresses colon carcinogenesis through induction of tumor cell differentiation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In this study, we analyzed global gene expressions of colon tumors from DNA hypomethylated and the control mice. We found that DNA hypomethylated tumors express significantly higher levels of intestinal differentiation-related genes when compared with the control tumors. These results suggest that DNA methylation may play a role in the maintenance of undifferentiated state of colon tumor cells.

Publication Title

Reducing DNA methylation suppresses colon carcinogenesis by inducing tumor cell differentiation.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP107301
Sema6D reverse signaling controls lipid metabolism for macrophage polarization linking mTOR to PPAR?
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study is to compare downstream genes of Sema6D signaling in both M1 and M2 macrophages. Overall design: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by IL-4 for 24 hrs.

Publication Title

Semaphorin 6D reverse signaling controls macrophage lipid metabolism and anti-inflammatory polarization.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP107300
Sema6D reverse signaling controls lipid metabolism for macrophage polarization linking mTOR to PPAR?
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goal of this study is to compare downstream genes of Sema6D signaling in LPS plus IFNg stimulated macrophages. Methods: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by LPS for 4 hrs. Results: According to this comparison, we found that 550 genes were downregulated in Sema6D-/- macrophages than WT macrophages in response to LPS. Conclusions: Our study represents 62 genes were supressed in both M1 and M2 Sema6D-/- macrophage than WT macrophages, suggesting of Sema6D reverse sigaling genes. Overall design: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by LPS for 4 hrs, then isolated total RNA by RNeasy kit.

Publication Title

Semaphorin 6D reverse signaling controls macrophage lipid metabolism and anti-inflammatory polarization.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP134274
Gene expression profiling in human nasal epithelial cells (HNEpCs) stimulated with eosinophil-derived neurotoxin (EDN)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study is to evaluate the function of eosinophil-derived neurotoxin (EDN) in eosinophilic chronic rhinosinusitis (ECRS) pathogenesis and assess its potential as a disease activity marker. Overall design: To determine the pathological role of eosinophil-derived neurotoxin (EDN) in eosinophilic chronic rhinosinusitis (ECRS), we performed RNA sequencing to analyze gene expression in human nasal epithelial cells (HNEpCs) stimulated with EDN.

Publication Title

Eosinophil-derived neurotoxin enhances airway remodeling in eosinophilic chronic rhinosinusitis and correlates with disease severity.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE26484
Sema4A, a novel serum marker of multiple sclerosis, implicates Th17 pathology and efficacy of interferon-.
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system and the leading cause of lasting neurological disabilities in young adults. Increasing evidence suggests that early treatment prevents the development of disability. However, there have been no reliable serum markers to assist the early diagnosis. In addition, interferon (IFN)-, which is the major treatment for MS, is not always effective. Therefore, the development of simple serological test to help the early diagnosis and predict responsiveness to IFN- is of clinical importance. On the other hand, a transmembrane-type semaphorin, Sema4A, has been implicated in experimental autoimmune encephalomyelitis (EAE) by regulating helper T (Th) cell differentiation. Thus, we aimed to identify the implications of Sema4A in diagnosis and pathogenesis of MS. Methods: We assayed serum Sema4A in 59 patients with relapsing-remitting MS (RRMS), 22 patients with clinically isolated syndrome (CIS) and 126 patients with other neurological diseases (OND) by developing a sandwich ELISA. To identify a source of soluble Sema4A and characteristics of MS patients with high levels of Sema4A, we analyzed peripheral blood mononuclear cells (PBMCs) from MS patients and healthy controls by flow cytometry (FACS) and gene chip analysis. The effect of Sema4A was examined in vitro and in vivo using an EAE model. Findings: Sema4A was significantly increased in sera of patients with MS and CIS compared to controls. Sema4A expression was increased on the surface of DCs in MS patients and shed from these cells in a metalloproteinase-dependent manner, affecting the Th17skewing. In addition, patients with high Sema4A levels exhibited more severe disabilities, and IFN- treatment was not beneficial to those patients. Interpretation: Measuring Sema4A is a practical laboratory test to help diagnose MS and to predict responsiveness to IFN- therapy.

Publication Title

Elevation of Sema4A implicates Th cell skewing and the efficacy of IFN-β therapy in multiple sclerosis.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon GSE65350
Expression data from mouse embryo
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To understand the molecular mechanism by which regulate skeletal development, we attempted to identify transcription factors that were highly expressed in developing cartilage during the embryonic stage.

Publication Title

The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification.

Sample Metadata Fields

Specimen part

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accession-icon GSE37431
Endothelial cell-enriched genes expression in mouse embryo
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The early blood vessels of the embryo and yolk sac in mammals develop by aggregation of de novo forming angioblasts into a primitive vascular plexus, which then undergoes a complex remodeling process. Angiogenesis is also important for disease progression in the adult. However, the precise molecular mechanism of vascular development remains unclear.

Publication Title

Genome-wide identification of endothelial cell-enriched genes in the mouse embryo.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE66039
Global analysis of androgen-signaling reveals the function of miRNAs for the epigenomic regulation in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE14843
Altered Hepatic Gene Expression Profiles Associated with Myocardial Ischemia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

BackgroundAcute coronary syndrome (ACS) is sometimes accompanied by accelerated coagulability, lipid metabolism, and inflammatory responses, which are not attributable to the cardiac events alone. We hypothesized that the liver plays a pivotal role in the pathophysiology of ACS. We simultaneously analyzed the gene expression profiles of the liver and heart during acute myocardial ischemia in mice.

Publication Title

Altered hepatic gene expression profiles associated with myocardial ischemia.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE66038
Effects of miRNA-mediated TET2 in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men. We identified that miR-29 family is the most androgen-responsive miRNA in hormone-refractory prostate cancer cells. For the screening of miR-29b target, we performed microarray analysis in two prostate cancer cells. Because TET2 is the primary target of miR-29 family by our analysis, we also performed TET2 signaling by microarray.

Publication Title

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.

Sample Metadata Fields

Specimen part, Cell line

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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)

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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.

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