refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
    0
github link
Build and Download Custom Datasets
refine.bio helps you build ready-to-use datasets with normalized transcriptome data from all of the world’s genetic databases.
Showing
of 29 results
Sort by

Filters

Technology

Platform

accession-icon GSE78066
Global gene expression changes during immune complex-induced neutrophil activation (wild type and Card9/ cells)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

--- Raw data of the Supplementary Table 1 of the Nature Communications article 'Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo'

Publication Title

Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo.

Sample Metadata Fields

Treatment, Time

View Samples
accession-icon GSE72353
A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

- Gene expression changes linked to two step immortalization of human mammary epithelial cells (HMEC).

Publication Title

A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE47047
Gene expression data from immortal and arsenite-transformed malignant prostate epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells.

Publication Title

Coordinate H3K9 and DNA methylation silencing of ZNFs in toxicant-induced malignant transformation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE22325
Expression data from interleukin-stimulated HUVEC
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors.

Publication Title

Transcriptional profiling of the hematopoietic support of interleukin-stimulated human umbilical vein endothelial cells (HUVECs).

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE19240
Expression profile of IL-1beta stimulated and non-stimulated endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Complete identification of the bone marrow niche remains one of the most progressing fields. Attempts to identify soluble factors involved in stem cell renewal have been less successful. We have previously shown that endothelial cells (EC) can induce the long-term proliferation of hematopoietic progenitor cells (HPC), especially when they had been subjected to an inflammatory stimulus like interleukins (IL) 1.

Publication Title

Interleukin 32 promotes hematopoietic progenitor expansion and attenuates bone marrow cytotoxicity.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE46866
Early induction of the type I interferon response in neurological forms of Gaucher disease
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neuroinflammation is a key phenomenon in the pathogenesis of many neurodegenerative diseases. Understanding the mechanisms by which brain inflammation is engaged and delineating the key players in the immune response and their contribution to brain pathology is of great importance for the identification of novel therapeutic targets for these devastating diseases. Gaucher disease, the most common lysosomal storage disease, is caused by mutations in the GBA1 gene and is a significant risk factor for Parkinson?s disease; in some forms of Gaucher disease, neuroinflammation is observed. An unbiased gene profile analysis was performed on a severely affected brain area of a neurological form of a Gaucher disease mouse at a pre-symptomatic stage; the mouse used for this study, the Gbaflox/flox; nestin-Cre mouse, was engineered such that GBA1 deficiency is restricted to cells of neuronal lineage, i.e., neurons and macroglia. The 10 most up-regulated genes in the ventral posteromedial/posterolateral region of the thalamus were inflammatory genes, with the gene expression signature significantly enriched in interferon signaling genes. Our results imply that the type I interferon response is involved in the development of nGD pathology, and support the notion that interferon signaling pathways play a vital role in the sterile inflammation that often occurs during chronic neurodegenerative diseases in which neuroinflammation is present.

Publication Title

Induction of the type I interferon response in neurological forms of Gaucher disease.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE78757
Cortical transcriptional changes in a chemically-induced neuronopathic Gaucher disease mouse model
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Great interest has been shown in understanding the pathology of Gaucher disease (GD) due to the recently-discovered genetic relationship with Parkinsons disease. For such studies, suitable animal models of GD are required. Chemical induction of GD by inhibition of acid -glucosidase (GCase) using the irreversible inhibitor, conduritol-B-epoxide (CBE), is particularly attractive, although few systematic studies examining the effect of CBE on development of symptoms associated with neurological forms of GD have been performed. We now demonstrate a correlation between the amount of CBE injected into mice and levels of accumulation of the GD substrates, glucosylceramide and glucosylsphingosine, and show that disease pathology, indicated by altered levels of pathological markers, depends on the dose of CBE and its time of injection. Gene array analysis shows a remarkable similarly in the gene expression profile of CBE-treated mice and a genetic GD mouse model, the Gbaflox/flox;nestin-Cre mouse, with 120 of the 144 genes up-regulated in CBE-treated mice also up regulated in Gbaflox/flox;nestin-Cre mice. Finally, we demonstrate that some aspects neuropathology and some behavioral abnormalities can be arrested upon cessation of CBE treatment during a specific time window. Together, our data demonstrate that injection of mice with CBE provides a rapid and relatively easy way to induce symptoms typical of neuronal forms of GD, which will prove particularly useful when examining the role of specific biochemical pathways in GD pathology, since CBE can be injected into mice defective in components of putative pathological pathways, alleviating the need for time consuming crossing of mice.

Publication Title

Identification of Modifier Genes in a Mouse Model of Gaucher Disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE29367
Expression data from human squamous cell lung cancer line HARA and highly bone metastatic subline HARA-B4.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We investigated the molecular mechanisms for osteolytic bone metastasis by selecting human lung cancer cell line subpopulations with elevated metastatic activity and validating genes that are overexpressed in these cells. A bone-seeking squamous lung cancer cell line (HARA-B4) was established by sequentially injecting parental HARA cells into the left ventricle of male 5-week-old nude mice 4 times.

Publication Title

Involvement of CXCL14 in osteolytic bone metastasis from lung cancer.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE42743
Oral Cavity Cancer Compared to Adjacent "Normal" Tissue [Validation Set]
  • organism-icon Homo sapiens
  • sample-icon 99 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oral Cavity Cancer

Publication Title

A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE41613
A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation
  • organism-icon Homo sapiens
  • sample-icon 94 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

OSCC is associated with substantial mortality and morbidity. In this study, we built on our previous molecular work to identify and validate a prognostic 13-gene signature that showed a higher ability than tumor stage in predicting survival for patients with

Publication Title

A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.

Sample Metadata Fields

Sex, Specimen part, Treatment

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