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accession-icon GSE42441
PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE42440
Gene expression profile of KM-H2 cells conditional expressing PU.1
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

PU.1 is an Ets family transcription factor that is essential for the differentiation of both myeloid and lymphoid cells. PU.1 is down-regulated in classical Hodgkin lymphoma cells via methylation of the PU.1 promoter. To evaluate whether down-regulation of PU.1 is essential for the growth of cHL cells, we generated KM-H2 derived cell lines conditionally express PU.1 by tet-off system (designated KM-H2tetPU.1). Conditonally expressed PU.1 by tetracycline removal induced complete growth arrest and apoptosis in KM-H2 cells. To elucidate the mechanisms underlying cell cycle arrest and apoptosis induced by PU.1, we compared gene expression profiles of KM-H2tetPU.1 cells 0, 1 and 3 days after PU.1 induction, by DNA microarray.

Publication Title

PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE109696
ERG and FLI1 in endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.

Sample Metadata Fields

Specimen part

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accession-icon GSE75690
Expression data from CD8alpha positive dendritic cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We screened a number of interferon inducible genes that may be involved in impeding HBV replication and found an anti-HBV activity in ISG20. ISG20 is an IFN-inducible 3- to 5-exonuclease, that degrades DNA and RNA and reduces antigen production in hepatocyte-derived cells

Publication Title

Interferon-stimulated gene of 20 kDa protein (ISG20) degrades RNA of hepatitis B virus to impede the replication of HBV in vitro and in vivo.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE59695
Role of histone lysine demethylase LSD2 in hepatic metabolism
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Lysine-specific demethylase 2 suppresses lipid influx and metabolism in hepatic cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE43762
Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation.

Publication Title

Glioma initiating cells form a differentiation niche via the induction of extracellular matrices and integrin αV.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE109662
Expression data in HUVECs treated with siERG, siFLI1, or both
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Endothelial-to-mesenchymal transition (EndMT) in which endothelial cells lose their characteristics and acquire mesenchymal property has recently been recognized as a driver of disease progression in wide range of pathologies. However, the regulatory mechanism of EndMT has not been fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induced EndMT. Hence, we analyzed functions of ERG and FLI1 using gene expression microarray and ChIP-seq to elucidate the regulatory mechanism of EndMT.

Publication Title

Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE100589
Gene expression profiling of SAS cell line transfected with siRNA targeting CYLD
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oral squamous cell carcinoma (OSCC) has a very poor prognosis due to its highly invasive nature, and 5-year survival rate has not changed apparently for the past 30 years. Although cylindromatosis (CYLD) is thought as a potent tumor suppressor, its biological and clinical significances in OSCC are largely unknown. The aim of this study was to clarify roles of CYLD in OSCC progression. Our immunohistochemical analyses revealed that CYLD expression was significantly reduced at invasive lesions in OSCC tissues whereas it was conserved in normal epithelium and carcinoma in situ. Accordingly, downregulation of CYLD by siRNA led to an acquisition of mesenchymal state and increased migratory and invasive activities in OSCC cells and HaCaT keratinocytes. Interestingly, CYLD knockdown promoted TGF-beta signaling by inducing TGF-beta receptor I (ALK5) stabilization in a cell autonomous fashion. In addition, the response to exogenous TGF-beta stimulation was enhanced by CYLD downregulation. The invasive phenotype induced by CYLD knockdown were completely blocked by an ALK5 inhibitor. Furthermore, lower CYLD expression was significantly associated with deep invasion, poor overall survival, and increased Smad3 phosphorylation which is an indicator of TGF-beta signaling activation in invasive OSCC. These findings suggest that downregulation of CYLD promotes invasion with mesenchymal transition via ALK5 stabilization in OSCC cells.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE18600
Importance of histone demethylation in adipogenic differentiation and function
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56645
Transcriptome analysis of LSD2-depleted HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcriptome analysis of LSD2-depleted HepG2 cells revealed that many of the target genes were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism.

Publication Title

Lysine-specific demethylase 2 suppresses lipid influx and metabolism in hepatic cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
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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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