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accession-icon GSE65480
Expression data at each site in colon cancer
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Colon cancer invade to depper layer and the expression of major molecules at cancer front change. But the screening of expression changing at cancer front has not be adequtely clarified.

Publication Title

Microarray Analysis of Gene Expression at the Tumor Front of Colon Cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE27881
Effect of ablation of Max gene expression on ES cells cultured under conventional or 2i/Nam condition.
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

c-Myc is one of key players that are crucially involved in maintaining the undifferentiated state and the self-renewal of ESCs. To understand the mechanism by which c-Myc helps preserve these prominent characteristics of ESCs, we generated null-ES cells for the Max gene, which encodes the best characterized partner protein for all Myc family proteins. Although Myc/Max complexes have been widely regarded as crucial regulators of the ESC status, our data reveal that ESCs do not absolutely require these complexes in so-called ground state or related conditons and that this requirement is restricted to conventional ES culture conditions without using a MAPK inhibitor.

Publication Title

Indefinite self-renewal of ESCs through Myc/Max transcriptional complex-independent mechanisms.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE37917
Sirt1, p53 and p38MAPK are crucial regulators of detrimental phenotypes of ESCs with Max expression ablation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ablation of expression of the Max gene encoding a Myc protein partner in ES cells provoked two major phenomena, i.e. loss of pluripotency and apoptotic cell death. We found that nicotinamide (Nam) significantly alleviates these Max expression ablation-coupled phenotypes in ES cells. To see the alleviation effect of Nam on the overall expression profile of Max-null ES cells whose Max expression is controlled by the tet-off system, we eliminated Max expression by adding doxycycline (Dox) in the presence of Nam.

Publication Title

Sirt1, p53, and p38(MAPK) are crucial regulators of detrimental phenotypes of embryonic stem cells with Max expression ablation.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE59410
Expression data from heterotopically grafted mouse small intestinal epithelium and the normal colonic epithelium
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Epithelia of small and large intestines differ in their structures and functions. Such heterogeneity between these two epithelial tissues might be controlled by both epithelium-intrinsic and -extrinsic programs. By employing the cell transplantation technique developed in our laboratory, we investigated how adult SI epithelial cells behave when heterotopically transplanted onto colon. Then the gene expression profiles of small intestinal epithelium heterotopically transplanted onto colon and control colonic epithelium were compared.

Publication Title

Small intestinal stem cell identity is maintained with functional Paneth cells in heterotopically grafted epithelium onto the colon.

Sample Metadata Fields

Specimen part

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accession-icon SRP009882
mRNA-seq and expression profile of mouse ES OS25 cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

mRNA-seq and expression profile of mouse ES OS25 cells Overall design: Gene expression (mRNA-Seq) in mouse ES cells

Publication Title

Polycomb associates genome-wide with a specific RNA polymerase II variant, and regulates metabolic genes in ESCs.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP152857
Functional characteristics of novel pancreatic Pax6 regulatory using a mouse pancreatic cell model
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptome profiling using RNA-seq of ß-TC3 cell, a mouse pancreatic cell line used in the study of novel Cis-regulatory elements for the Pax6 gene . Overall design: Total RNA was collected and a Illumina sequencing libraries prepared from two biological replicates of cultured ß-TC3 cells.

Publication Title

Functional characteristics of novel pancreatic Pax6 regulatory elements.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE32547
Expression data of HUVEC cells after statin treatment
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, statins, are known to exert endothelial athero-protective effects through the induction of specific transcriptional factors and their downstream target genes besides lowering LDL-cholesterol. However its critical mechanism has not still been elucidated. Here we report the comprehensive change of transcripts induced by pitavastatin.

Publication Title

Direct evidence for pitavastatin induced chromatin structure change in the KLF4 gene in endothelial cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE32693
Expression data of statin treated HUVEC cells transfected siRNA KLF2 or KLF4.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

KLF2 and KLF4 are important transcriptional factors in endothelial cells, however their roles in statin treatment has not been elucidated. Here we report the comprehensive change of transcripts of statin treated HUVECs transfected with siRNA KLF2 or KLF4.

Publication Title

Direct evidence for pitavastatin induced chromatin structure change in the KLF4 gene in endothelial cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE30540
A new classification of chromosome instability (CIN) phenotype, CIN-high and CIN-low
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Samples were taken from colorectal cancers in surgically resected specimens in 35 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype.

Publication Title

Chromosomal instability (CIN) phenotype, CIN high or CIN low, predicts survival for colorectal cancer.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE34489
A new classification of chromosome instability (CIN) phynotype, CIN-high and CIN-low (validation dataset)
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Samples were taken from colorectal cancers in surgically resected specimens in 33 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype

Publication Title

Chromosomal instability (CIN) phenotype, CIN high or CIN low, predicts survival for colorectal cancer.

Sample Metadata Fields

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

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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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