refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 178 results
Sort by

Filters

Technology

Platform

accession-icon GSE25465
Expression data from SSEA1+ c-kit+ differentiated murine embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

SSEA1+ c-kit+cells sorted from mouse embryonic stem cells differentiated for 4 days in 10uM Retinoic acid do not form teratomas when transplated into SCID mice while Pten-/- cells do.

Publication Title

Loss of Pten causes tumor initiation following differentiation of murine pluripotent stem cells due to failed repression of Nanog.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE76848
Expression data from mouse intestinal organoids II
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

APC inactivation is the early process in the tumorigenesis of colorectal cancer. We established organoid cultures from intestines of genetically modifeid mice harboring Apcfl/fl, Tacc3wt/wt or Apcfl/fl, Tacc3fl/fll and R26CreERT2 allele

Publication Title

Suppression of intestinal tumors by targeting the mitotic spindle of intestinal stem cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE53680
Expression data of macrophage phenotypes treated with interleukin-1alpha
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Identification of the difference in responsiveness to interleukin-1alpha between M1 and M2 macrophage phenotypes.

Publication Title

Perivascular leukocyte clusters are essential for efficient activation of effector T cells in the skin.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE38412
Identification of genes regulated by knockdown of HSF1 or RPA1
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transcription factor access to regulatory elements is prevented by the nucleosome. Heat shock factor 1 (HSF1) is a winged helix transcription factor that plays roles in control and stressed conditions by gaining access to target elements, but mechanisms of HSF1 access have not been well known in mammalian cells. We show a physical interaction between the wing motif of human HSF1 and replication protein A (RPA), which is involved in DNA metabolism. Depletion of RPA1 abolishes HSF1 access to the promoter of HSP70 in unstressed conditions, and delays its rapid activation in response to heat shock. The HSF1-RPA complex leads preloading of RNA polymerase II and opens chromatin structure by recruiting a histone chaperone FACT. Furthermore, this interaction is required for melanoma cell proliferation. These results provide a mechanistic basis for constitutive HSF1 access to nucleosomal DNA, which is important for both basal and inducible gene expression.

Publication Title

RPA assists HSF1 access to nucleosomal DNA by recruiting histone chaperone FACT.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE67418
Expression data from mouse embryonic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In addition to transcriptional regulation, mRNA degradation critically contributes to gene expression as shown by various biological analysis. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation.

Publication Title

CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE68525
Disruption of Cytochrome c Oxidase Function Induces Warburg Effect and Metabolic Reprogramming
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Defects in mitochondrial oxidative phosphorylation complexes, altered bioenergetics and metabolic shift are often seen in cancers. Here we show a role for the dysfunction of electron transport chain component, cytochrome c oxidase (CcO) in cancer progression. We show that genetic silencing of the CcO complex by shRNA expression and loss of CcO activity in multiple cell types from the mouse and human sources resulted in metabolic shift to glycolysis, loss of anchorage dependent growth and acquired invasive phenotypes. Disruption of CcO complex caused loss of transmembrane potential and induction of Ca2+/Calcineurin-mediated retrograde signaling. Propagation of this signaling, includes activation of PI3-kinase, IGF1R and Akt, Ca2+ sensitive transcription factors and also, TGF1, MMP16, periostin that are involved in oncogenic progression. Whole genome expression analysis showed up regulation of genes involved in cell signaling, extracellular matrix interactions, cell morphogenesis, cell motility and migration. The transcription profiles reveal extensive similarity to retrograde signaling initiated by partial mtDNA depletion, though distinct differences are observed in signaling induced by CcO dysfunction. The possible CcO dysfunction as a biomarker for cancer progression was supported by data showing that esophageal tumors from human patients show reduced CcO subunits IVi1 and Vb in regions that were previously shown to be hypoxic core of the tumors. Our results show that mitochondrial electron transport chain defect initiates a retrograde signaling. These results suggest that a defect in CcO complex can potentially induce tumor progression.

Publication Title

Disruption of cytochrome c oxidase function induces the Warburg effect and metabolic reprogramming.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE43378
Expression data from glioma patients
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to select the genes associated glioma patients survival.

Publication Title

Gene expression signature-based prognostic risk score in patients with glioblastoma.

Sample Metadata Fields

Sex, Age, Disease, Disease stage

View Samples
accession-icon SRP097006
Distinct roles for matrix metalloproteinases 2 and 9 in hematopoietic stem cell emergence, migration and niche colonization
  • organism-icon Danio rerio
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We report gene expression data for FACS sorted zebrafish mpeg1:mCherry + and mpx:EGFP + cells collected from whole embryos at 72 hours post fertilization (hpf). We also report gene expression data for the remaining, transgene negative, portion of these embryos. Overall design: ~1,000 mpeg1:mCherry+; mpx:EGFP+ transgenic embryos were homogenized, filtered, and sorted using FACS into PBS, collecting >50,000 cells for each of the three populations: mpeg1:mCherry+, mpx:EGFP+ and double negative (no double positive cells were collected as there was almost no overlap between mCherry and EGFP expression).

Publication Title

Distinct Roles for Matrix Metalloproteinases 2 and 9 in Embryonic Hematopoietic Stem Cell Emergence, Migration, and Niche Colonization.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE99080
Expression data from NRF3 knocked-down DLD-1 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Accumulated evidences suggest physiological relevance between the transcription factor NRF3 (NFE2L3) and cancers. However NRF3 target genes in cancer cells remain poorly understood.

Publication Title

Multiple regulatory mechanisms of the biological function of NRF3 (NFE2L3) control cancer cell proliferation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE26387
Methanol is an endogenous elicitor molecule upon senescence of detached rice leaves
  • organism-icon Oryza sativa
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

During senescence of detached rice leaves, tryptophan (Trp) and Trp-derived secondary metabolites such as serotonin and 4-coumaroylserotonin accumulated in concert with methanol (MeOH) production. This senescence-induced MeOH induction was closely associated with levels of pectin methylesterase (PME)1 mRNA and PME enzyme activity. Exogenous challenge of detached rice leaves with 1% MeOH accelerated Trp and serotonin biosynthesis with induction of the corresponding genes. No other solvents including ethanol resulted in a Trp-inducing effect. This MeOH-induced Trp synthesis was positively regulated by abscisic acid but negatively regulated by cytokinin, suggesting hormonal involvement on the action of MeOH. Endogenous overproduction or suppression of MeOH either by PME1 overexpression or RNAi gene silencing revealed that PME1 overexpressing lines produced twofold higher Trp levels with elevated Trp biosynthetic gene expression, whereas RNAi lines showed twofold reduction in Trp level in healthy control rice leaves, suggesting that MeOH acts as an endogenous elicitor to enhance Trp biosynthesis. Among many transcription factors induced following MeOH treatment, the WRKY family showed significant induction patterns of which WRKY14 appeared to play a key regulatory role in MeOH-induced Trp and Trp-derived secondary metabolite biosynthesis.

Publication Title

Methanol is an endogenous elicitor molecule for the synthesis of tryptophan and tryptophan-derived secondary metabolites upon senescence of detached rice leaves.

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

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