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accession-icon GSE26933
Effects of polyglutamine expansion and subcellular localization of C-terminal fragment of Cav2.1 in PC12 rat pheochromocytoma cells
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Polyglutamine(polyQ) expansion of 1A voltage-dependent calcium channel (Cav2.1) is the causative mutation of spinocerebellar ataxia type 6 (SCA6). The C-terminal fragment (CTF) of Cav2.1 makes aggregates in the cytoplasm of SCA6 Purkinje cells and may relate to the pathogenesis. In order to identify genes associated with polyQ expansion and subcellular localization of CTF, we analyzed gene expression profiles of PC12 rat pheochromocytoma cells using Tet-off system.

Publication Title

Cytoplasmic location of α1A voltage-gated calcium channel C-terminal fragment (Cav2.1-CTF) aggregate is sufficient to cause cell death.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP186416
RNA-sequencing of Wnt-dependent and Wnt-independent of Glioblastoma stem cell cultures
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Four Wnt-dependent and four Wnt-independent GSC cultures were grown in stem cell media and RNA expression between the two subsets evaluated Overall design: Four biological replicates each of Wnt-dependent and Wnt-independent GSC cultures

Publication Title

Wnt and Notch signaling govern self-renewal and differentiation in a subset of human glioblastoma stem cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE35108
Expression data from patient iPSC and iPSC-derived cardiomyocytes
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Dilated cardiomyopathy (DCM) is the leading cause of heart failure and transplantation worldwide. We used iPSCs to model this disease and compared gene expression change before and after gene therapy of cardiomyocytes derived from DCM-specific iPSCs.

Publication Title

Patient-specific induced pluripotent stem cells as a model for familial dilated cardiomyopathy.

Sample Metadata Fields

Specimen part

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accession-icon GSE62714
Gene expression data from PNU 96415E treated human glioblastoma derived neural stem cells (GNS)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Glioblastomas grow in a rich neurochemical mileu, but targeting neurochemical signaling as a potential therapeutic avenue for these incurable tumors has been underexplored. Thus, we probed patient derived glioblastoma stem cells with a focused library of neurochemicals, to identify new therapeutic targets. Dopaminergic, serotonergic and cholinergic pathways were found to be active against glioblastoma. In particular, dopamine receptor D4 (DRD4) antagonists selectively inhibited glioblastoma growth in vitro and in vivo, in addition to showing synergistic effect with temozolomide. Small molecule or genetic antagonism of DRD4 suppressed ERK1/2 signaling and impaired autophagic flux causing accumulation of autophagic vacuoles and ubiquitinated proteins, associated with G0/G1 cell cycle arrest. These data suggest a new mechanism for treating glioblastoma through modulating dopamine DRD4 signaling.

Publication Title

Inhibition of Dopamine Receptor D4 Impedes Autophagic Flux, Proliferation, and Survival of Glioblastoma Stem Cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP147557
Mechanism sharing between genetic and gestational hypoxia-induced cardiac anomalies
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: Mutations in several genetic loci lead to cardiac anomalies, with mutations in transcription factor NKX2-5 gene being one of the largest mutations known. Gestational hypoxia, such as seen in high-altitude pregnancy, has been known to affect cardiac development, and this paper aims to uncover information about the underlying mechanisms of this phenomena. Methods: Wild-type female mice were mated with Nkx2-5 mutant males, to produce offsprings. The pregnant females were then separated into two groups, one left in normal air and one breathing hypoxic, 14% oxygen, air from gestation day 10.5 to 12.5. Hearts were dissected from E12.5 embryos, subjected to RNA purification followed by RNA-seq. Wild-hypoxia and mutant-normoxia were compared to control wild-normoxia. Conclusions: The results of our study provide insights into a common molecular mechanism underlying non-genetic/epigenetic and genetic cardiac anomalies. Overall design: Embryonic mice were produced with either wild-type or mutant genomes, and some from each group were exposed to hypoxia during gestation, then physical analysis and RNA sequencing was done on the embryos.

Publication Title

Mechanism Sharing Between Genetic and Gestational Hypoxia-Induced Cardiac Anomalies.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE58331
Gene expression in human orbit
  • organism-icon Homo sapiens
  • sample-icon 168 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Diagnosis of inflamed human orbit tissue with standard clinical and histopathology evaluation data is imprecise. A large number of these patients are diagnosed with the catch-all classification of nonspecific orbital inflammation (NSOI).

Publication Title

Orbital pseudotumor can be a localized form of granulomatosis with polyangiitis as revealed by gene expression profiling.

Sample Metadata Fields

Sex, Specimen part, Disease

View Samples
accession-icon GSE104003
Analysis of transcriptome changes arising from MIR205HG modulation in prostate cells
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE103655
Effects of deletion of a portion of the Alu element from MIR205HG transcript
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We aimed at analyzing the transcriptome changes associated with the deletion of a portion of the Alu element from MIR205HG transcript

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE103656
Effects of MIR205HG silencing
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE105149
Gene Expression in the Human Lacrimal Gland
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Diagnosis of inflamed human lacrimal gland with standard clinical and histopathology evaluation data is imprecise. A large number of these patients are diagnosed with the catch-all classification of nonspecific orbital inflammation (NSOI).

Publication Title

Gene Expression Profiling and Heterogeneity of Nonspecific Orbital Inflammation Affecting the Lacrimal Gland.

Sample Metadata Fields

Sex, Specimen part, Disease

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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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