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accession-icon GSE30654
Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Recurrent variations in DNA methylation in human pluripotent stem cells and their differentiated derivatives.

Sample Metadata Fields

Sex, Specimen part, Disease, Cell line, Subject

View Samples
accession-icon GSE30652
Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives [Illumina HT12v3 Gene Expression]
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Human pluripotent stem cells (hPSCs) are potential sources of cells for modeling disease and development, drug discovery, and regenerative medicine. However, it is important to identify factors that may impact the utility of hPSCs for these applications. In an unbiased analysis of 205 hPSC and 130 somatic samples, we identified hPSC-specific epigenetic and transcriptional aberrations in genes subject to X chromosome inactivation (XCI) and genomic imprinting, which were not corrected during directed differentiation. We also found that specific tissue types were distinguished by unique patterns of DNA hypomethylation, which were recapitulated by DNA demethylation during in vitro directed differentiation. Our results suggest that verification of baseline epigenetic status is critical for hPSC-based disease models in which the observed phenotype depends on proper XCI or imprinting, and that tissue-specific DNA methylation patterns can be accurately modeled during directed differentiation of hPSCs, even in the presence of variations in XCI or imprinting.

Publication Title

Recurrent variations in DNA methylation in human pluripotent stem cells and their differentiated derivatives.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE59484
Expression data for miR-33a over-expression in CD133-negative D456MG cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

MiR-33a is involved in the maintenance of Glioma Initiating Cells (GIC) and tumor progression. MicroRNA-33a could promote GIC growth and self-renewal by regulating two pathways including cAMP/PKA pathway and Notch pathway. We used microarrays to identify the direct target genes of miR-33a in a glioblastoma cell line D456MG.

Publication Title

miR-33a promotes glioma-initiating cell self-renewal via PKA and NOTCH pathways.

Sample Metadata Fields

Cell line

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accession-icon SRP064317
Expression data for KDM1B knockdown in Glioma-Initiating Cells (GICs)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. KDM1B is involved in regulating GICs'' responses to hypoxia, since over-expression of KDM1B delays the cell growth under hypoxia while knocking-down of KDM1B in GICs promotes their survival and tumorigenic abilities. Overall design: We used RNA-Sequencing to detail the global change of gene expression in GICs with knockdown of KDM1B, and identified de-regulated genes and pathways downstream of KDM1B. CD133+ D456MG GICs were infected with non-targeting control and shRNA of KDM1B. Then RNA was extracted and gene expression was profiled by RNA-Seq.

Publication Title

MiR-215 Is Induced Post-transcriptionally via HIF-Drosha Complex and Mediates Glioma-Initiating Cell Adaptation to Hypoxia by Targeting KDM1B.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15918
Torcetrapib induces aldosterone and cortisol production in an intracellular calcium-dependent mechanism
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

ILLUMINATE (Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events), the phase 3 morbidity and mortality trial of torcetrapib, a cholesteryl ester transfer protein (CETP) inhibitor, identified previously undescribed changes in plasma levels of potassium, sodium, bicarbonate, and aldosterone. A key question after this trial is whether the failure of torcetrapib was a result of CETP inhibition or of some other pharmacology of the molecule. The direct effects of torcetrapib and related molecules on adrenal steroid production were assessed in cell culture using the H295R as well as the newly developed HAC15 human adrenal carcinoma cell lines. Torcetrapib induced the synthesis of both aldosterone and cortisol in these two in vitro cell systems. Analysis of steroidogenic gene expression indicated that torcetrapib significantly induced the expression of CYP11B2 and CYP11B1, two enzymes in the last step of aldosterone and cortisol biosynthesis pathway, respectively. Transcription profiling indicated that torcetrapib and angiotensin II share overlapping pathways in regulating adrenal steroid biosynthesis. Hormone-induced steroid production is mainly mediated by two messengers, calcium and cAMP. An increase of intracellular calcium was observed after torcetrapib treatment, whereas cAMP was unchanged. Consistent with intracellular calcium being the key mediator of torcetrapibs effect in adrenal cells, calcium channel blockers completely blocked torcetrapib-induced corticoid release and calcium increase. A series of compounds structurally related to torcetrapib as well as structurally distinct compounds were profiled. The results indicate that the pressor and adrenal effects observed with torcetrapib and related molecules are independent of CETP inhibition.

Publication Title

Torcetrapib induces aldosterone and cortisol production by an intracellular calcium-mediated mechanism independently of cholesteryl ester transfer protein inhibition.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon GSE40584
Analysis of Nkx2-1-regulated gene expression in A549 lung carcinoma cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A transcription factor Nkx2-1 (also known as TTF-1) regulates the expression of different sets of genes. Gene expression analysis was performed using mRNAs from Nkx2-1-induced A549 cells compared to that from the control A549 cells. We used microarrays to detail the global program of gene expression controlled by Nkx2-1 and identified distinct classes of up-regulated and down-regulated genes.

Publication Title

Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.

Sample Metadata Fields

Cell line

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accession-icon GSE40508
Expression data of mouse mucinous lung tumors
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice.

Publication Title

Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.

Sample Metadata Fields

Specimen part

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accession-icon E-MEXP-891
Transcription profiling by array of mammary gland from Akt1 knock-out mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

A comparison of gene expression in the mammary gland of lactating mice at day 9 after parturition between Akt -/- and wildtype individuals.

Publication Title

Isoform-specific requirement for Akt1 in the developmental regulation of cellular metabolism during lactation.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

View Samples
accession-icon SRP063496
Gene expression of baseline biopsies from etrolizumab-treated ulcerative colitis (UC) patients
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

RNA sequencing was performed on RNA isolated from baseline biopsies from UC patients enrolled in the Phase II EUCALYPTUS study of etrolizumab. Gene expression differences were identified in a subset of anti-TNF naïve patients that achieved clinical remission at 10 weeks in response to etrolizumab. Overall design: Baseline colonic biopsies from UC patients treated with etrolizumab were sequenced by the Illumina HiSeq 2000 Sequencing System.

Publication Title

Association Between Response to Etrolizumab and Expression of Integrin αE and Granzyme A in Colon Biopsies of Patients With Ulcerative Colitis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE49283
Translational activation of developmental mRNAs during neonatal mouse testis development
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The sequence of gene regulatory events that drive neonatal germ cell development in the mammalian testis is not yet clear. We assessed changes in mRNA utilization in the neonatal testis at 1 and 4 dpp, times when the testis contains quiescent gonocytes (1 dpp) and proliferating spermatogonia (4 dpp). There are not thought to be major changes in the nature or number of somatic cells over that interval.

Publication Title

Translational activation of developmental messenger RNAs during neonatal mouse testis development.

Sample Metadata Fields

Age, 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)

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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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