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accession-icon E-MEXP-1282
Transcription profiling by array of grape cultivar Pinot Noir berry development during three seasons
  • organism-icon Vitis vinifera
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Vitis vinifera (Grape) Genome Array (vitisvinifera)

Description

Global gene expression analysis of grapevine cv. Pinot Noir berries during development and ripening. Time-course comparison of samples collected at three developmental stages (stages 33, 34 and 36 according to the modified E-L system, ref: Coombe BG, Aust J Grape Wine Res 1995, 1: 104-110) during three seasons (2003, 2005 and 2006).

Publication Title

Genome-wide transcriptional analysis of grapevine berry ripening reveals a set of genes similarly modulated during three seasons and the occurrence of an oxidative burst at vèraison.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon GSE31674
Pinot Noir berry transcriptome during ripening.
  • organism-icon Vitis vinifera
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Vitis vinifera (Grape) Genome Array (vitisvinifera)

Description

Global gene expression analysis of grapevine cv. Pinot Noir berries during development and ripening. Time-course comparison of samples collected at three developmental stages (stages 33, 34 and 36 according to the modified E-L system, ref: Coombe BG, Aust J Grape Wine Res 1995, 1: 104-110) during three seasons (2003, 2005 and 2006). Data for each of the three seasons were normalized independently within each season, using gcRMA.

Publication Title

Genome-wide transcriptional analysis of grapevine berry ripening reveals a set of genes similarly modulated during three seasons and the occurrence of an oxidative burst at vèraison.

Sample Metadata Fields

Specimen part

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accession-icon GSE60578
Regulatory logic of the coupled diurnal and feeding cycles in the mouse liver
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study is a follow-up to GSE35790.

Publication Title

Transcriptional regulatory logic of the diurnal cycle in the mouse liver.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE14807
Investigation of over-expressing Annexin receptor cell line with and without agonists
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The therapeutic potential of pro-resolution factors in determining the outcome of inflammatory events has gained ground over the past decade. However, the attention has been focused on the non-genomic effects of these endogenous, anti-inflammatory substances. In this study, we have focused our attention on identifying specific annexin 1 (AnxA1) protein/ALX receptor mediated gene activation, in an effort to identify down-stream genomic targets of this well-known, glucocorticoid induced, pro-resolution factor.

Publication Title

Downstream gene activation of the receptor ALX by the agonist annexin A1.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP166961
Linking YAP to Müller glia quiescence exit in the degenerative retina
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

Contrasting with fish or amphibian, retinal regeneration from Müller glial cells is largely limited in mammals. In our quest towards the identification of molecular cues that may boost their stemness potential, we investigated the involvement of the Hippo pathway effector YAP, which we previously found to be upregulated in Müller cells following retinal injury. We report that conditional Yap deletion in Müller cells prevents the upregulation of cell cycle genes that normally accompanies reactive gliosis upon photoreceptor cell death. This occurs as a consequence of defective EGFR signaling. Consistent with a function of YAP in triggering Müller glia cell cycle re-entry, we further show that in Xenopus, a species endowed with efficient regenerative capacity, YAP is required for their injury-dependent proliferative response. Finally, and noteworthy, we reveal that YAP overactivation in mouse Müller cells is sufficient to induce their reprogramming into highly proliferative cells. Overall, we unravel a pivotal role for YAP in tuning Müller cell response to injury and highlight a novel YAP-EGFR axis by which Müller cells exit their quiescence state, a critical step towards regeneration. Overall design: Retinal samples were harvested from Yapflox/flox; Rax-CreERT2 mouse line allowing for Cre-mediated conditional gene ablation specifically in Müller cells. It is named Yap CKO while “control” refers to Yapflox/flox mice. Yap deletion was induced in fully differentiated Müller cells, through 4-hydroxytamoxifen (4-OHT) intraperitoneal injection at P10. All animals were injected with 4-OHT. Each sample included 1 frozen retina and experiments were performed in triplicate. RNA-seq transcriptome libraries were constructed from 1 ug of total RNA.

Publication Title

Linking YAP to Müller Glia Quiescence Exit in the Degenerative Retina.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE42902
FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Glucocorticoid excess is linked to central obesity, adipose tissue insulin resistance and type 2 diabetes mellitus. The aim of our study was to investigate the effects of dexamethasone on gene expression in human subcutaneous and omental adipose tissue, in order to identify potential novel mechanisms and biomarkers for glucocorticoid-induced insulin resistance in adipose tissue. Dexamethasone changed the expression of 527 genes in both subcutaneous and omental adipose tissue. FKBP5 and CNR1 were the most responsive genes in both depots (~7-fold increase). Dexamethasone increased FKBP5 gene and protein expression in a dose-dependent manner in both depots, but FKBP5 protein levels were 10-fold higher in omental than subcutaneous adipose tissue. FKBP5 gene expression in subcutaneous adipose tissue was positively correlated with serum insulin, HOMA-IR and subcutaneous adipocyte diameter, while fold change in gene expression by dexamethasone was negatively correlated with clinical markers of insulin resistance, i.e. HbA1c, BMI, HOMA-IR and serum insulin. Only one gene, SERTM1, clearly differed in response to dexamethasone between the two depots. Dexamethasone at high concentrations, influences gene expression in both subcutaneous and omental adipose tissue in a similar pattern and promotes gene expression of FKBP5, a gene that may be implicated in glucocorticoid-induced insulin resistance.

Publication Title

FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE7948
In vitro modeling of primordial germ cell development
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transgenic StellaGFP ESCs were used to derive primordial germ cells during embryoid body (EB) differentiation, and microarry analysis used to compared FACS sorted Stella-positive cells of day 7 Ebs with the parental ESCs and Stella-negative cells of day 7 Ebs.

Publication Title

A role for Lin28 in primordial germ-cell development and germ-cell malignancy.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP078060
Regulators of cellular heterogeneity in basal-like breast cancer influence symmetric versus asymmetric division rates (shRNA targeting)
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Differentiation events contribute to cellular heterogeneity within tumors and influence disease progression and response to therapy. Here we dissect the mechanisms controlling intratumoral heterogeneity within basal-like breast cancers. We show that cancer cells can transition between a differentiation state related to that of normal luminal progenitors and a state closer to that of mature luminal cells, and that this occurs through asymmetric cell divisions. The Polycomb factor EZH2 and the Notch pathway act to increase the rates of symmetric divisions that produce progenitor-like cells, while the FOXA1 transcription factor promotes asymmetric divisions that reduce the numbers of such cells. Through functional screening, we identified a group of regulators that control cancer cell differentiation state and the relative proportions of tumor cell subpopulations. Our findings highlight the regulation of asymmetric cell divisions as a mechanism controlling intratumoral heterogeneity, and identify molecular pathways that control breast cancer cellular composition. Overall design: Expression profiles of HCC70 cells expressing shRNAs targeting regulatory factors that influence basal-like cancer cell population composition

Publication Title

Regulation of Cellular Heterogeneity and Rates of Symmetric and Asymmetric Divisions in Triple-Negative Breast Cancer.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP077979
Regulators of cellular heterogeneity in basal-like breast cancer influence symmetric versus asymmetric division rates (Expression profiles)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Differentiation events contribute to cellular heterogeneity within tumors and influence disease progression and response to therapy. Here we dissect the mechanisms controlling intratumoral heterogeneity within basal-like breast cancers. We show that cancer cells can transition between a differentiation state related to that of normal luminal progenitors and a state closer to that of mature luminal cells, and that this occurs through asymmetric cell divisions. The Polycomb factor EZH2 and the Notch pathway act to increase the rates of symmetric divisions that produce progenitor-like cells, while the FOXA1 transcription factor promotes asymmetric divisions that reduce the numbers of such cells. Through functional screening, we identified a group of regulators that control cancer cell differentiation state and the relative proportions of tumor cell subpopulations. Our findings highlight the regulation of asymmetric cell divisions as a mechanism controlling intratumoral heterogeneity, and identify molecular pathways that control breast cancer cellular composition. Overall design: Expression profiles of three cell subpopulations – K18+, K18+K14+ and K18+Vim+ – sorted from the breast cancer cell lines HCC70 and MDA-MB-468

Publication Title

Regulation of Cellular Heterogeneity and Rates of Symmetric and Asymmetric Divisions in Triple-Negative Breast Cancer.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE19383
Altered gene expression in normal breast and ovarian epithelial cells from BRCA1 and BRCA2 mutation carriers
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Early genetic changes during cancer initiation may provide targets for agents that delay, or even prevent, cancer. We hypothesized that cells bearing a single inherited hit in a tumor suppressor gene express an altered mRNA repertoire that may identify targets for measures that could delay or even prevent progression to carcinoma. Here, we report on the transcriptomes of primary breast and ovarian epithelial cells cultured from BRCA1 and BRCA2 mutation-carriers and controls. Our comparison analyses identified multiple changes in gene expression, in both tissues for both mutations that were independently validated by real-time RT-PCR analysis. Several of the differentially expressed genes had been previously proposed as cancer markers including, mammaglobin in breast cancer and serum amyloid in ovarian cancer. These findings demonstrate that heterozygosity for a mutant tumor suppressor gene can alter the expression profiles of phenotypically normal epithelial cells in a gene-specific manner, and that these detectable effects of one-hit represent early molecular changes in tumorigenesis that may serve as novel biomarkers of cancer risk and as targets for chemoprevention

Publication Title

Altered gene expression in morphologically normal epithelial cells from heterozygous carriers of BRCA1 or BRCA2 mutations.

Sample Metadata Fields

Specimen part

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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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