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accession-icon GSE71272
Paracrine effects of estrogen on 231BR cells, through ER+ astrocytes
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

The objective of this study was to determine the extent to which paracrine action of 17-beta-estradiol on ER+ mouse astrocytes, affect gene expression of MDA231-derived brain trophic 231BR cells.

Publication Title

No associated publication

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE108607
SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Luminal breast cancers express estrogen (ER) and progesterone (PR) receptors, and respond to endocrine therapies. However, some ER+PR+ tumors display intrinsic or acquired resistance, possibly related to PR. Two PR isoforms, PR-A and PR-B, regulate distinct gene subsets that may differentially influence tumor fate. A high PR-A:PR-B ratio is associated with poor prognosis and tamoxifen resistance. We speculate that excessive PR-A marks tumors that will relapse early. Here we address mechanisms by which PR-A regulate transcription, focusing on SUMOylation. We use receptor mutants and synthetic promoter/reporters to show that SUMOylation deficiency or the deSUMOylase SENP1 enhance transcription by PR-A, independent of the receptors dimerization interface or DNA binding domain. De-SUMOylation exposes the agonist properties of the antiprogestin RU486. Thus, on synthetic promoters, SUMOylation functions as an independent brake on transcription by PR-A. What about PR-A SUMOylation of endogenous human breast cancer genes? To study these, we used gene expression profiling. Surprisingly, PR-A SUMOylation influences progestin target genes differentially, with some upregulated, others downregulated, and others unaffected. Hormone-independent gene regulation is also PR-A SUMOylation dependent. Several SUMOylated genes were analyzed in clinical breast cancer database. In sum, we show that SUMOylation does not simply repress PR-A. Rather, it regulates PR-A activity in a target selective manner including genes associated with poor prognosis, shortened survival, and metastasis.

Publication Title

SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE55232
Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart
  • organism-icon Homo sapiens
  • sample-icon 129 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE55231
Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart: gene expression
  • organism-icon Homo sapiens
  • sample-icon 129 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

In recent years genome-wide association studies (GWAS) have uncovered numerous chromosomal loci associated with various electrocardiographic traits and cardiac arrhythmia predisposition. A considerable fraction of these loci lie within inter-genic regions. Trait-associated SNPs located in putative regulatory regions likely exert their effect by modulating gene expression. Hence, the key to unraveling the molecular mechanisms underlying cardiac traits is to interrogate variants for association with differential transcript abundance by expression quantitative trait locus (eQTL) analysis. In this study we conducted an eQTL analysis of human heart. To this end, left ventricular mycardium samples from non-diseased human donor hearts were hybridized to Illumina HumanOmniExpress BeadChips for genotyping (n = 129) and Illumina Human HT12 Version 4 BeadChips (n = 129) for transcription profiling.

Publication Title

Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE141515
6 Gy gamma-irradiation of mouse small intestinal organoids at 24h, 48h and 96h after irradiation
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The intact intestinal epithelial barrier protects our body from a range of immune mediated diseases. The epithelial layer has an impressive ability to reconstitute and repair upon damage and this process of repair is increasingly seen as a therapeutic target. In vitro models to study this process in primary intestinal cells are lacking. Therefore we established and characterized an in vitro model of intestinal damage and repair by applying γ-radiation on small intestinal organoids. We then used this model to identify novel regulators of intestinal regeneration.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE9150
Primary nasal epithelium exposed to house dust mite extract shows activated expression in allergics
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Response to allergen was studied in epithelial cells derived from allergic pantients and from healthy controls. Cells were cultured after isolation from a nasal biopsy. Cells were exposed to Housed dust mite or vessel (saline)

Publication Title

Primary nasal epithelium exposed to house dust mite extract shows activated expression in allergic individuals.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE143509
Driver mutations of the adenoma-carcinoma sequence govern the intestinal epithelial global translational capacity.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

In colorectal cancer, the role of the most common driver mutations in APC, KRAS, SMAD4 and TP53, on global mRNA translation are incompletely understood. To adress this, we generated and characterised mouse intestinal organoid models with oncogenic mutations in each of these genes using Cre-Lox recombination in ex vivo organoid cultures combined with stable expression of short hairpin RNAs. Microarray analysis was used to characterise transcriptomic reprogramming that supports altered global translation rates in mutant cells.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE142065
ATF2 and ATF7 mediation of intestinal repair in murine colitis model
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

AP1 transcription factor family members: activating transcription factor 2 (ATF2) and activating transcription factor 7 (ATF7) have highly redundant functions due to homology and hence overlapping DNA-binding sites. The role of these transcription factors in intestinal epithelial homeostasis and repair has not been critically examined. Here, by using an intestine-specific deletion of ATF2 combined with body wide deletion of ATF7 in mice we assess the role of these proteins during intestinal homeostasis and repair after inflammation.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE141518
Small intestinal tissue 96h after 14 Gy whole body gamma-irradiation of VillinCreERT2 Hnf4a knockout mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This experiment was performed to assess the effect of loss of Hnf4a in the intestinal epithelium on the regeneration process after irradiation. Intestinal epithelium specific knockout was obtained by oral adminstration of tamoxifen to VillinCreERT2+-Hnf4afl/fl mice and VillinCreERT2--Hnf4afl/fl mice (which served as controls). 3 weeks after the tamoxifen administration, mice received 14 Gy whole-body gamma-irradiation. RNA was extracted from small intestinal tissue 96 hours after irradiation.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE6406
Effect on gene expression after administration of siRNA/siLNA targeting GFP
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

siRNA mediated gene knockdown has been shown to be extremely sequence specific. However, off-target gene regulation due to partial sequence homology has also been reported. Furthermore, sequence unrelated effects on gene regulation can occur when siRNA is applied in vivo. In this experiment we investigated off target gene regulation due to treatment of mice with siRNA and LNA modified siRNA targeting GFP. Off target gene regulation was observed and was markedly reduced upon introduction of LNA modifiecation in siRNA.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
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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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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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