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accession-icon E-TABM-585
Transcription profiling by array of human lung cancer cells after treatment with dasatinib, imatinib, nilotinib or PD0325901
  • organism-icon Homo sapiens
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.

Publication Title

Transcriptional profiling of the dose response: a more powerful approach for characterizing drug activities.

Sample Metadata Fields

Disease, Cell line, Compound, Time

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accession-icon E-TABM-450
Transcription profiling by array of human lung cancer cells after treatment with various inhibitors of LIMK1 and LIMK2
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To investigate an unknown mechanism of cytotoxicity, A549 human lung-cancer cells were treated with compounds from a series of inhibitors developed against the human LIM kinases LIMK1 and LIMK2. Compounds 1 and 2 inhibit LIM kinase activity in vitro and affect cell proliferation and survival in vivo. Compounds 3 and 4 inhibit LIM kinases but do not affect cell survival or proliferation. Compounds 5 and 6 affect proliferation and survival but do not inhibit LIM kinases. Nocodazole was included as a comparator because the compounds were known to affect microtubule stability. A treatment of 7 hours was used to examine events prior to apoptosis, while the dose levels captured both cytotoxicity and inhibition of LIMKs (Compounds 1 and 2), LIMK inhibition alone ( Compounds 3 and 4) or cytotoxicity alone (Compounds 5, 6, and Nocodazole).

Publication Title

Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors.

Sample Metadata Fields

Cell line, Subject, Compound

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accession-icon GSE23711
Expression profiling of nhp6 mutants and wildtype yeast cells (Saccharomyces cerevisiae)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The basic unit of genome packaging is the nucleosome, and nucleosomes have long been proposed to restrict DNA accessibility both to damage and to transcription. However, nucleosome number in cells was considered fixed, and no condition was described where nucleosome number was reduced. We show here that mammalian cells lacking High Mobility Group Box 1 protein (HMGB1) contain a reduced amount of core, linker and variant histones, and a correspondingly reduced number of nucleosomes. Yeast nhp6 mutants lacking NHP6A and B proteins, which are related to HMGB1, also have a reduced amount of histones and fewer nucleosomes. Nucleosome limitation in both mammalian and yeast cells increases the sensitivity of DNA to damage, increases transcription globally, and the relative expression of about 10% of genes. In yeast nhp6 cells the loss of more than one nucleosome in four does not affect the location of nucleosomes and their spacing, but nucleosomal occupancy. The decrease in nucleosomal occupancy is non-uniform, and our results can be modelled assuming that different nucleosomal sites compete for the available histones: sites with high affinity are almost always packaged into nucleosomes both in wt and nucleosome-depleted cells, whereas sites with low affinity are less frequently packaged in nucleosome-depleted cells. We suggest that by modulating the occupancy of nucleosomes histone availability may constitute a novel layer of epigenetic regulation.

Publication Title

Substantial histone reduction modulates genomewide nucleosomal occupancy and global transcriptional output.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE110545
Transcriptome data from Eomes-overexpressing Th17 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Th17 cells were sorted ex vivo from PB of healthy donors as CD4+CD161+CCR6+CXCR3-. Following, cells were transduced with a lentiviral vector carrying the Eomes gene or with an empty vector. Infected cells were then enriched by MACS separation using the reporter gene NGFR as selection marker. Finally, cells were frozen for RNA analysis.

Publication Title

Eomes controls the development of Th17-derived (non-classic) Th1 cells during chronic inflammation.

Sample Metadata Fields

Cell line

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accession-icon GSE31189
Molecular Biomarker Signature for Bladder Cancer Detection
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study we applied differential gene expression analysis to exfoliated human urothelia obtained from patients of known bladder disease status. Selected targets from the microarray data were validated in an independent set of samples using a quantitative PCR approach.

Publication Title

A candidate molecular biomarker panel for the detection of bladder cancer.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE24917
Genome wide gene expression profiles of Drosophila l(3)mbt larval brains and cultured tumors
  • organism-icon Drosophila melanogaster
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Mutants in the Drosophila gene lethal (3) malignant brain tumor cause malignant growth in the larval brain. This data shows the changes in gene expression profile associated to mutations in l(3)mbt, both in situ in third instar larval brains and in tumors cultured for 1 5 and 10 (T1, T5, T10) rounds of allograft culture

Publication Title

Ectopic expression of germline genes drives malignant brain tumor growth in Drosophila.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25316
FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

FOXA1 is a key determinant of estrogen receptor function and endocrine response.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE25314
FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part I)
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts.

Publication Title

FOXA1 is a key determinant of estrogen receptor function and endocrine response.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE25315
FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part II)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts.

Publication Title

FOXA1 is a key determinant of estrogen receptor function and endocrine response.

Sample Metadata Fields

Treatment

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accession-icon SRP031504
RNA-seq transcriptome profiling of equine inner cell mass and trophectoderm
  • organism-icon Equus caballus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptomic analysis of ICM and TE from in vivo-derived equine blastocysts using Illumina sequencing technology Overall design: RNA was extracted from individual equine blastocyst ICM and TE (Arcturus Picopure), cDNA was synthesized and amplified (Nugen Ovation V2) and indexed libraries were created for sequencing (TruSeq DNA V1)

Publication Title

RNA-seq transcriptome profiling of equine inner cell mass and trophectoderm.

Sample Metadata Fields

Specimen part, Subject

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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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