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accession-icon GSE45516
Expression data from human Huntington fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profile comparison from fibroblasts of Huntington individuals and normal ones

Publication Title

Gene expression profile in fibroblasts of Huntington's disease patients and controls.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon SRP068907
mRNA-seq of nuclear RNA extracted from T4 and T5 neurons of D. melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

T4 and T5 neurons are components of the neuronal circuit for motion vision in flies. To identify genes involved in neuronal computation of T4 and T5 neurons, we perfomed transcriptome analysis. Nuclei of T4 and T5 neurons were immunoprecipitated, total RNA was harvested and used for mRNA-seq with Illumina technology. In two biological replicates, we mapped 154 and 119 million reads to D. melanogaster genome. mRNA-seq provided information about expression levels of 17,468 annotated transcripts in the T4 and T5 neurons. Overall design: Cell type – specific transcriptome analysis of the RNA isolated from immunoprecipitated nuclei, performed in two biological replicates

Publication Title

RNA-Seq Transcriptome Analysis of Direction-Selective T4/T5 Neurons in Drosophila.

Sample Metadata Fields

Subject

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accession-icon GSE18113
Expression data from Human MicroVascular Endothelial Cells (HMVECS)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The activation of endothelium by tumor cells is one of the main steps by tumor metastasis. The role of the blood components (platelets and leukocytes) in this process remain unclear.

Publication Title

Selectin-mediated activation of endothelial cells induces expression of CCL5 and promotes metastasis through recruitment of monocytes.

Sample Metadata Fields

Specimen part

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accession-icon GSE26231
Noggin vs BMP4 overexpression Epidermis
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The study was performed to determine if there were alterations in the total RNA pool among the epidermal keratinocytes of K14 promotor-driven noggin overexpression compared with K14 promotor-driven BMP4 overexpression transgenic animals, which will directly relate to cellular chemistry and immune and sensory function. The total study is also aimed at determining alterations of transcrption factors and/or regulation of gene function, including methylation states and micro RNA control in keratinocytes following sensory challenge, particularly neuropathic and chronic pain conditions.

Publication Title

Keratinocyte expression of calcitonin gene-related peptide β: implications for neuropathic and inflammatory pain mechanisms.

Sample Metadata Fields

Specimen part

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accession-icon GSE90970
Mesenchymal Stromal Cells Induce Ex Vivo Proliferation and Erythroid Commitment of Cord Blood Haematopoietic Stem Cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A human bone marrow-derived mesenchymal stromal cell (MSCs) and cord blood-derived CD34+ stem cell co-culture system was set up in order to evaluate the proliferative and differentiative effects induced by MSCs on CD34+ stem cells, and the reciprocal influences on gene expression profiles

Publication Title

Mesenchymal stromal cells (MSCs) induce ex vivo proliferation and erythroid commitment of cord blood haematopoietic stem cells (CB-CD34+ cells).

Sample Metadata Fields

Specimen part

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accession-icon GSE9000
Effect of HDAC inhibitors on expression of androgen induced genes
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to assemble a coactivator/RNA polymerase II complex after AR binds to the enhancers of target genes. Failed complex assembly is associated with a phase shift in the cyclical wave of AR recruitment that typically occurs in response to ligand treatment. HDAC inhibitors retain the ability to block AR activity in hormone refractory prostate cancer models and therefore merit clinical investigation in this setting. HDAC-regulated AR target genes defined here can serve as biomarkers to ensure sufficient levels of HDAC inhibition.

Publication Title

Histone deacetylases are required for androgen receptor function in hormone-sensitive and castrate-resistant prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12438
Effect of individual HDAC knockdown on expression of androgen induced genes
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to assemble a coactivator/RNA polymerase II complex after AR binds to the enhancers of target genes. Failed complex assembly is associated with a phase shift in the cyclical wave of AR recruitment that typically occurs in response to ligand treatment. HDAC inhibitors retain the ability to block AR activity in hormone refractory prostate cancer models and therefore merit clinical investigation in this setting. HDAC-regulated AR target genes defined here can serve as biomarkers to ensure sufficient levels of HDAC inhibition.

Publication Title

Histone deacetylases are required for androgen receptor function in hormone-sensitive and castrate-resistant prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP058071
ABCC5 functions as a transporter of glutamate conjugates and analogs
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The ubiquitous efflux transporter ATP-binding cassette sub-family C member 5 (ABCC5) is present at high levels in the blood-brain barrier, neurons and glia, but its in vivo substrates and function are not known. Untargeted metabolomic screens revealed that Abcc5-/- mice accumulate endogenous glutamate conjugates and analogs in several tissues, but brain in particular. The abundant neurotransmitter N-acetylaspartylglutamate (NAAG), for example, was over 2-fold higher in Abcc5-/- brain. In line with ABCC5-mediated transport, the metabolites that accumulated in Abcc5-/- tissues were depleted in cultured cells that overexpressed human ABCC5. Using membrane vesicles, we show that ABCC5 not only transports the metabolites detected in our screen, but also a wide range of peptides containing a C-terminal glutamate. Glutamate conjugates are of physiological relevance because they can affect the function of glutamate, the principal excitatory neurotransmitter in the brain. We found that ABCC5 also transports exogenous glutamate analogs, like the classic excitotoxic neurotoxins kainic acid, domoic acid and N-methyl-D-aspartate (NMDA) and the therapeutic glutamate analog ZJ43. Taken together, we have identified ABCC5 as a general glutamate conjugate and analog transporter that affects the disposition of endogenous metabolites, toxins and drugs. Overall design: A set of 5 wildtype brains was compared to a set of 5 Abcc5-knockout mouse brains

Publication Title

ATP-binding Cassette Subfamily C Member 5 (ABCC5) Functions as an Efflux Transporter of Glutamate Conjugates and Analogs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP042045
Transposon expression kinetics in Dnmt3L-/- developing testes [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We examined the kinetics of production of mRNAs and small RNAs derived from transposable elements during mouse spermatogenesis, in whole gonads of wildtype and DNA methylation-deficient males (Dnmt3L and Miwi2 mutants). We found that in absence of DNA methylation, transposon reactivation is not constitutive but rather occurs in a class- and development-specific manner : both the intensity of reactivation and the number of reactivated transposon classes increased as germ cells progress in meiosis. Moreover, we observed that transposon silencing before meiosis is not due to increased cleavage by the piRNA machinery. In contrast, the burst of transposon transcripts occurring at meiosis in the absence of DNA methylation serve as substrates for increased piRNA production Overall design: Six whole testis samples were analyzed, corresponding to three time points (16.5dpc, 10dpp and 20dpp) each for Dnamt3L-/- animals and control littermates. For 16.5dpc, testes from 7/8 mice were pooled per genotype. For the other stages, three mice were pooled per genotype.

Publication Title

DNA methylation restrains transposons from adopting a chromatin signature permissive for meiotic recombination.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE55616
ARRB1 regulates prostate cancer cell metabolism
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Nuclear ARRB1 induces pseudohypoxia and cellular metabolism reprogramming in prostate cancer.

Sample Metadata Fields

Specimen part, Cell line

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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)

fund-icon Fund the CCDL

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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