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accession-icon GSE51447
Microarray data from CREB inhibited and control mesothelioma cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Cyclic AMP response element binding protein (CREB) is known to play important roles in growth and drug resistance of various cancers. Here we show roles of inhibition of CREB1 on gene expression profile of malignant mesothelioma (MM) cells (Hmeso and H2373/PPMMill).

Publication Title

CREB-induced inflammation is important for malignant mesothelioma growth.

Sample Metadata Fields

Cell line

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accession-icon SRP007885
CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. Overall design: CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.

Publication Title

CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP187109
RNA-seq of microglia isolated from aged mice treated with IgG or anti-CD22.
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Sequencing data related to the manuscript entitled, "CD22 blockade restores homeostatic microglial phagocytosis in the aging brain." Overall design: To assess the transcriptional effects of CD22 blockade, we implanted aged mice with osmotic pumps to continuously infuse a CD22 blocking antibody or an IgG control antibody directly into the cerebrospinal fluid for one month. Following one month of continuous infusion, we performed RNA-seq on purified microglia from the hemi-brains of these mice contralateral to the cannulation site to minimize injury-induced confounding factors. Primary mouse microglia were isolated by gentle dounce homogenization of the brain, magentic myelin removal, and FACS-purification of ~20,000 live CD11b+CD45lo cells. Microglia were sorted into RLT Plus buffer (Qiagen) containing beta-mercaptoethanol. RNA was extracted using a RNeasy Micro Plus kit (Qiagen) according the manufacturer's protocol. RNA integrity was assessed on a Bioanalyzer (Agilent), and high quality samples were used for library preparation. cDNA synthesis and amplification was performed using the SmartSeq v4 Ultra-low input kit (Takara), and libraries were tagmented, adaptor ligated, and indexed using the Nextera XT kit (Illumina). After normalization and pooling, libraries were sequenced on a Hiseq 4000 (Illumina) using paired-end 100bp reads. Raw sequencing files were demultiplexed with bcl2fastq, reads were aligned using STAR, the count matrix was generated using SummarizedExperiment, and differential expression analysis was performed using DESeq2 with standard settings.

Publication Title

CD22 blockade restores homeostatic microglial phagocytosis in ageing brains.

Sample Metadata Fields

Age, Cell line, Subject

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accession-icon GSE66925
A Comparative Study of Global Transcriptomic Responses under Excess or deficient Phosphate (Pi) Regime reveals ethylene mediated signaling in Arabidopsis.
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

Phosphorus is an essential macronutrient element, but some time causes problems if present in excess. Unlike the enormous molecular and morphophysiological information available in plants regarding phosphate (Pi) deficiency, little is known about the effect of excess Pi on plants, which is indeed essential for its remediation. Here, we have carried out a comparative study of plant molecular responses under excess Pi (20 mM) or without Pi (0 mM) at transcriptome level. The 1.25 mM treatment concentration of Pi used as a control to obtain differentially regulated genes under above mentioned Pi regimes. A novel whole-transcript expression array, i.e. Arabidopsis Gene 1.0 ST Array, was used to perform these experiments. The most distinctly regulated groups of genes represent modulation in ethylene mediated signaling, Fe deficiency response, and root development. We have also identified some defensin like genes, possessing a gibberellic acid regulated domain (GASA like) under excess Pi treatment. Overall, this study will not only help in dissecting the mechanism of plant responses under excess Pi but also provide the clues about the unknown genes involved in phosphorus homeostasis.

Publication Title

Comprehensive study of excess phosphate response reveals ethylene mediated signaling that negatively regulates plant growth and development.

Sample Metadata Fields

Specimen part

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accession-icon GSE55436
Genome-wide transcriptome analysis reveals ABA mediated response in Arabidopsis during gold (Aucl4-) treatment
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

Genome-wide transcriptome analysis was carried out in root tissue of Arabidopsis seedlings treated with gold (Au) as Chloroauric acid (HAuCl4). This study demonstrated remarkable changes in root transcriptome within the 12 h exposure. Most of the genes differentially expressed were related to glutathione binding, methylations, secondary metabolism, sugar metabolism, ABA, ethylene, auxin related signalling, transport and signal-transduction pathways.

Publication Title

Genome wide transcriptome analysis reveals ABA mediated response in Arabidopsis during gold (AuCl(-) 4) treatment.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP050954
Differential susceptibility of human pleural and peritoneal mesothelial cells to asbestos exposure
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq1000

Description

We hypothesize that the observed differences in incidences of pleural and peritoneal malignant mesothelioma (MM) are the result of differences in the direct response of these cell types to asbestos rather than to differences mediated by the in vivo microenvironment. To test this hypothesis, we characterized cellular responses to asbestos in a controlled environment using high-throughput RNA sequence and other assays. Overall design: Examination of asbestos-treated versus untreated mesothelial cells from four cell lines representing two tissue types in culture.

Publication Title

Differential Susceptibility of Human Pleural and Peritoneal Mesothelial Cells to Asbestos Exposure.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE97493
Altered expression of the Cdk5 activator-like protein, Cdk5, causes neurodegeneration, in part by accelerating the rate of aging.
  • organism-icon Drosophila melanogaster
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Altered expression of the Cdk5 activator-like protein, Cdk5α, causes neurodegeneration, in part by accelerating the rate of aging.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE97491
Altered expression of the Cdk5 activator-like protein, Cdk5, causes neurodegeneration, in part by accelerating the rate of aging.
  • organism-icon Drosophila melanogaster
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

Aging is the greatest risk factor for neurodegeneration, but the connection between the two processes remains opaque. This is in part for want of a rigorous way to define physiological age, as opposed to chronological age. Here, we develop a comprehensive metric for physiological age in Drosophila, based on genome-wide expression profiling. We applied this metric to a model of adult-onset neurodegeneration, increased or decreased expression of the activating subunit of the Cdk5 protein kinase, encoded by the gene Cdk5, the ortholog of mammalian p35. Cdk5-mediated degeneration was associated with a 27-150% acceleration of the intrinsic rate of aging, depending on the tissue and genetic manipulation. Gene ontology analysis and direct experimental tests revealed that affected age-associated processes included numerous core phenotypes of neurodegeneration, including enhanced oxidative stress and impaired proteostasis. Taken together, our results suggest that Cdk5-mediated neurodegeneration results from accelerated aging, in combination with cell-autonomous neuronal insults. These data fundamentally recast our picture of the relationship between neurodegeneration and its most prominent risk factor, natural aging.

Publication Title

Altered expression of the Cdk5 activator-like protein, Cdk5α, causes neurodegeneration, in part by accelerating the rate of aging.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE97492
Altered expression of the Cdk5 activator-like protein, Cdk5, causes neurodegeneration, in part by accelerating the rate of aging.
  • organism-icon Drosophila melanogaster
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

Aging is the greatest risk factor for neurodegeneration, but the connection between the two processes remains opaque. This is in part for want of a rigorous way to define physiological age, as opposed to chronological age. Here, we develop a comprehensive metric for physiological age in Drosophila, based on genome-wide expression profiling. We applied this metric to a model of adult-onset neurodegeneration, increased or decreased expression of the activating subunit of the Cdk5 protein kinase, encoded by the gene Cdk5, the ortholog of mammalian p35. Cdk5-mediated degeneration was associated with a 27-150% acceleration of the intrinsic rate of aging, depending on the tissue and genetic manipulation. Gene ontology analysis and direct experimental tests revealed that affected age-associated processes included numerous core phenotypes of neurodegeneration, including enhanced oxidative stress and impaired proteostasis. Taken together, our results suggest that Cdk5-mediated neurodegeneration results from accelerated aging, in combination with cell-autonomous neuronal insults. These data fundamentally recast our picture of the relationship between neurodegeneration and its most prominent risk factor, natural aging.

Publication Title

Altered expression of the Cdk5 activator-like protein, Cdk5α, causes neurodegeneration, in part by accelerating the rate of aging.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE113322
Expression data after PAK2 knockdown in head and neck cancer cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Epigenetic mechanisms play an important role in the cellular development and maintenance of cellular homeostasis. Any alteration of epigenetic mechanisms via the changes in DNA methylation and histone modification may lead to various diseases including cancer. The differential expression of histone modifiers has been observed in various malignancies.

Publication Title

PAK2-c-Myc-PKM2 axis plays an essential role in head and neck oncogenesis via regulating Warburg effect.

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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