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accession-icon GSE7441
Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Amyotrophic lateral sclerosis (ALS) is caused by the progressive degeneration of motor neurons. Mutations in the Cu/Zn superoxide dismutase (SOD1) are found in about 20% of patients with familial ALS. Mutant SOD1 causes motor neuron death through an acquired toxic property. Although, molecular mechanism underlying this toxic gain-of-function remains unknown, evidence support the role of mutant SOD1 expression in non-neuronal cells in shaping motor neuron degeneration. We have previously found that in contrast to non-transgenic, SOD1G93A-expressing astrocytes induced apoptosis of co-cultured motor neurons. This prompted us to investigate whether the effect on motor neuron survival was related to a change in the gene expression profile. Through high-density oligonucletide microarrays we found changes in the expression of genes involved in transcription, signaling, cell proliferation, extracellular matrix construction, response to stress and steroid and lipid metabolism. Decorin, a small multifunctional proteoglycan, was the most up-regulated gene. Down-regulated genes included the insulin-like growth factor-1 receptor and the RNA binding protein ROD1. We also analyzed the expression of selected genes in purified motor neurons expressing SOD1G93A and in spinal cord of asymptomatic and early symptomatic ALS-rodent model.

Publication Title

Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8442
Profiling of Angiotensin II Rapid Response Genes in Human, Bovine, and Rat Adrenocortical Cells.
  • organism-icon Bos taurus, Homo sapiens, Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Angiotensin II (Ang-II) regulates adrenal steroid production and gene transcription through several signaling pathways. Changes in gene transcription occur within minutes after Ang-II stimulation, causing an acute increase in aldosterone production and subsequent increase in the overall capacity to produce aldosterone. Our goal was to compare the Ang-II regulation of early gene expression and confirm the upregulation of selected genes using quantitative real-time RT-PCR (qPCR) across three species: human, bovine, and rat.

Publication Title

Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP051155
A multi-scale approach reveals that NFkB cRel enforces a B-cell decision to divide.
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The transcriptomes of individual small and large B cells after 24 h of stimulation were sequenced and genes upregulated in small or large cells were found and analyzed to provide a global charactarization of transcription patterns in growing B cells. Overall design: We identified 5 large and 5 small viable B cells from images of the C1 IFC containing captured cells. We prepared libraries for the 10 individual cells, a positive bulk control (containing diluted bulk cDNA), a negative control containing only the ERCC spikeins, and a 0h bulk control.

Publication Title

A multi-scale approach reveals that NF-κB cRel enforces a B-cell decision to divide.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE86842
Changes in gene expression upon treatment of SH-SY5Y cells to cisplatin
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

In this study we investigated the changes in mRNA expression upon treatment of SH-SY5Y cells to 10M cisplatin for 72h.

Publication Title

Calcium-regulatory proteins as modulators of chemotherapy in human neuroblastoma.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE115455
A cancer avatar models prospectively guides therapy
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of transcriptomic fidelity between primary and pdx tumor. The hypothesis tested in the present study was that pdx can serve as high fidelity models of human cancer and guide longitudinal care. Results provide important information on the response of preservation of gene expression changes between the primary tumor and the first generation pdx.

Publication Title

Case study: patient-derived clear cell adenocarcinoma xenograft model longitudinally predicts treatment response.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE60187
Evaluation of Niacinamide effects on murine primary macrophage transcriptional regulation and cell cycle progression.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Murine MafB/c-MAF double KO (Maf-DKO) primary macrophages are known for their unlimited non-tumorigenic self-renewal ability (Aziz et al., 2009). In an in vitro screen for cytokines and small molecules we identified Niacinamide (NAM) a potent inhibitor of their proliferative potential characterized by a reversible cell cycle arrest.

Publication Title

SIRT1 regulates macrophage self-renewal.

Sample Metadata Fields

Specimen part

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accession-icon GSE44057
Tissue macrophage subsets derived from regenerating muscle
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Muscle injury was elicited by cardiotoxin injection into the tibialis anterior muscle. Macrophages were isolated 2 days post-injury from the regenerating muscle.

Publication Title

Tissue LyC6- macrophages are generated in the absence of circulating LyC6- monocytes and Nur77 in a model of muscle regeneration.

Sample Metadata Fields

Specimen part

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accession-icon GSE35248
Analysis of the Pseudomonas aeruginosa regulon controlled by the sensor kinase KinB and sigma factor RpoN
  • organism-icon Pseudomonas aeruginosa pao1
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Alginate overproduction by P. aeruginosa, also known as mucoidy is associated with chronic endobronchial infections in cystic fibrosis (CF). Alginate biosynthesis in this bacterium is initiated by the extracytoplasmic function sigma factor (22, AlgU/T). In the wild type (wt) nonmucoid strains, such as PAO1, AlgU is sequestered by the anti-sigma factor MucA that inhibits alginate production. However, the degradation of MucA by activated intramembrane proteases AlgW and/or MucP can lead to the conversion from nonmucoid strains to mucoid. Previously we reported that the absence of the sensor kinase KinB in PAO1 causes the initiation of AlgW-dependent proteolysis of MucA resulting in alginate overproduction. In the kinB mutant this activation requires alternate sigma factor RpoN (54). To determine the RpoN-dependent KinB regulon, microarray and proteomic analyses were performed on a mucoid kinB mutant and an isogenic nonmucoid kinB rpoN double mutant. In the kinB mutant, RpoN controlled the expression of approximately 20% of the genome. Besides alginate biosynthesis and regulator genes such as AlgW, KinB, in concert with RpoN, also control a large number of genes including: those involved in carbohydrate metabolism, quorum sensing, iron regulation, rhamnolipid production, and motility. In an acute pneumonia murine infection model, mice exhibited better survival when challenged with the kinB mutant than wt PAO1. Together, these data strongly suggest that KinB controls virulence factors important for acute pneumonia and conversion to mucoidy.

Publication Title

Analysis of the Pseudomonas aeruginosa regulon controlled by the sensor kinase KinB and sigma factor RpoN.

Sample Metadata Fields

Treatment

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accession-icon GSE94340
Expression data from skin biopsies in patients with systemic sclerosis treated with beta-catenin inhibitor (C82) and placebo
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Wnt signaling pathway is thought to have a role in skin fibrosis in Systemic slcerosis. This Randomized, Placebo-Controlled trial examines the effect of beta catenin inhibition on skin expression.

Publication Title

Inhibition of β-Catenin Signaling in the Skin Rescues Cutaneous Adipogenesis in Systemic Sclerosis: A Randomized, Double-Blind, Placebo-Controlled Trial of C-82.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE8700
Expression data from epididymal fat tissues of diet induced obese rats
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Analysis of gene expression profiles of epididymal fat from DIO rats

Publication Title

Assessment of diet-induced obese rats as an obesity model by comparative functional genomics.

Sample Metadata Fields

No sample metadata fields

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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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