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accession-icon GSE18935
Effects on small RNA MgrR in Escherichia coli
  • organism-icon Escherichia coli k-12
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

MgrR is a newly characterized Hfq dependent small RNA RNA. The expression of MgrR is regulated by Two component system, PhoPQ regulon, which senses low Mg2+ in environment. It has been reported that Hfq-binding sRNAs base pair with target RNAs, frequently leading to rapid degradation of target messages or, less frequently, to stabilization, both of which can be assayed by using microarrays. In order to search for the target genes of MgrR, we therefore examined the consequences of MgrR expression on mRNA abundance under two conditions. In condition 1, the chromosomal copy of mgrR was deleted and MgrR was expressed for 15 from an induced plac-mgrR plasmid and compared to cells carrying a vector induced for the same period. In condition 2, the expression of mRNAs was compared in wild-type cells (mgrR+) and the mgrR deletion strain, both grown in LB; because MgrR levels are fairly high under our normal growth conditions, this allowed analysis of both the direct and indirect (long-term) effects of MgrR.

Publication Title

A PhoQ/P-regulated small RNA regulates sensitivity of Escherichia coli to antimicrobial peptides.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12332
Mating induces an immune response and developmental switch in the Drosophila oviduct
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Mating triggers physiological and behavioral changes in females.

Publication Title

Mating induces an immune response and developmental switch in the Drosophila oviduct.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10345
Genome-wide analysis of transcriptional termination in E. coli
  • organism-icon Escherichia coli
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Transcription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA.

Publication Title

Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.

Sample Metadata Fields

Compound

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accession-icon GSE8832
K562 Gene Expression Control vs 1R-Chl treatments
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined.

Publication Title

Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia.

Sample Metadata Fields

Sex, Age, Disease

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accession-icon GSE5040
Polyamides alleviate transcription inhibition associated with long GAATTC repeats in Friedreichs ataxia
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Lymphoblast cells from a patient with Freidriech's Ataxia were incubated with pyrrole-imidazole polyamides targeted to the GAA triplet repeat in the intron 1. The polyamides were shown in cell culture to increase levels of endogenous frataxin mRNA. A normal sibling derived lymphoblast cell line was used as a control.

Publication Title

DNA sequence-specific polyamides alleviate transcription inhibition associated with long GAA.TTC repeats in Friedreich's ataxia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24460
Prolonged Drug Selection of Breast Cancer Cells and Enrichment of Cancer Stem Cell Characteristics.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Background: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters. We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells.

Publication Title

Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE10745
HDAC Inhibitors Correct Frataxin Deficiency in a Friedreich Ataxia Mouse Model
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

Background: Friedreich ataxia, an autosomal recessive neurodegenerative and cardiac disease, is caused by abnormally low levels of frataxin, an essential mitochondrial protein. All Friedreich ataxia patients carry a GAA/TTC repeat expansion in the first intron of the frataxin gene, either in the homozygous state or in compound heterozygosity with other loss-of-function mutations. The GAA expansion inhibits frataxin expression through a heterochromatin-mediated repression mechanism. Histone modifications that are characteristic of silenced genes in heterochromatic regions occur at expanded alleles in cells from Friedreich ataxia patients, including increased trimethylation of histone H3 at lysine 9 and hypoacetylation of histones H3 and H4.

Publication Title

HDAC inhibitors correct frataxin deficiency in a Friedreich ataxia mouse model.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7753
Gene Expression Profiling in Peripheral Blood in Untreated New Onset Systemic Juvenile Idiopathic Arthritis
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Systemic Juvenile Idiopathic Arthritis (sJIA) has been strongly associated with macrophage activation syndrome (MAS). To better understand the pathogenesid of sJIA and to facilitate the search for MAS biomarkers, we examine gene expression profiles in untreated new onset sJIA.

Publication Title

Gene expression profiling of peripheral blood from patients with untreated new-onset systemic juvenile idiopathic arthritis reveals molecular heterogeneity that may predict macrophage activation syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13849
Expression Signatures in Polyarticular JIA Show Heterogeneity and Offer a Molecular Classification of Disease Subsets
  • organism-icon Homo sapiens
  • sample-icon 110 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective. Microarray analysis was used to determine whether children with recent onset polyarticular juvenile idiopathic arthritis (JIA) exhibit biologically or clinically informative gene expression signatures in peripheral blood mononuclear cells (PBMC). Methods. Peripheral blood samples were obtained from 59 healthy children and 61 children with polyarticular JIA prior to treatment with second-line medications, such as methotrexate or biological agents. RNA was purified from Ficoll-isolated mononuclear cells, fluorescently labeled and then hybridized to Affymetrix U133 Plus 2.0 GeneChips. Data were analyzed using ANOVA at a 5% false discovery rate threshold after Robust Multi-Array Average pre-processing and Distance Weighted Discrimination normalization. Results. Initial analysis revealed 873 probe sets for genes that were differentially expressed between polyarticular JIA and controls. Hierarchical clustering of these probe sets distinguished three subgroups within polyarticular JIA. Prototypical subjects within each subgroup were identified and used to define subgroup-specific gene expression signatures. One of these signatures was associated with monocyte markers, another with transforming growth factor-beta-inducible genes, and a third with immediate-early genes. Correlation of these gene expression signatures with clinical and biological features of JIA subgroups suggests direct relevance to aspects of disease activity and supports the division of polyarticular JIA into distinct subsets. Conclusions. PBMC gene expression signatures in recent onset polyarticular JIA reflect discrete disease processes and offer a molecular classification of disease.

Publication Title

Gene expression signatures in polyarticular juvenile idiopathic arthritis demonstrate disease heterogeneity and offer a molecular classification of disease subsets.

Sample Metadata Fields

Sex, Specimen part, Race

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accession-icon GSE45405
Examination of the MAPK pathway gene expression in patient samples
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina humanRef-8 v2.0 expression beadchip

Description

Microarray analysis of total RNA isolated from samples of circulating tumor cells from 7 patients before romidepsin infusion (0 hours), at 4 h after initiation of the infusion (4 hours) and 24 h after initiation of the infusion (24 hours).

Publication Title

MAPK pathway activation leads to Bim loss and histone deacetylase inhibitor resistance: rationale to combine romidepsin with an MEK inhibitor.

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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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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