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accession-icon E-MEXP-3764
Transcription profiling by array of Pseudomonas aeruginosa treated with fosfomycin, tobramycin or a combination of both drugs under aerobic and anaerobic conditions
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

The experiment aimed to characterise the transcriptional response of a clinical CF P. aeruginosa isolate to sub-inhibitory concentrations of fosfomycin, tobramycin and a novel 4/1 (w/w) combination of the two (FT) under both aerobic and anaerobic conditions

Publication Title

Fosfomycin and tobramycin in combination downregulate nitrate reductase genes narG and narH, resulting in increased activity against P. aeruginosa under anaerobic conditions.

Sample Metadata Fields

Compound

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accession-icon GSE8510
RAR-PLZF overcomes PLZF-mediated repression of CRABPI contributing to retinoid resistance in t(11;17) APL
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This study supports an active role for PLZF and RAR-PLZF in leukemogenesis, identifies upregulation of CRABPI as a novel mechanism contributing to retinoid resistance and reveals the ability of the reciprocal fusion gene products to mediate distinct

Publication Title

RARalpha-PLZF overcomes PLZF-mediated repression of CRABPI, contributing to retinoid resistance in t(11;17) acute promyelocytic leukemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56640
Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Affymetrix Human Exon 1.0 ST Array [AltAnalyze 2.0.6 beta probeset-to-Ensembl mapping (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress.

Sample Metadata Fields

Treatment

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accession-icon GSE25130
Novel virulence factors in host-adapted Pseudomonas aeruginosa infection of the Cystic Fibrosis airways
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Pseudomonas aeruginosa airway infection is the primary cause of death in Cystic Fibrosis (CF). During early infection P. aeruginosa produces multiple virulence factors, which cause acute pulmonary disease and are largely regulated by quorum sensing (QS) intercellular signalling networks. Longitudinal clinical studies have observed the loss, through adaptive mutation, of QS and QS-related virulence in late chronic infection. Although the mechanisms are not understood, infection with QS mutants has been linked to a worse outcome for CF patients. By comparing QS-active and QS-inactive P. aeruginosa CF isolates, we have identified novel virulence factors and pathways associated with QS disruption. In particular, we noted factors implicating increased intra-phagocyte survival. Our data present novel targets as candidates for future CF therapies. Some of these targets are already the subject of drug development programmes for the treatment of other bacterial pathogens and may provide cross-over benefit to the CF population.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE25128
Gene expression data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Pseudomonas aeruginosa is a common pathogen in the lungs of the cystic fibrosis patients. As infection develops the organism progressively adapts to its environment and its mode of pathogenesis alters, frequently including the loss of quorum sensing regulated virulence factors.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE57187
Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [Affymetrix]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [AltAnalyze 2.0.6 beta probeset-to-Ensembl mapping (huex10st)

Description

In response to genotoxic stress the TP53 tumour suppressor activates target gene expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage. These canonical activities can be repressed by TP63 in normal stratifying epithelia to maintain proliferative capacity or drive proliferation of squamous cell carcinomas, where TP63 is frequently overexpressed/amplified. Here we use ChIP-sequencing, integrated with microarray analysis, to define the genome wide interplay between TP53 and TP63 in response to genotoxic stress in normal cells. We reveal that TP53 and TP63 bind to overlapping, but distinct cistromes of sites through utilization of distinctive consensus motifs and that TP53 is constitutively bound to a number of sites. We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity. Collectively, this results in a global TP53 dependent repression of cell cycle progression, mitosis and DNA damage repair concomitant with activation of anti-proliferative and pro-apoptotic canonical target genes. Further analyses reveals that in the absence of genotoxic stress TP63 plays an important role in maintaining expression of DNA repair genes, loss of which results in defective repair

Publication Title

Genome-wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress.

Sample Metadata Fields

Treatment

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accession-icon GSE110126
The impact of DSF and C23 on P. aeruginosa physiology
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

To verify the imapct of DSF and C23 on P. aeruginosa during infection

Publication Title

No associated publication

Sample Metadata Fields

Time

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accession-icon GSE86445
Integrated analysis of the molecular action of Vorinostat identifies epi-sensitised targets for combination therapy
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Acute myeloid leukaemia (AML) is a highly heterogeneous entity of disorders in haematopoietic progenitors, characterised by an arrest in differentiation and an outgrowth of myeloid blasts in the bone marrow. AML is a disease of the aging, many patients are unable to withstand standard chemotherapy therefore novel approaches for anti-cancer agents has arisen in the understanding of epigenetic regulation in cancer cells, such as chromatin remodelling. Acetylation of histones is a reversible process, whereby acetyl groups are transferred on the -amino groups of specific lysine residues by a specific group of enzymes, histone acetyltransferases (HATs) and removed by histone deacetylase complexes (HDACs). HDACs are involved in regulating a number of processes in the cell, such as cell proliferation, differentiation as well as apoptosis. Deregulation of the activity of these enzymes is associated with cancer; therefore it is important that the HAT and HDAC equilibrium is regained. This equilibrium can be improved through the inhibition of HDAC enzymes using HDAC inhibitors. Vorinostat is a HDAC inhibitor, clinically approved for the treatment of CTCL, and is in phase II clinical trials for AML and a number of haematological malignancies. Studies have shown that some patients are non-responsive/resistant to Vorinostat; therefore a fuller characterisation of Vorinostat needs to be made so an adequate combination drug can be identified, as understanding of resistance is crucial to overcoming it. The purpose of this study was to provide a comprehensive analysis of Vorinostat in AML cell lines and to identify potential synergistic therapies that could be used in combination with Vorinostat to provide a better outlook in AML. The global identification of genes associated with Vorinostat induced histone H3 lysine 9 (H3K9) acetylation, investigated using chromatin immunoprecipitation coupled with next generation sequencing (ChIP-SEQ), was integrated with data from gene expression studies to provide a comprehensive approach to understanding Vorinostat. This study has identified the sonic hedgehog homolog (SHH) as a rational and potential therapeutic target for combination therapy with Vorinostat

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE16756
Expression data from retinas of wildtype and Nhlh2 knockout mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Nhlh2 is a neuronal helix-loop-helix transcription factor. The goal of this study was to determine the pattern of gene expression in wildtype mouse retina and to compare it to that in the retinas of mice in which the nhlh2 gene had been knocked out.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE25129
Comparative genomic hybridisation data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Pseudomonas aeruginosa is a common pathogen in the lungs of the cystic fibrosis patients. As infection develops the organism progressively adapts to its environment and its mode of pathogenesis alters, frequently including the loss of quorum sensing (QS) regulated virulence factors.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
...

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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