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accession-icon GSE17364
Sodium arsenate response of wild type and slt2 deficient cells
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Wild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization.

Publication Title

Slt2 MAPK pathway is essential for cell integrity in the presence of arsenate.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-2064
Transcription profiling of Drosophila after exposure to microgravity in the International Space Station and in a microgravity simulator
  • organism-icon Drosophila melanogaster
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Larvae-Pupae transition flies (Drosophila) were recovered and transport for 3 days at 12-14ºC to arrest development until the launch site, then exposed to RT (18-20ºC) for some hours including the launch and trip to the International Space Station, then pupae were exposed to microgravity in the ISS for 4 days and a half at 22ºC. Finally pupae were fixed on acetone and frozen until recovery on Earth.<br></br><br></br><br></br><br></br>Four groups of samples: 1 ISS (+ground control) as described, 2 RPM (microgravity simulator on Earth) as described, 3 RPM without constrains (No MAMBA container and only 5 days exposure without cold transport) and 4 centrifuge 10g without constrains control..

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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accession-icon GSE80394
Expression data from yeast exposed to Caspofungin (wild type strain and rlm1, slt2, msn2/4 and bcy1 mutants) and Aminocandin (wild type strain)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

We did transcription profiling on the effect of rlm1 (MAPK Slt2 transcription factor) deletion, slt2 (MAPK of Cell wall intregity pathway) deletion, bcy1 (Regulatory subunit of the cyclic AMP-dependent protein kinase (PKA)) deletion and msn2/4 (Stress-responsive transcriptional activators) deletion in genes involved in Caspofungin response (2 hours of treatment). In addition, we analyzed the genome-wide expression profile of the wild type strain in response to Aminocandin (2 hours of treatment).

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71433
Expresion data from yeast (wild type and gcn5 mutants) exposed to Congo Red (CR)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

We analyzed the genome-wide expression profile of the wild type strain and the gcn5 mutant (component of the SAGA complex) under basal and cell wall stress (CR during 3 hours) conditions.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29245
Amplified genes are not necessarily over expressed, they can be unchanged or down regulated in cervical cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Mapping 50K Hind240 SNP Array (mapping50khind240), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE29216
Amplified genes are not necessarily over expressed, they can be unchanged or down regulated in cervical cancer cell lines [expression array data]
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Mapping 50K Hind240 SNP Array (mapping50khind240)

Description

Several copy number altered regions (CNA) have been identified in the genome of cervical cancer, especially amplifications of 3q and 5p. However, the contribution of those alterations to cervical carcinogenesis is still a matter of debate, since genome-wide, there is a lack of correlation between CNAs and gene expression. In this study, we investigated whether the CNAs in cell lines (CaLo, CasKi, HeLa, SiHa), at a gene-by-gene level, are related to changes in gene expression. On average 19.2% of the whole genome of cell lines had CNA. However, only 2.4% consisted of minimal recurrent regions (MRR), common to all cell lines. Whereas 3q had just some sparse common gains (13%), 5p was entirely duplicated recurrently. Genome-wide, only 11% of genes located in CNAs changed gene expression. In contrast, the rate increased over 3 fold times in MRRs. Chr 5p was confirmed entirely amplified by FISH. In spite of this, at most 32.9% of the explored genes in 5p (n=202) were de-regulated. In 3q, the rate was just 11.8%. Even in 3q26, which had five MRRs and 38.7% of SNPs was gained recurrently, the rate rose slightly to 13.6% (10 out of 73). Interestingly, up to 16% of de-regulated genes in 5p and 80% in 3q26 were down-regulated, suggesting additional factors are involved in gene repression. The de-regulated genes in 3q and 5p were found in clusters, suggesting local chromatin factors may also influence gene expression. In regions amplified discontinuously, the rate of down-regulated genes rose steadily as the number of amplified SNPs increased (p<0.01, Spearman's correlation). This suggests partial gene amplification as a mechanism of silencing gene expression. Additional genes were identified up- or down-regulated in 5p and 3q, which could be involved in cervical carcinogenesis, especially implicated in apoptosis. Those include CLPTM1L, AHRR, PDCD6 and DAP in 5p and TNFSF10 and ECT2 in 3q. Overall, the gene expression and copy number profiles suggest other factors, like epigenetic or chromatin domains, may influence gene expression within the entirely amplified genome segments. Further studies are needed to elucidate how these mechanisms regulate gene expression.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Cell line

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accession-icon GSE22596
Time course of the transcriptional response of three porcine intestinal sections to Salmonella typhimurium infection
  • organism-icon Sus scrofa
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

The GeneChip Porcine Genome Array was used to identify the transcriptional response upon Salmonella typhimurium infection in three porcine intestinal sections (jejumun, ileum and colon) along a time course of 1,2 and 6 days post infection.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE96955
Lysine 100 acetylation effect of CRP (catabolite activator protein) in gene expression in Escherichia coli
  • organism-icon Escherichia coli k-12
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

cAMP receptor protein (CRP, also known as the catabolite activator protein [CAP]) is arguably the best-studied of the global transcription factors of E coli. CRP alone is responsible for regulating at least 283 operons. Upon binding cAMP, the CRP dimer binds DNA and directly interacts with RNA polymerase (RNAP). At Class II promoters, CRP binds near position -41,5 relative to the transcription start site and contacts the amino-terminal domain of the RNAP subunit (RNAP-NTD). This interaction requires AR2, a patch of primarily positively charged residues (H19, H21, E96, and K101) that interact with negatively charged residues on RNAP-NTD. Acetylome analyses consistently detect lysine 100 (K100) of CRP as acetylated. Since K100 is adjacent to the positively charged AR2, we hypothesized that the K100 positive charge may also play a role in CRP function. We further hypothesized that acetylation of K100 would neutralize this positive charge, leading to a potential regulatory mechanism

Publication Title

Influence of Glucose Availability and CRP Acetylation on the Genome-Wide Transcriptional Response of &lt;i&gt;Escherichia coli&lt;/i&gt;: Assessment by an Optimized Factorial Microarray Analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE47176
Candidate transcriptomic sources of inbreeding depression in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

The genomic causes of inbreeding depression are poorly known. Several studies have found widespread transcriptomic alterations in inbred organisms, but it remains unclear which of these alterations are causes of the depression and which are mere responses to the ensuing physiological stress.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE68169
Expression data from mouse brain
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A detailed knowledge of the mechanisms underlying brain aging is fundamental to understand its functional decline and the baseline upon which brain pathologies superimpose. Endogenous protective mechanisms must contribute to the adaptability and plasticity still present in the healthy aged brain. Apolipoprotein D (ApoD) is one of the few genes with a consistent and evolutionarily conserved up-regulation in the aged brain. ApoD protecting roles upon stress or injury are well known, but a study of the effects of ApoD expression in the normal aging process is still missing. Using an ApoD-knockout mouse we analyze the effects of ApoD on factors contributing to the functional maintenance of the aged brain. We focused our cellular and molecular analyses in cortex and hippocampus at an age representing the onset of senescence where mortality risks are below 25%, avoiding bias towards long-lived animals. Lack of ApoD causes a prematurely aged brain without altering lifespan. Age-dependent hyperkinesia and memory deficits are accompanied by differential molecular effects in cortex and hippocampus. Transcriptome analyses reveal distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus, with different cell-type contributions to age-regulated gene expression. Markers of glial reactivity, proteostasis, and oxidative and inflammatory damage reveal early signs of aging and enhanced brain deterioration in the ApoD-knockout brain. The lack of ApoD results in an age-enhanced significant reduction in neuronal calcium-dependent functionality markers and signs of early reduction of neuronal numbers in the cortex, thus impinging upon parameters clearly differentiating neurodegenerative conditions from healthy brain aging. Our data support the hypothesis that the physiological increased brain expression of ApoD represents a homeostatic anti-aging mechanism.

Publication Title

Aging without Apolipoprotein D: Molecular and cellular modifications in the hippocampus and cortex.

Sample Metadata Fields

Sex, Age, Specimen part

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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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