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accession-icon GSE106865
A longitudinal gene expression microarray analysis of skeletal muscle resistance training
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Skeletal muscle adapts to resistance exercise (RE) performance acutely and chronically. An important regulatory step of muscle adaptation to RE is gene expression. Microarray analysis can be used as an exploratory method to investigate how genes and gene clusters are modulated acutely and chronically by RE. The purpose of the present study was to investigate the effect of training status in the basal (rested) and pre- to 24h post-RE on the global transcriptome in vastus lateralis muscle biopsies of young men. Muscle biopsies of nine young men who undertook RE training for 10-wks were collected pre and 24h post-RE at the first (W1) and last (W10) weeks of training and analysed using microarray. An unaccustomed RE bout (at W1) up-regulated muscle gene transcripts related to stress (e.g., heat shock proteins), damage and inflammation, structural remodelling, protein turnover and increased translational capacity. Trained muscles (at W10) became more efficient metabolically, as training favoured a more oxidative metabolism, refined response to stress, showed by genes suppression related to RE-induced stress and inflammation, and up-regulated genes indicating greater muscle contractile efficiency and contribution to promote muscle growth and development. These data highlight that chronic repetition of RE increases muscle efficiency and adapt muscles to respond more specifically and accurately to RE-induced stress.

Publication Title

Resistance training in young men induces muscle transcriptome-wide changes associated with muscle structure and metabolism refining the response to exercise-induced stress.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE103935
A bright side of Zika: potent and selective oncolytic properties against aggressive human CNS embryonal tumors
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Zika virus (ZIKV) is largely known for causing brain abnormalities due to its ability to infect neural progenitor stem cells (NPC) during early development. Here we show that ZIKV is also capable of infecting and destroying stem-like cancer cells from aggressive human embryonal tumors of the central nervous system (CNS). When evaluating the oncolytic properties of Brazilian Zika virus strain (ZIKVBR) against human breast, prostate, colorectal and embryonal CNS tumor cell lines, a selective infection of CNS tumor cells, followed by a massive necrotic tumor cell death, was verified. Notably, ZIKVBR was more efficient in destroying CNS tumorspheres than normal stem cell neurospheres. A single intracerebroventricular injection of ZIKVBR in BALB/c nude mice bearing orthotopic human embryonal CNS tumor xenografts resulted in a significantly longer survival, reduced tumor burden, fewer metastasis and complete remission in some animals. Tumor cells closely resembling neural stem cells at the molecular level were more susceptible to ZIKVBR oncolytic effects. Altogether, these preclinical findings indicate that ZIKV could be an efficient oncolytic agent to treat aggressive forms of embryonal CNS tumors. Considering the poor effectiveness and severe side effects of available treatments for these tumors and that most ZIKV infections are asymptomatic, our findings open new avenues for novel therapies.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE38749
Expression data of Human Gastric Adenocarcinoma
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Anatomical staging is a critical, although imperfect, instrument to assess gastric cancer prognosis and define indication for surgery and adjuvant therapy. Despite recent advances, treatment results, as a whole, remain less than satisfactory. Thus, biomarkers are sorely needed to improve risk categorization and define new molecular targets for therapy.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE33427
Genome-wide Response of Saccharomyces cerevisiae upon Arsenate Exposure
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Arsenic metalloid is a double-edge sword. On the one hand it is a very toxic and powerful carcinogen, and on the other it has been successfully used in the treatment of acute promyelocytic leukemia. In order to prevent the deleterious effects caused by arsenic compounds, almost all living organisms have developed mechanisms to eliminate it. In this study genome-wide response of S. cerevisiae to arsenic shows that this metal interferes with genes involved in the iron homeostasis including those encoding proteins that function in iron uptake, incorporation into FeS clusters, and more. In addition our data indicate that Yap1 transcriptionally controls the iron homeostasis regulator AFT2 as well as its direct target, MRS4. Most importantly in response to arsenate exposure Yap1 strongly regulates the expression of several genes involved in the Fe-S proteins biosynthesis, namely NBP35 and YFH1. Interestingly mRNA levels encoding Fet3, Ferro-O2-oxidoreductase required for high-affinity iron uptake, are drastically destabilized upon arsenic exposure. Such destabilization is due to the 5 to 3 exonuclease Xrn1 localized in the P Bodies. Moreover FET3 mRNA decay is not mediated by Cth2 and is independent on the formation of ROS responsible for the toxic effects of arsenic compounds. Strikingly, in presence of arsenate fet3 mutant shows resistance over the wild-type which leads us to suggest that Fet3 has a role in arsenic toxicity. Unexpectedly arsenic treatment seems to activate the non-reductive iron uptake in order to maintain the cellular iron homeostasis. Furthermore our genetic, biochemical, and physiological analysis demonstrate that aft1 mutant is sensitive to arsenic compounds and such phenotype is reversible upon addition of iron. We also show that arsenic exposure induces iron deficiency in aft1 mutant. In conclusion this work shows for the first time that arsenic, a chemotherapy drug used to treat a specific type of acute promyelocytic leukemia (APL), disrupts iron homeostasis and our results suggest that this disruption is independent on ROS generation. Finally we provide preliminary data confirming that such disruption also takes place in mammalian cells, an observation that can be very relevant in term of clinical applications.

Publication Title

Arsenic stress elicits cytosolic Ca(2+) bursts and Crz1 activation in Saccharomyces cerevisiae.

Sample Metadata Fields

Time

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accession-icon GSE13982
Effect of CORM-2 on E. coli transcriptome
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

We recently reported that carbon monoxide (CO) has bactericidal activity. To understand its mode of action we analysed the gene expression changes occurring when Escherichia coli, grown aerobically and anaerobically, is treated with the carbon monoxide releasing molecule, CORM-2. The E. coli microarray analysis shows that E. coli CORM-2 response is multifaceted with a high number of differentially regulated genes spread through several functional categories, namely genes involved in inorganic ion transport and metabolism, regulators, and genes implicated in posttranslational modification, such as chaperones. CORM-2 has higher impact in E. coli cells grown anaerobically, as judged by the existence of repressed genes belonging to eight functional classes which are absent in aerobically CORM-2 treated cells. In spite of the relatively stable nature of the CO molecule, our results show that CO is able to trigger a significant alteration in the transcriptome of E. coli which necessarily has effects in several key metabolic pathways.

Publication Title

Exploring the antimicrobial action of a carbon monoxide-releasing compound through whole-genome transcription profiling of Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE58509
BolA is a transcriptional switch that turns off motility and turns on biofilm development
  • organism-icon Escherichia coli str. k-12 substr. mg1655
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Bacteria are extremely versatile organisms which rapidly adapt to changing environments. When Escherichia coli cells switch from planktonic growth to biofilm, flagellum formation is turned off, and the production of fimbriae and extracellular polysaccharides is switched on. Here we show that BolA protein is a new bacterial transcription factor which modulates the switch from planktonic to sessile lifestyle. BolA negatively modulates flagella biosynthesis and thus swimming capacity. Furthermore, BolA overexpression favors biofilm formation and involvesinvolving fimbriae-like adhesins and curli production. Our results unraveled for the first time that BolA is a protein with high affinity to DNA, involved in the regulation of several genes of E. coli at a genome-wide scale level. Moreover, this observation further demonstrated that the most significant targets of this protein involved a complex network of genes encoding proteins extremely necessary in biofilm development processes. Herein we propose that BolA is a motile/adhesive transcriptional switch, specifically involved in the transition between the planktonic and the attachment stage of biofilm formation process.

Publication Title

BolA is a transcriptional switch that turns off motility and turns on biofilm development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE66521
Transcriptomic response of Saccharomyces cerevisiae in mixed-culture wine fermentation with Hanseniaspora guilliermondii
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Natural grape-juice fermentations involve the sequential development of different yeast species which strongly influence the chemical and sensorial traits of the final product. In the present study,we aimed to examine the transcriptomic response of Saccharomyces cerevisiae to the presence of Hanseniaspora guilliermondii wine fermentation.

Publication Title

Genomic expression program of Saccharomyces cerevisiae along a mixed-culture wine fermentation with Hanseniaspora guilliermondii.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE26941
CpG Oligodeoxynucleotides treatment of Anopheles mosquitoes
  • organism-icon Anopheles gambiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

In the present study, we have investigated the effect of CpG Oligodeoxynucleotides (CpG-ODN) on the outcome of Plasmodium infection of the mosquito vectors Anopheles stephensi and Anopheles gambiae and on the modulation of mosquito immunity to Plasmodium. Anopheles mosquitoes inoculated with CpG-ODN showed significant reduction of Plasmodium infection rate and intensity. Microarrays were used to profile transcription of fat-body from CpG-ODN-treated mosquitoes. Mosquitoes were dissected 18h after ODN inoculation (immediately before feeding). Batches of 20 to 30 fat bodies (abdomen without midgut, ovaries and malpighian tubule]) were dissected in cold DEPC-treated phosphate-buffered saline (PBS) and processed for RNA preparation. Mosquitoes treated with CpG-ODNs are less susceptible to Plasmodium infection. Transcription profile of fat body indicates that protection was associated with coagulation/wound healing, while melanization appears to be depressed.

Publication Title

CpG-containing oligodeoxynucleotides increases resistance of Anopheles mosquitoes to Plasmodium infection.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE6011
Expression data from quadriceps muscle of young DMD patients and age matched controls
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Albeit increased serum CK level and abnormal muscle histology are always present, boys with DMD are phenotipically indistinguishable from the normal ones at birth and, in their first years of life, acquire early motor milestones at normal times. A clear defect in muscle function becomes generally apparent by the end of the second year. As the disease is typically diagnosed between the ages of 3 and 7, the first two years are often considered and referred to as clinically presymptomatic.

Publication Title

Gene expression profiling in the early phases of DMD: a constant molecular signature characterizes DMD muscle from early postnatal life throughout disease progression.

Sample Metadata Fields

Sex, Age

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accession-icon GSE18662
Expression data of human perirenal adipose tissue-derived mesenchymal stem cells cultured under various conditions
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Human mesenchymal stem cells (MSC) derived from perirenal adipose tissue (PV) of living kidney donors were cultured under various conditions, namely (1) control (medium+foetal bovine serum(FBS)) or (2) control (medium+heat-inactivated FBS); (3) with mixed-lympohocyte reactions (MLR) in transwell culture systems for 4 days; (4) with mixed-lympohocyte reactions (MLR) in transwell culture systems for 7 days; or (5)with pro-inflammatory cytokines(IFNgamma, TNFalpha and interleukin 6).

Publication Title

Inflammatory conditions affect gene expression and function of human adipose tissue-derived mesenchymal stem cells.

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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