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accession-icon GSE49959
Expression data from larvae body wall expressing LaminC transgenes
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Expression of mutant lamins in human muscle causes muscular dystrophy. We have generated a drosophila model that expresses mutant lamins, modeled after those that cause disease in humans.

Publication Title

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway.

Sample Metadata Fields

Specimen part

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accession-icon GSE43760
Metabolic syndrome exercise training
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We assessed vastus lateralis muscle gene expression levels of 12 women with the metabolic syndrome before and after a 6 month exercise training program

Publication Title

Upregulation of skeletal muscle inflammatory genes links inflammation with insulin resistance in women with the metabolic syndrome.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment, Subject, Time

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accession-icon GSE33886
Vastus lateralis muscle gene expression after local physical deconditioning and exercise training
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The leg of healthy volunteers was locally deconditioned using three weeks of unilateral lower limb suspension (ULLS). The extremely deconditioned legs of subjects with a spinal cord injury (SCI) were trained using eight weeks of functional electrical stimulation (FES) exercise, 2-3 times per week (total 20 sessions).

Publication Title

Expression of genes involved in fatty acid transport and insulin signaling is altered by physical inactivity and exercise training in human skeletal muscle.

Sample Metadata Fields

Subject, Time

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accession-icon E-ATMX-13
Transcription profiling by array of Arabidopsis cell suspensions after treatment with methyl jasmonate
  • organism-icon Arabidopsis thaliana
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The transcriptional response of Arabidopsis thaliana cell suspensions following treatment with the stress hormone methyl jasmonate (MeJA) was monitored over time 16 hours after subcultivation. Three time points were included: 30 minutes, 2 hours and 6 hours after elicitation with 50µm MeJA or DMSO as a control.

Publication Title

Mapping methyl jasmonate-mediated transcriptional reprogramming of metabolism and cell cycle progression in cultured Arabidopsis cells.

Sample Metadata Fields

Compound, Time

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accession-icon GSE17617
Gene profiling within the orexin-producing neurons
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness and attacks of muscle atonia triggered by strong emotions (cataplexy). The best biological marker of narcolepsy is orexin deficiency with dramatic loss in hypothalamic orexin-producing neurons. Together with a tight HLA and T-cell receptor alpha(5) association, narcolepsy is believed to be autoimmune although all attempts to prove it have failed.To characterize orexin specific peptides we produced a transgenic mouse model to access to the orexin neurons transcription profile. We generated BAC-based transgenic mice by replacing the orexin coding sequence by a flag-tagged poly(A) binding protein (Pabp1) cDNA sequence. The basis of this construct is to take advantage of the ability of Pabp1 to bind to the poly(A) tails of mRNAs in vivo. Thus mRNAs from orexin cells are expected to be enriched by cross-linking them to the flag-tagged PABP and then co-immunoprecipitating this complex with a specific anti-flag monoclonal antibody.

Publication Title

Elevated Tribbles homolog 2-specific antibody levels in narcolepsy patients.

Sample Metadata Fields

Age

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accession-icon SRP010646
Caenorhabditis elegans strain:N2, adr-1, adr-2, adr-1;adr-2 Transcriptome or Gene expression
  • organism-icon Caenorhabditis elegans
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Competition between ADAR and RNAi pathways for an extensive class of RNA targets.

Publication Title

Competition between ADAR and RNAi pathways for an extensive class of RNA targets.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE46515
Expression data from mouse model using targeted deletion of hepatic RICTOR (Albumin-Cre Rictor LoxP/LoxP)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Recent work using mouse models has revealed that mTORC2, which unlike mTORC1 is not acutely sensitive to rapamycin, plays a key role in the regulation of organismal physiology. The substrates and pathways regulated by mTORC2 are at present relatively unknown

Publication Title

Hepatic signaling by the mechanistic target of rapamycin complex 2 (mTORC2).

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE38063
Comparison of the long-term effects of calorie restriction without malnutrition on global gene expression profiles of rat and human skeletal muscle
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina Rat Ref-12 v1

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.

Sample Metadata Fields

Specimen part

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accession-icon GSE38012
Comparison of the long-term effects of calorie restriction without malnutrition on global gene expression profiles of rat and human skeletal muscle [Human]
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

With the population of older and overweight individuals on the rise in the Western world, there is an ever greater need to slow the aging processes and reduce the burden of age-associated chronic disease that would significantly improve the quality of human life and reduce economic costs. Caloric restriction (CR), is the most robust and reproducible intervention known to delay aging and to improve healthspan and lifespan across species (1); however, whether this intervention can extend lifespan in humans is still unknown. Here we report that rats and humans exhibit similar responses to long-term CR at both the physiological and molecular levels. CR induced broad phenotypic similarities in both species such as reduced body weight, reduced fat mass and increased the ratio of muscle to fat. Likewise, CR evoked similar species-independent responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with improved health and survival: IGF-1/insulin signaling, mitochondrial biogenesis and inflammation. To our knowledge, these are the first results to demonstrate that long-term CR induces a similar transcriptional profile in two very divergent species, suggesting that such similarities may also translate to lifespan-extending effects in humans as is known to occur in rodents. These findings provide insight into the shared molecular mechanisms elicited by CR and highlight promising pathways for therapeutic targets to combat age-related diseases and promote longevity in humans.

Publication Title

Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE64647
Expression data from diploid human pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human pluripotent stem cells (hPSCs) tend to acquire chromosomal aberrations in culture, which may increase their tumorigenicity. However, the cellular mechanism(s) underlying these aberrations are largely unknown. Here we show that the DNA replication in aneuploid hPSCs is perturbed, resulting in high prevalence of defects in chromosome condensation and segregation. Global gene expression analyses in aneuploid hPSCs revealed decreased levels of actin cytoskeleton genes and their common transcription factor SRF. Down-regulation of SRF or chemical perturbation of actin cytoskeleton organization in diploid hPSCs resulted in increased replication stress and perturbation of chromosome condensation, recapitulating the findings in aneuploid hPSCs. Altogether, our results revealed that in hPSCs DNA replication stress results in a distinctive defect in chromosome condensation, underlying their ongoing chromosomal instability. Our results shed a new light on the mechanisms leading to ongoing chromosomal instability in hPSCs, and may be relevant to tumor development as well.

Publication Title

Genomic Instability in Human Pluripotent Stem Cells Arises from Replicative Stress and Chromosome Condensation Defects.

Sample Metadata Fields

Specimen part, Cell line

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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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