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accession-icon GSE35661
A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE35659
A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype (resting muscle after endurance training)
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The molecular pathways which are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ~800 gene transcripts are regulated following 6 weeks of supervised endurance training in young sedentary males, referred to as the training responsive transcriptome (TRT). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as over-represented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9 and PAX3 were down-regulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, pro-angiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA level validation there were several DNA variants that associated with VO(2)max trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.

Publication Title

A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE18583
Baseline skeletal muscle gene expression
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Muscle biopsy samples were obtained from two groups of male subjects prior to endurance training. The samples were used to predict training responses.

Publication Title

Using molecular classification to predict gains in maximal aerobic capacity following endurance exercise training in humans.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE59880
Stockholm dataset for ageing prototype diagnostic
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Muscle biopsy samples from healthy male subjects at the baseline belonging to either <29y or >59y age range. These samples were used to design a prototype of multi-tissue molecular diagnostic of healthy physiological age.

Publication Title

Using molecular classification to predict gains in maximal aerobic capacity following endurance exercise training in humans.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE21419
Laser Capture Microdissection of Hyperlipidemic Mouse Aorta Atherosclerosis
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Atherosclerosis is a transmural chronic inflammatory condition of small and large arteries that is associated with adaptive immune responses at all disease stages. However, impacts of adaptive immune reactions on clinically apparent atherosclerosis such as intima lesion (plaque) rupture, thrombosis, myocardial infarction, and aneurysm largely remain to be identified. It is increasingly recognized that leukocyte infiltrates in plaque, media, and adventitia are distinct but their specific roles have not been defined. To map these infiltrates, we employed laser capture microdissection (LCM) to isolate the three arterial wall laminae using apoE-/- mouse aorta as a model. RNA from LCM-separated tissues was extracted and large scale whole genome expression microarrays were prepared. We observed that the quality of the resulting gene expression maps was compromised by tissue RNA carried over from adjacent laminae during LCM. To account for these flaws, we established quality controls and algorithms to improve the predictive power of LCM-derived microarray data. Our approach creates robust transcriptome atlases of normal and atherosclerotic aorta. Assessing LCM transcriptomes for immunity-related mRNAs indicated markedly distinctive gene expression patterns in the three laminae of the atherosclerotic aorta. These mouse mRNA expression data banks can now be mined to address a wide range of questions in cardiovascular biology.

Publication Title

The lamina adventitia is the major site of immune cell accumulation in standard chow-fed apolipoprotein E-deficient mice.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE17383
Toward a Better Understanding of Potential Roles of Astrocytes in HIV-1-associated Neurocognitive Disorders
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We present a microarray analysis of primary mouse astrocytes exposed to HIV-1 in culture. Results are compared with previous genomic studies of HIV-1 effect in human astrocytes and human and macaque brains.

Publication Title

Gene expression profiles of HIV-1-infected glia and brain: toward better understanding of the role of astrocytes in HIV-1-associated neurocognitive disorders.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE7772
Comparison between mRNAs of how germ-line clones embryos and WT embryos at 3-5 h AEL
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Mutant embryos lacking maternal and zygotic HOW exhibit defects in mesoderm development. How is an RNA binding protein that regulates the levels of mRNAs by controling RNA metabolism.

Publication Title

Post-transcriptional repression of the Drosophila midkine and pleiotrophin homolog miple by HOW is essential for correct mesoderm spreading.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13093
Feeding schedule and the circadian clock shape rhythms in hepatic gene expression
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13060
The effects of temporally restricted feeding on hepatic gene expression
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Temporally restricted feeding is known to impact the circadian clock. This dataset shows the effects of temporally restricted feeding on the hepatic transcriptome.

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13062
The effects of temporally restricted feeding on hepatic gene expression of Cry1, Cry2 double KO mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
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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)

fund-icon Fund the CCDL

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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