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accession-icon GSE57999
Expression data from baseline and post-endurance training in human PBMCs
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

There is an association between transcriptome and the exercise-related phenotype. Peripheral blood cells suffer alterations in the gene expression pattern in response to perturbations caused by exercise. The acute response to endurance activates stress and inflammation, as well as growth and tissue repair responses.

Publication Title

PBMCs express a transcriptome signature predictor of oxygen uptake responsiveness to endurance exercise training in men.

Sample Metadata Fields

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

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accession-icon SRP014147
Bos taurus Transcriptome or Gene expression
  • organism-icon Bos taurus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

Sequencing of a pool of 9 bulls of varying conception rate (CR) scores from -2.9 to 3.5.

Publication Title

Cryopreserved bovine spermatozoal transcript profile as revealed by high-throughput ribonucleic acid sequencing.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29806
Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in NOD mice
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Vertebrates typically harbor a rich gastrointestinal microbiota, which has co-evolved with the host over millennia and is essential for several of its physiological functions, in particular maturation of the immune system. Recent studies have highlighted the importance of a single bacterial species, segmented filamentous bacteria (SFB), in inducing a robust T helper (Th)17 population in the small intestinal lamina propria (SI-LP) of the mouse gut. Consequently, SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encephalomyelitis. Here, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to explore its impact on the incidence and course of type-1 diabetes in this prototypical, spontaneous model. There was a strong co-segregation of SFB-positivity and diabetes protection in females, but not in males, which remained relatively disease-free regardless of the SFB status. In contrast, insulitis did not depend on SFB colonization. SFB-positive, but not SFB-negative, females had a substantial population of Th17 cells in the SI-LP, which was the only significant, repeatable difference in the examined T cell compartments of the gut, pancreas or systemic lymphoid tissues. Th17 signature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4+ T cells. Thus, a single bacterium, and the gut immune system alterations associated with it, can either promote or protect from autoimmunity in predisposed mouse models, likely reflecting their variable dependence on different Th subsets.

Publication Title

Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in nonobese diabetic mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE62064
Radial glia require PDGFD/PDGFRB signaling in human but not mouse neocortex
  • organism-icon Homo sapiens
  • sample-icon 87 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of gene expression over serial 150um sections of a single gestational week 14.5 human neocortical specimen. The hypothesis tested with this dataset was that a transcriptional signature of radial glia (neural stem cells) could be isolated via unsupervised gene coexpression analysis due to variation in the abundance of this cell type from section to section. This dataset is the first of its kind generated using this method (Gene Coexpression Analysis of Serial Sections, or GCASS).

Publication Title

Radial glia require PDGFD-PDGFRβ signalling in human but not mouse neocortex.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP065040
A Primate lncRNA Mediates Notch Signaling During Neuronal Development by Sequestering miRNA [single cell sequencing analysis]
  • organism-icon Homo sapiens
  • sample-icon 240 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Long non-coding RNAs (lncRNAs) are a diverse category of transcripts with poor conservation and have expanded greatly in primates, particularly in their brain. We identified a lncRNA, which has acquired 16 microRNA response elements (MREs) for miR-143-3p in the Catarrhini branch of primates. This lncRNA termed LncND (neuro-development) gets expressed in neural progenitor cells and then declines in mature neurons. Binding and release of miR-143-3p, by LncND, can control the expression of Notch. Its expression is highest in radial glia cells in the ventricular and outer subventricular zones of human fetal brain. Down-regulation of LncND in neuroblastoma cells reduced cell proliferation and induced neuronal differentiation, an effect phenocopied by miR-143-3p over-expression and supported by RNA-seq analysis. These findings support a role for LncND in miRNA-mediated regulation of Notch signaling in the expansion of the neural progenitor pool of primates and hence contributing to the rapid growth of the cerebral cortex. Overall design: Cerebral organoids were generated as in Lancaster et al. (Lancaster and Knoblich, 2014). Organoids were dissociated into single cells and captured on C1 Single-Cell Auto Prep Integrated Fluidic Circuit (IFC) (Fluidigm). The RNA extraction and amplification was performed on the chip as described by the manufacturer. We captured 68 single-cells on a C1 Single-Cell Auto Prep System (Fluidigm) and sequenced the RNA on a NextSeq500 System (Illumina) (Pollen et al., 2014). Out of 68 cells, we obtained 60 high quality cells.

Publication Title

A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064761
A Primate lncRNA Mediates Notch Signaling During Neuronal Development by Sequestering miRNA [SHSY5Y cells]
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Long non-coding RNAs (lncRNAs) are a diverse category of transcripts with poor conservation and have expanded greatly in primates, particularly in their brain. We identified a lncRNA, which has acquired 16 microRNA response elements (MREs) for miR-143-3p in the Catarrhini branch of primates. This lncRNA termed LncND (neuro-development) gets expressed in neural progenitor cells and then declines in mature neurons. Binding and release of miR-143-3p, by LncND, can control the expression of Notch. Its expression is highest in radial glia cells in the ventricular and outer subventricular zones of human fetal brain. Down-regulation of LncND in neuroblastoma cells reduced cell proliferation and induced neuronal differentiation, an effect phenocopied by miR-143-3p over-expression and supported by RNA-seq analysis. These findings support a role for LncND in miRNA-mediated regulation of Notch signaling in the expansion of the neural progenitor pool of primates and hence contributing to the rapid growth of the cerebral cortex. Overall design: SHSY5Y cells treated either with miR-143-3p mimic or 100 nM of siRNA specific for LncND were sequenced on NextSeq500 platform. Scrambled siRNA or miRNA sequences were used as a negative control.

Publication Title

A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32012
Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Recurrent Copy Number Variations (CNVs) of human 16p11.2 have been associated with a variety of developmental/neurocognitive syndromes. In particular, deletion of 16p11.2 is found in patients with autism, developmental delay, and obesity. Patients with deletions or duplications have a wide range of clinical features, and siblings carrying the same deletion often have diverse symptoms. To study the consequence of 16p11.2 CNVs in a systematic manner, we used chromosome engineering to generate mice harboring deletion of the chromosomal region corresponding to 16p11.2, as well as mice harboring the reciprocal duplication. These 16p11.2 CNV models have dosage-dependent changes in gene expression, viability, brain architecture, and behavior. For each phenotype, the consequence of the deletion is more severe than that of the duplication. Of particular note is that half of the 16p11.2 deletion mice die postnatally; those that survive to adulthood are healthy and fertile, but have alterations in the hypothalamus and exhibit a behavior trap phenotypea specific behavior characteristic of rodents with lateral hypothalamic and nigrostriatal lesions. Our findings indicate that 16p11.2 CNVs cause both brain and behavioral anomalies, providing new insight into human neurodevelopmental disorders.

Publication Title

Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism.

Sample Metadata Fields

Sex

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accession-icon SRP106491
Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4 [mRNA]
  • organism-icon Rattus norvegicus
  • sample-icon 117 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the changes in left ventricle mRNA abundance in response to 5/6 nephrectomy surgery Overall design: Ten week old male Sprague Dawley rats were subjected to the excision model of 5/6 nephrectomy (5/6Nx) or sham surgery. Left ventricle tissue was collected 2, 4, 5 or 7 weeks later for mRNAsequencing.

Publication Title

MicroRNA-21 regulates peroxisome proliferator-activated receptor alpha, a molecular mechanism of cardiac pathology in Cardiorenal Syndrome Type 4.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP106489
Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4 [anti-miR-21]
  • organism-icon Rattus norvegicus
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the changes in left ventricle mRNA abundance in response to miR-21-5p suppression in 5/6 nephrectomized rats. Overall design: Ten week old male Sprague Dawley rats were subjected to the excision model of 5/6 nephrectomy (5/6Nx) surgery. LNA-anti-scrambled or LNA-anti-miR-21-5p was delivered intravenously in 3 daily doses of 1 mg/kg at 1 and 4 weels post-surgery. Left ventricle tissue was collected for mRNA sequencing 7 weeks after surgery.

Publication Title

MicroRNA-21 regulates peroxisome proliferator-activated receptor alpha, a molecular mechanism of cardiac pathology in Cardiorenal Syndrome Type 4.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26626
mRNAs associated with human Pumilio2 protein (PUM2)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The presence of the PUF (Pumilio/FBF) domain defines a conserved family of RNA-binding proteins involved in repressing gene expression. It has been suggested that a conserved function of PUF proteins is to repress differentiation and sustain the mitotic proliferation of stem cells. In humans, Pumilio2 (PUM2) is expressed in embryonic stem cells and adult germ cells.

Publication Title

PUMILIO-2 is involved in the positive regulation of cellular proliferation in human adipose-derived stem cells.

Sample Metadata Fields

Specimen part, Subject

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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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