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accession-icon GSE64345
Neuronal changes induced by Varicella Zoster Virus in a rat model of Post Herpetic Neuralgia
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Neuronal reactivation of latent varicella zoster virus (VZV) causes debilitating and protracted pain (post herpetic neuralgia: PHN) in a significant fraction of patients.

Publication Title

Neuronal changes induced by Varicella Zoster Virus in a rat model of postherpetic neuralgia.

Sample Metadata Fields

Sex

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accession-icon SRP153814
Dissecting the autonomy of the liver circadian clock
  • organism-icon Mus musculus
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver Overall design: 8-12 week-old, female WT, KO and Liver-RE BMAL1-stop-FL mice (see referenced paper for details) were fed ad libitum normal chow under 12hr light/ 12hr dark schedule. Livers were harvested every 4 hours over the circadian cycle at ZT0, 4, 8, 12, 16, 20 (n=3 per time point per group). Total RNA was extracted and used for RNA-seq.

Publication Title

Defining the Independence of the Liver Circadian Clock.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP185806
RNA sequencing of wild-type Drosophila melanogaster brains in sated, fasted, or refed nutritional states
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the application of RNA-sequencing technology for high-throughput profiling of RNA abundance in Drosophila melanogaster brains. By obtaining RNA-sequencing reads, we generated quantitative transcriptome-wide measures in three nutritional states: sated, fasted, refed. Overall design: RNA sequencing of wild-type Drosophila melanogaster brains in sated, fasted, or refed nutritional states

Publication Title

Rapid metabolic shifts occur during the transition between hunger and satiety in Drosophila melanogaster.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP100793
Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease [2]
  • organism-icon Homo sapiens
  • sample-icon 189 Downloadable Samples
  • Technology Badge Icon

Description

Intestinal health is sustained by cooperation between diverse cell types, including epithelial cells, immune cells and stromal cells. Colonic stromal cells provide critical structural support but also regulate mucosal immunity, tolerance and inflammatory responses. Although mucosal stromal cells display substantial variability and plasticity, a paucity of unique genetic markers has precluded the identification of distinct stromal populations and functions. We used single-cell RNA-sequencing to uncover heterogeneity and subtype-specific markers of individual colonic stromal cells in health and ulcerative colitis (UC). Marker-free transcriptional clustering revealed four distinct stromal populations in healthy colon, corresponding to myofibroblasts and three previously unknown distinct subsets of fibroblasts. These fibroblast subsets were substantially remodeled in UC compared to healthy colon: inflamed UC colon was depleted for a healthy fibroblast subpopulation associated with epithelial cell homeostasis, and enriched for a novel disease-associated subtype expressing pro-inflammatory genes. Thus, we have discovered new, molecularly distinct colonic stromal cell subtypes that are altered in human disease. Overall design: Colonic lamina propria mesenchymal cells from 3 healthy donors. 183 single cell libraries, 6 bulk controls, 3 empty well controls. Individual donors processed as separate batches with Fluidigm C1 IFCs and pooled for sequencing (2 x Illumina HiSeq 2500 lanes).

Publication Title

Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP100795
Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease [3]
  • organism-icon Homo sapiens
  • sample-icon 162 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Intestinal health is sustained by cooperation between diverse cell types, including epithelial cells, immune cells and stromal cells. Colonic stromal cells provide critical structural support but also regulate mucosal immunity, tolerance and inflammatory responses. Although mucosal stromal cells display substantial variability and plasticity, a paucity of unique genetic markers has precluded the identification of distinct stromal populations and functions. We used single-cell RNA-sequencing to uncover heterogeneity and subtype-specific markers of individual colonic stromal cells in health and ulcerative colitis (UC). Marker-free transcriptional clustering revealed four distinct stromal populations in healthy colon, corresponding to myofibroblasts and three previously unknown distinct subsets of fibroblasts. These fibroblast subsets were substantially remodeled in UC compared to healthy colon: inflamed UC colon was depleted for a healthy fibroblast subpopulation associated with epithelial cell homeostasis, and enriched for a novel disease-associated subtype expressing pro-inflammatory genes. Thus, we have discovered new, molecularly distinct colonic stromal cell subtypes that are altered in human disease. Overall design: Ulcerative colitis colonic lamina propria mesenchymal cells from 3 donors. 178 single cell libraries, 7 bulk controls, 7 empty well controls. Individual donors processed as separate batches on Fluidigm C1 IFCs and pooled for sequencing (1 x Illumina HiSeq 4000 lane).

Publication Title

Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease.

Sample Metadata Fields

Disease, Subject

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accession-icon SRP100786
Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease [1]
  • organism-icon Homo sapiens
  • sample-icon 89 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Intestinal health is sustained by cooperation between diverse cell types, including epithelial cells, immune cells and stromal cells. Colonic stromal cells provide critical structural support but also regulate mucosal immunity, tolerance and inflammatory responses. Although mucosal stromal cells display substantial variability and plasticity, a paucity of unique genetic markers has precluded the identification of distinct stromal populations and functions. We used single-cell RNA-sequencing to uncover heterogeneity and subtype-specific markers of individual colonic stromal cells in health and ulcerative colitis (UC). Marker-free transcriptional clustering revealed four distinct stromal populations in healthy colon, corresponding to myofibroblasts and three previously unknown distinct subsets of fibroblasts. These fibroblast subsets were substantially remodeled in UC compared to healthy colon: inflamed UC colon was depleted for a healthy fibroblast subpopulation associated with epithelial cell homeostasis, and enriched for a novel disease-associated subtype expressing pro-inflammatory genes. Thus, we have discovered new, molecularly distinct colonic stromal cell subtypes that are altered in human disease. Overall design: Colonic epithelial cells from 3 healthy donors. 92 single cell libraries, 3 bulk controls, 1 empty well control. Individual donors processed as separate batches on Fluidigm C1 IFCs and pooled for sequencing (1 x Illumina HiSeq 2500 lane).

Publication Title

Structural Remodeling of the Human Colonic Mesenchyme in Inflammatory Bowel Disease.

Sample Metadata Fields

Disease, Subject

View Samples
accession-icon SRP063059
Transcriptome-wide Quantitative Analysis of XLPDR-derived human dermal fibroblasts with POLA1 deficiency
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The goal of this study is to analyzed transcriptome changes caused by POLA1 deficiency. Our data represents the first detailed analysis of molecular basis of XLPDR syndrome. We report than POLA1 deficiency leads to over-activation of IRF and NF-kB pathways with overexpression of typical markers of autoimmune syndromes. Overall design: Wild type and XLPDR-derived dermal fibroblasts are analyzed under non-stimulated (basal) conditions, after TNF treatment (2 and 12 h, 1000 U/mL), and poly(dA:dT) stimulation (16h, 1 mkg/mL). Obtained data were confirmed using the cellular model of XLPDR - normal dermal fibroblasts pretreated with control or anti-POLA1 siRNA and stimulated in analogous way.

Publication Title

NK cell defects in X-linked pigmentary reticulate disorder.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36895
Molecular Genetic Classification of clear-cell Renal Cell Carcinoma (ccRCC) based on the Gene Expression Profiling of Tumors and Tumorgrafts deficient for BAP1 or PBRM1
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice exhibited similar gene expression profiling to corresponding primary tumors. Gene expression profiling of tumors and tumorgrafts displayed different signatures for BAP1- and PBRM1-deficient samples. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities.

Publication Title

BAP1 loss defines a new class of renal cell carcinoma.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Subject

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accession-icon GSE29515
The transcriptional program controlled by Runx1 during early hematopoietic development
  • organism-icon Mus musculus
  • sample-icon 4 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

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29112
The transcriptional program controlled by Runx1 during early hematopoietic development (expression data)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcription factors have long been recognised as powerful regulators of mammalian development, yet it is largely unknown how individual key regulators operate within wider regulatory networks. Here we have used a combination of global gene expression and chromatin-immunoprecipitation approaches across four ES-cell-derived populations of increasing haematopoietic potential to define the transcriptional programme controlled by Runx1, an essential regulator of blood cell specification. Integrated analysis of these complementary genome-wide datasets allowed us to construct a global regulatory network model, which suggested that core regulatory circuits are activated sequentially during blood specification, but will ultimately collaborate to control many haematopoietically expressed genes. Using the CD41/integrin alpha 2b gene as a model, cellular and in vivo studies showed that CD41 is controlled by both early and late circuits in fully specified blood cells, but initiation of CD41 expression critically depends on a later subcircuit driven by Runx1. Taken together, this study represents the first global analysis of the transcriptional programme controlled by any key haematopoietic regulator during the process of early blood cell specification. Moreover, the concept of interplay between sequentially deployed core regulatory circuits is likely to represent a design principle widely applicable to the transcriptional control of mammalian development.

Publication Title

The transcriptional programme controlled by Runx1 during early embryonic blood development.

Sample Metadata Fields

Specimen part, Cell line

View Samples
...

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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