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accession-icon GSE75441
Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

One of the challenges of current research in prostate cancer is to improve the differential non-invasive diagnosis of prostate cancer (PCa) and benign prostate hyperplasia (BPH). Extracellular vesicles (EV) are emerging structures with promising properties for intercellular communication. In addition, the characterization of EV in biofluids is an attractive source of non-invasive diagnostic, prognostic and predictive biomarkers. Here we show that urinary EV (uEV) from prostate cancer patients exhibit genuine and differential physical and biological properties. Importantly, transcriptomics characterization of uEVs led us to define the decreased abundance of Cadherin 3, type 1 (CDH3) transcript in uEV from PCa patients. Tissue and cell line analysis strongly suggested that the status of CDH3 in uEVs is a distal reflection of changes in the expression of this cadherin in the prostate tumor. Our results reveal that uEVs could represent a non-invasive tool to inform about the molecular alterations in prostate cancer.

Publication Title

Transcriptomic profiling of urine extracellular vesicles reveals alterations of CDH3 in prostate cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE12304
Albumin, TGF-Beta1 and Blood-Brain Barrier opening induce cortical epileptogenesis.
  • organism-icon Rattus norvegicus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Insults to the cerebral cortex, such as trauma, ischemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Previous studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the underlying mechanisms are unknown. As with BBB opening, treatment with albumin or with TGF-1 results in the development of hypersynchronized epileptiform activity. Given the latent period before the appearance of epileptiform activity, we hypothesized the underlying mechanism is a transcriptional response which would be similar for BBB breakdown and exposure to albumin or TGF-1. In search of a common pathway and transcriptional activation pattern we performed a genome wide analysis. Genomic expression analyses demonstrated similar expression patterns for BBB opening, albumin and TGF-1 exposure. Most importantly, TGF- pathway blockers suppressed most albumin-induced transcriptional changes.

Publication Title

Astrocytic dysfunction in epileptogenesis: consequence of altered potassium and glutamate homeostasis?

Sample Metadata Fields

Sex

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accession-icon GSE13190
Global gene-expression analyses of the Esrrb reprogrammed cells and Esrrb knockdown cells
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming.

Publication Title

Reprogramming of fibroblasts into induced pluripotent stem cells with orphan nuclear receptor Esrrb.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13212
Global gene-expression analyses of the Esrrb knockdown cells
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming.

Publication Title

Reprogramming of fibroblasts into induced pluripotent stem cells with orphan nuclear receptor Esrrb.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13211
Global gene-expression analyses of the Esrrb reprogrammed cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming.

Publication Title

Reprogramming of fibroblasts into induced pluripotent stem cells with orphan nuclear receptor Esrrb.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE7148
Differential gene expression in peripheral blood leukocytes from CHASRS particpants
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene expression profiling was carried out on peripheral blood leukocytes from 14 healthy older adults. The primary research question is whether gene expression differs in individuals experiencing chronically high levels of social isolation (by UCLA Loneliness Scale) vs chronically low levels of social isolation.

Publication Title

Social regulation of gene expression in human leukocytes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP107205
Epigenetic restriction of embryonic and extraembryonic lineages mirrors the somatic transition to cancer (Perturbation-RNAseq)
  • organism-icon Mus musculus
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Concerted efforts over past decades have established a thorough understanding of the canonical somatic DNA methylation landscape as well as its systematic misregulation across most human cancers. However, the underlying mechanism that directs this genome-scale transformation remains elusive, with no clear model for its acquisition or understanding of its potential developmental utility. Here we present base pair resolution analysis of global remethylation from the hypomethylated state of the preimplantation embryo into the early epiblast and extraembryonic ectoderm. We show that these two states acquire highly divergent genomic distributions: while the proximal epiblast establishes a canonical CpG-density dependent pattern found in somatic cells, the extraembryonic epigenome becomes substantially more mosaic. Moreover, this alternate pattern includes specific de novo methylation of hundreds of CpG island promoter containing genes that function in early embryonic development and are orthologously methylated across an extensive cohort of human cancers. From these data, we propose a model where the evolutionary innovation of extraembryonic tissues in eutherian mammals required cooption of DNA methylation-based suppression as an alternate pathway to the embryonically utilized Polycomb group proteins, which otherwise coordinate germ layer formation in response to extraembryonic cues at the onset of gastrulation. Moreover, we establish that this decision is made deterministically downstream of the promiscuously utilized, and frequently oncogenic, FGF signaling pathway and utilizes a novel combination of epigenetic cofactors. Recruitment of this silencing mechanism to developmental genes during cancer therefore reflects the misappropriation of an innate regulatory pathway that may be spontaneously sampled as an alternate epigenetic landscape within somatic cells. Overall design: Comparison of gene expression patterns in Extraembryonic Ectoderm and cancer

Publication Title

Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP043093
Transcriptome comparison of mouse pancreatic islets cultured at low vs high ambient glucose
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Islets are known to respond to changes in ambient glucose. To quantify the transcriptome-wide changes in ambient glucose, we compared transcriptome of islets exposed to low and high glucose. Overall design: Isolated islets from wild type male mice. Islets from adult males were pooled, cultured overnight in RPMI containing 11 mM glucose. The next day, all islets were starved in RPMI containing 2.8 mM glucose for 2 hours before stimulation with 2.8 mM glucose or 16.8 mM glucose for 12 hours. Islets were lysed in Trizol for RNA isolation and library construction.

Publication Title

The transcriptional landscape of mouse beta cells compared to human beta cells reveals notable species differences in long non-coding RNA and protein-coding gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP033135
Pseudo-temporal ordering of individual cells reveals regulators of differentiation
  • organism-icon Homo sapiens
  • sample-icon 384 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500, IlluminaHiSeq2000

Description

Single-cell expression profiling by RNA-Seq promises to exploit cell-to-cell variation in gene expression to reveal regulatory circuitry governing cell differentiation and other biological processes. Here, we describe Monocle, a novel unsupervised algorithm for ordering cells by progress through differentiation that dramatically increases temporal resolution of expression measurements. This reordering unmasks switch-like changes in expression of key regulatory factors, reveals sequentially organized waves of gene regulation, and exposes regulators of cell differentiation. A functional screen confirms that a number of these regulators dramatically alter the efficiency of myoblast differentiation, demonstrating that single-cell expression analysis with Monocle can uncover new regulators even in well-studied systems. Overall design: We selected primary human myoblasts as a model system of cell differentiation to investigate whether ordering cells by progress revealed new regulators of the process. We sequenced RNA-Seq libraries from each of several hundred cells taken over a time-course of serum-induced differentiation. Please note that this dataset is a single-cell RNA-Seq data set, and each cell comes from a capture plate. Thus, each well of the plate was scored and flagged with several QC criteria prior to library construction, which are provided as sample characteristics; CONTROL indicates that this library is a off-chip tube control library constructed from RNA of approximately 250 cells and ''DEBRIS'' indicates that the well contained visible debris (and may or may not include a cell). Libraries marked DEBRIS thus cannot be confirmed to come from a single cell.

Publication Title

The dynamics and regulators of cell fate decisions are revealed by pseudotemporal ordering of single cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE93987
Distinctive transcriptome alterations of prefrontal pyramidal neurons in schizophrenia and schizoaffective disorder
  • organism-icon Homo sapiens
  • sample-icon 207 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Schizophrenia is associated with alterations in working memory that reflect dysfunction of dorsolateral prefrontal cortex (DLPFC) circuitry. Working memory depends on the activity of excitatory pyramidal cells in DLPFC layer 3, and to a lesser extent in layer 5.

Publication Title

Distinctive transcriptome alterations of prefrontal pyramidal neurons in schizophrenia and schizoaffective disorder.

Sample Metadata Fields

Specimen part

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)

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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