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accession-icon SRP136102
Systemic Lupus Erythematosus patient blood with controls
  • organism-icon Homo sapiens
  • sample-icon 120 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The experiment consists of 31 Systemic Lupus Erythematosus patient blood samples and 29 healthy donor blood samples. Overall design: Whole blood was collected in PaxGene tubes from 31 SLE and 29 healthy donors.

Publication Title

Machine learning applied to whole-blood RNA-sequencing data uncovers distinct subsets of patients with systemic lupus erythematosus.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE49804
Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone

Publication Title

Caveolin-1 regulates genomic action of the glucocorticoid receptor in neural stem cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP132018
In-vitro stimulation of healthy donor blood with IL-3 cytokine
  • organism-icon Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

This experiment was designed to look for in vitro IL-3 gene signature in donor blood at two different time points (6 and 24 hours). RNA from lysed whole blood cells was used for the sequencing. Overall design: Lysed whole blood from seven healthy donors was stimulated with recombinant human IL-3 for 6 hours, or 24 hours, prior to RNA extraction for next-generation sequencing on the Illumina HiSeq platform. Unstimulated samples were included as controls.

Publication Title

A potential association between IL-3 and type I and III interferons in systemic lupus erythematosus.

Sample Metadata Fields

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

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accession-icon SRP067022
Expression data from dexamethasone treated mouse embryonic hypothalamic progenitor/stem cells isolated from wild type C57Bl/6 male or female mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used RNA-Seq to detail the global program of sexually dimorphic dexamethasone regulated gene expression in embryonic hypothalamic neural progenitor/stem cells. Overall design: RNAseq on Primary E14.5 mouse hyothalamic neurosphere cultures. 4 conditions - Male Dex, Male EtOH, Female Dex and Female EtOH. There are 3 biological replicates for each condition and all the 12 samples are run on two lanes (techinical duplicates).

Publication Title

Research Resource: The Dexamethasone Transcriptome in Hypothalamic Embryonic Neural Stem Cells.

Sample Metadata Fields

Sex, Cell line, Treatment, Subject

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accession-icon SRP071837
Stimulation of isolated plasmacytoid dendritic cells (pDCs) with TLR9 agonist CpG C (CpG) and TLR7 agonist imiquimod (IMQ)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The purpose of this experiment was to assess the genes upregulated when pDCs were stimulated with TLR7 agonist imiquimod and TLR9 agonist CpG C. Overall design: pDCs were isolated from six healthy donors by FACS sorting, and were stimulated with CpG and imiquimod for 18 hours, after which RNA was extracted for next generation sequencing on the Illumina HiSeq platform. Unstimulated samples were included as controls.

Publication Title

A cytotoxic anti-IL-3Rα antibody targets key cells and cytokines implicated in systemic lupus erythematosus.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37700
Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE37699
Aberrant ERK signaling causes resistance to EGFR kinase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models harboring EGFR T790M, resistance to WZ4002 develops through aberrant activation of ERK signaling caused by either an amplification of MAPK1 or by downregulation of negative regulators of ERK signaling. Inhibition of MEK or ERK restores sensitivity to WZ4002, and the combination of WZ4002 and a MEK inhibitor prevents the emergence of drug resistance. The WZ4002 resistant MAPK1 amplified cells also demonstrate an increase both in EGFR internalization and a decrease in sensitivity to cytotoxic chemotherapy compared to the parental counterparts. Our findings provide insights into mechanisms of drug resistance to EGFR kinase inhibitors and highlight rational combination therapies that should be evaluated in clinical trials.

Publication Title

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE38431
Gene expression from induced CB-derived neurons at different time of differentiation
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Gene expression from cord blood stem cells and respective derived neuronal cells at different times point of differentiation:CD133+ cells;

Publication Title

Cord blood-derived neuronal cells by ectopic expression of Sox2 and c-Myc.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP031857
Transcriptome Sequencing During Mouse Brain Development Identifies Long Non-Coding RNAs Functionally Involved in Neurogenic Commitment
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem cell commitment during neurogenesis. “LncRNAs control neurogenesis” Aprea, Prenninger, Dori, Monasor, Wessendof, Zocher, Massalini, Ghosh, Alexopoulou, Lesche, Dahl, Groszer, Hiller, Calegari, The EMBO Journal (In Press) Overall design: mRNA profiles of Proliferating Progenitors, Differentiating Progenitors and Neurons from lateral cortex of E14.5 mouse embryos. Each cell type in three biological replicates.

Publication Title

Transcriptome sequencing during mouse brain development identifies long non-coding RNAs functionally involved in neurogenic commitment.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE43794
Differentiation of human fetal multipotential neural progenitor cells to astrocytes reveals susceptibility factors for JC Virus
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Viral infections of the CNS are of increasing concern, especially among immunocompromised populations. Rodent models are often inappropriate for studies of CNS infection, as many viruses, including JC Virus (JCV) and HIV, cannot replicate in rodent cells. Consequently, human fetal brain-derived multipotential CNS progenitor cells (NPCs) that can be differentiated into neurons, oligodendrocytes, or astrocytes, have served as a model for CNS studies. NPCs can be non-productively infected by JCV, while infection of progenitor-derived astrocytes (PDAs) is robust. We profiled cellular gene expression at multiple times during differentiation of NPCs to PDAs. Several activated transcription factors show commonality between cells of the brain in which JCV replicates and lymphocytes in which JCV is likely latent. Bioinformatic analysis determined transcription factors that may influence the favorable transcriptional environment for JCV in PDAs. This study attempts to provide a framework for understanding the functional transcriptional profile necessary for productive JCV infection.

Publication Title

Differentiation of human fetal multipotential neural progenitor cells to astrocytes reveals susceptibility factors for JC virus.

Sample Metadata Fields

Specimen part, Time

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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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