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accession-icon GSE92530
Genome-wide gene expression analysis of BQ.Ncf1m1J mutated and BQ wild type mice during collagen induced arthritis
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Whole blood and spleen tissue was collected 15 (d15) or 44 (d44) days postimmunization from mice immunized with type II collagen on day 0 and immunostimulated on day 21.

Publication Title

Reactive Oxygen Species Regulate Both Priming and Established Arthritis, but with Different Mechanisms.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP078976
Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response (UPR) pathway
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We examined the transcriptional changes modulated by KDM1A inhibitor NCD-38 by performing global transcriptome analysis. Glioma Stem Cells (GSC10) were treated with either vehicle or NCD-38 for 24 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that NCD-38 modulated several genes that are involved in unfolded protein response, endoplasmic reticulum stress pathway and NRF-2 mediated oxidative stress response. Overall design: Total RNA was isolated from the GSC10 cells that were treated with vehicle or NCD-38 for 24 hours. Illumina TruSeq RNA Sample Preparation was performed following manufacturer''s protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.

Publication Title

Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response pathway.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE75701
Human expression data from iPSCs, motor neurons derived from iPSCs and ESCs, and fetal spinal cords
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compare transcriptomic profiles of human induced pluripotent stem cells (iPSCs), motor neurons (MNs) in vitro differentiated from iPSCs or human ESCs containing a HB9::GFP reporter for MNs, and human fetal spinal cords.

Publication Title

ALS disrupts spinal motor neuron maturation and aging pathways within gene co-expression networks.

Sample Metadata Fields

Sex

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accession-icon SRP165889
Estrogen receptor beta enhances chemotherapy response of GBM cells by down regulating DNA damage response pathways
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We examined the transcriptional changes modulated by estrogen receptor beta (ERß) by performing global transcriptome analysis. U87 cells were transduced with lentiviral particles carrying either empty vector or ERß-FLAG expression vector and the RNA was isolated and utilized for RNA-seq analysis. Our results demonstrated that ERß modulated genes were related to homologous recombination, DNA damage response, ATM signaling and cell cycle pathways. Overall design: Total RNA was isolated from U87 cells expressing either empty vector or ERß expression vector. Illumina TruSeq RNA Sample Preparation was performed following manufacturer's protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat2. Genes were annotated and quantified by HTSeq-DESeq pipeline.

Publication Title

Estrogen receptor beta enhances chemotherapy response of GBM cells by down regulating DNA damage response pathways.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP062536
The Estrogen Receptor Co-Regulator Protein, Proline Glutamic Acid and Leucine Rich Protein 1 (PELP1) Mediates Estrogen Rapid Signaling and Neuroprotection in the Brain
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We examined the role of PELP1 in E2-ER-mediated transcription in the hippocampus under conditions of GCI by perfroming global transcriptome analysis. E2-treated FLOX and PELP1 FBKO mice were subjected to GCI followed by 24 h reperfusion and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that PELP1 is needed for optimal activation of E2-regulated genes following GCI. Overall design: Total RNA was isolated from the hippocampus of ovariectomized FLOX and PELP1 FBKO mice (implanted with E2 mini pumps) that were subjected to GCI followed by 24 h reperfusion. Illumina TruSeq RNA Sample Preparation was performed following manufacturer''s protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.

Publication Title

Proline-, glutamic acid-, and leucine-rich protein 1 mediates estrogen rapid signaling and neuroprotection in the brain.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP066968
Estrogen receptor coregulator binding modulators (ERXs) effectively target estrogen receptor positive human breast cancers
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We examined the transcriptional chagnes modulated by ECBI-11 by perfroming global transcriptome analysis. ZR75 cells were treated with either control or ECBI-11 in the presence of E2 for 48 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that ECBI modulated several genes that are involved in cell cycle, breast cancer signaling, estrogen signaling and apoptosis. Overall design: Total RNA was isolated from the ZR75 cells that were treated with vehicle or ECBI for 48 h. Illumina TruSeq RNA Sample Preparation was performed following manufacturer''s protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.

Publication Title

Estrogen receptor coregulator binding modulators (ERXs) effectively target estrogen receptor positive human breast cancers.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE24873
IL-17-induced NF-kB activation via CIKS/Act1: Physiologic significance and signaling mechanisms
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Interleukin-17 (IL-17) is essential in host defense against extracellular bacteria and fungi, especially at mucosal sites, but it also contributes significantly to inflammatory and autoimmune disease pathologies. Binding of IL-17 to its receptor leads to recruitment of the adaptor protein CIKS/Act1 via heterotypic association of their respective SEFIR domains and to activation of the transcription factor NF-kB; it is not known whether CIKS and/or NF-kB are required for all gene induction events. Here we report that CIKS is essential for all IL-17 induced immediate-early genes in primary mouse embryo fibroblasts, while NF-kB is profoundly involved. We also identify a novel sub-domain in the N-terminus of CIKS that is essential for IL-17-mediated NF-kB activation. This domain is both necessary and sufficient for the interaction between CIKS and TRAF6, an adaptor required for NF-kB activation. The ability of decoy peptides to block this interaction may provide a new therapeutic strategy for intervention in IL-17-driven autoimmune and inflammatory diseases.

Publication Title

IL-17-induced NF-kappaB activation via CIKS/Act1: physiologic significance and signaling mechanisms.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP032798
iPSC derived motor neuron cultures from C9ORF72 carriers
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord. Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9ORF72 gene are the most common cause of the familial form of ALS (C9-ALS), as well as frontotemporal lobar degeneration and other neurological diseases. How the repeat expansion causes disease remains unclear, with both loss of function (haploinsufficiency) and gain of function (either toxic RNA or protein products) proposed. We report a cellular model of C9-ALS with motor neurons differentiated from induced pluripotent stem cells (iPSCs) derived from ALS patients carrying the C9ORF72 repeat expansion. No significant loss of C9ORF72 expression was observed, and knockdown of the transcript was not toxic to cultured human motor neurons. Transcription of the repeat was increased, leading to accumulation of GGGGCC repeat–containing RNA foci selectively in C9-ALS iPSC-derived motor neurons. Repeat-containing RNA foci colocalized with hnRNPA1 and Pur-a, suggesting that they may be able to alter RNA metabolism. C9-ALS motor neurons showed altered expression of genes involved in membrane excitability including DPP6, and demonstrated a diminished capacity to fire continuous spikes upon depolarization compared to control motor neurons. Antisense oligonucleotides targeting the C9ORF72 transcript suppressed RNA foci formation and reversed gene expression alterations in C9-ALS motor neurons. These data show that patient-derived motor neurons can be used to delineate pathogenic events in ALS. Overall design: Transcriptome profiling from iPSC derived motor neurons compared to controls

Publication Title

Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP106034
mRNA Sequencing of Human PromoCells Using 3''-directed Digital Gene Expression (3''-DGE) Technique
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The differential gene expression of human cardiomyocytes induced by kinase inhibitors sorafenib and sunitinib is measured by a high-throughput mRNA-sequencing approach called 3''-DGE, that is based on a 3'' end-focused reference sequence library and a transcript molecule counting method with unique molecular identifiers (UMI) for correcting PCR bias. Overall design: Cells were treated with sunitinib, sorafenib, or vehicle control for 48 hours, and gene expression levels of all samples were measured by 3''-DGE and conventional random-primed mRNA-sequencing methods using paired-end reading to obtain the genome-wide expression profiles for each sample.

Publication Title

A Comparison of mRNA Sequencing with Random Primed and 3'-Directed Libraries.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP079913
Effects of the expression of a samble mutant of Kif1-Binding Protein (KBP) on the transcriptome of self-renewing ES cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mouse ES cells were stably transduced with a lentivirus expressing either wild-type KBP or the stable mutant KBP(KK/RR) and maintained in self-renewing growth conditions. RNA-seq was performed to assess mRNA expression differences caused by the stabilization of KBP. Overall design: 6 samples [a triplicate set for ES cells expressing wild-type KBP and a triplicate set expressing KBP(KK/RR)] were analyzed.

Publication Title

The TDH-GCN5L1-Fbxo15-KBP axis limits mitochondrial biogenesis in mouse embryonic 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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