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accession-icon SRP052872
Differential expression between Sh2b3 knockout and wild type mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To validate the predicted Sh2b3 derived gene regulatory subnetwork using integrative network approach in human population study, we examined the gene expression levels of whole blood in WT (wild-type) and Sh2b3-/- mice by RNA sequencing, and identified the differentially expressed genes. Overall design: RNA sequencing whole blood samples from 4 WT and 4 Sh2b3-/- mice.

Publication Title

Integrative network analysis reveals molecular mechanisms of blood pressure regulation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE90696
Identification of evolutionary conserved gene networks that mediate neurodegenerative dementia
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 38 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

Identification of evolutionarily conserved gene networks mediating neurodegenerative dementia.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon SRP149532
Genome wide analysis of SAHA (vorinostat) treatment in human iPSC-derived neurons from Tau A152T patients and controls
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon

Description

Purpose: The goal of this study was to assess gene expression changes upon SAHA treatment in neurons derived from patients with A152T Tau mutation Overall design: iPSC derived neurons were treated with SAHA at different dosage for several days

Publication Title

Identification of evolutionarily conserved gene networks mediating neurodegenerative dementia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP149533
Genome wide analysis of SAHA (vorinostat) treatment in primary mouse cortical neurons upon miR-203 overexpression
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Purpose: The goal of this study was to assess gene expression changes upon SAHA treatment in cells overexpressing miR-203. Overall design: Primary cortical cultures were established using E15 cortical cultures from C57BL/6J mice. At DIV0, cells were infectd with either miR-203 (high titre - 1MOI) or intermediate titre (0.5MOI) or control (high 1MOI) lentivirus andalso treated with different dose of SAHA. At DIV8, total RNA was isolated using NucleoSpin RNA XS kit (Takara). Libraries were prepared using Standard illumina stranded mRNA-seq protocol.

Publication Title

Identification of evolutionarily conserved gene networks mediating neurodegenerative dementia.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE16214
Expression data from relapsing-remitting MS samples
  • organism-icon Homo sapiens
  • sample-icon 229 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

One of our new major finding among the genes that contributes to MS susceptibility is ICSBP1. The so called disease modifying therapies like interferon-beta (IFN-), possibly acting on the peripheral T-cells, reduce the disease activity and the clinical progression, with a MRI-detectable effect in preventing lesion burden and cerebral atrophy development in RR-MS. It suggests a critical role of peripheral blood mononuclear cells (PBMCs) immune response and modulation in developing inflammation in the brain. We tested the hypothesis that the genetic effect of the susceptible allele ICSBP1 can impact the gene expression profile of molecules belonging to the interferon pathway. We therefore interrogated the PBMC for changes in gene expression profile. We correlate those changes with the minor allele frequency for ICSBP1, performing independent quantitative trait analysis for each treatment category. Expression Quantitative Trait Loci Association with a p value < 0.05 have been used in follow up analysis. The regression coefficient of the Quantitative trait association represents the degree of correlation between the gene expression for each interrogated target gene and the minor allele frequency of the SNP for our gene of interest. This coefficient has been used as input in the subsequent Gene Set Enrichment Analysis performed in a pre-ranked approach. The resulting GSEA-SNP method rests on the assumption that SNPs underlying a disease phenotype might affect genes constituting a signaling pathway or genes with a common regulation. Therefore, GSEA-SNP can facilitate the identification of pathways or of underlying biological mechanisms.

Publication Title

Meta-analysis of genome scans and replication identify CD6, IRF8 and TNFRSF1A as new multiple sclerosis susceptibility loci.

Sample Metadata Fields

Specimen part

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accession-icon SRP090108
RNA Sequencing Quantitative Analysis of RNA editing sites of Wild Type and ADAR1 editing deficient (ADAR1E861A) murine fetal RNA of various tissues
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Adar1 deaminase inactive mutant mouse tissue samples were obtain from the Walkley lab as described in http://www.ncbi.nlm.nih.gov/pubmed/26275108. We performed mmPCR-seq on the samples and measured the editing levels of. Overall design: Fetal mRNA profiles of E12.5 wild type (WT) and ADAR E861A mutant mice were generated by deep sequencing using Illumina HiSeq 2000.

Publication Title

Dynamic landscape and regulation of RNA editing in mammals.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE58445
Gene expression signatures delineate biological and prognostic subgroups in peripheral T-cell lymphoma
  • organism-icon Homo sapiens
  • sample-icon 188 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Peripheral T-cell lymphoma (PTCL) encompasses a heterogeneous group of neoplasms with generally poor clinical outcome. Currently 50% of PTCL cases are not classifiable: PTCL-not otherwise specified (NOS). Gene-expression profiles on 372 PTCL cases were analyzed and robust molecular classifiers and oncogenic pathways that reflect the pathobiology of tumor cells and their microenvironment were identified for major PTCL-entities, including 114 angioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (ALK)-positive and 48 ALK-negative anaplastic large cell lymphoma, 14 adult T-cell leukemia/lymphoma and 44 extranodal NK/T-cell lymphoma that were further separated into NK-cell and gdT-cell lymphomas. Thirty-seven percent of morphologically diagnosed PTCL-NOS cases were reclassified into other specific subtypes by molecular signatures. Reexamination, immunohistochemistry, and IDH2 mutation analysis in reclassified cases supported the validity of the reclassification. Two major molecular subgroups can be identified in the remaining PTCL-NOS cases characterized by high expression of either GATA3 (33%; 40/121) or TBX21 (49%; 59/121). The GATA3 subgroup was significantly associated with poor overall survival (P=.01). High expression of cytotoxic genesignaturewithin the TBX21 subgroup also showed poor clinical outcome (P=.05). InAITL, high expression of several signatures associated with the tumor microenvironment was significantly associated with outcome. A combined prognostic score was predictive of survival in an independent cohort (P=.004).

Publication Title

Gene expression signatures delineate biological and prognostic subgroups in peripheral T-cell lymphoma.

Sample Metadata Fields

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

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accession-icon SRP061412
Transcriptome analysis of RANK-positive and RANK-negative luminal progenitor subpopulations in the human breast
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

RANK-positive and RANK-negative luminal progenitor cells were isolated by FACS from histologically normal human breast tissue from wild-type human donors. RNA-seq gene expression profiling was used to find differentially expressed genes between the RANK-positive and RANK-negative cell populations. Overall design: Cells were isolated from 4 human patients. A paired analysis was used to compare RANK-positive and RANK-negative cells within patients.

Publication Title

RANK ligand as a potential target for breast cancer prevention in BRCA1-mutation carriers.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31637
Tumor Suppressor BRCA1 epigenetically controls oncogenic miRNA-155
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

BRCA1, a well-known breast and ovarian cancer susceptibility gene with multiple interacting partners, is predicted to have diverse biological functions. However, to date its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate risk variant, and found that it does not impair DNA damage repair but abrogates the repression of miR-155, a bona fide oncomir. We further show that in the absence of functional BRCA1, miR-155 is up-regulated in BRCA1-deficient mouse mammary epithelial cells, human and mouse BRCA1-deficienct breast tumor cell lines as well as tumors. Mechanistically, we found that BRCA1 represses miR-155 expression via its association with HDAC2, which deacetylates H2A and H3 on the miR-155 promoter. Finally, we show that over-expression of miR-155 accelerates whereas the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Taken together, our findings demonstrate a new mode of tumor suppression by BRCA1 and reveal miR-155 as a potential therapeutic target for BRCA1-deficient tumors.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Sample Metadata Fields

Specimen part

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accession-icon GSE31611
Expression data from embryoid body with BRCA1 mutation [mRNA]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We examined the functional significance of the R1699Q variant of human BRCA1 gene using a mouse ES cell-based assay.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Sample Metadata Fields

Specimen part

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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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