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SRP090108
Mus musculus
43 Downloadable Samples
Illumina 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
View Samples- Mus musculus, Homo sapiens
- 38 Downloadable Samples
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
View Samples- Homo sapiens
- 35 Downloadable Samples
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
View Samples- Mus musculus
- 35 Downloadable Samples
- Illumina 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
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Using stem cellbased therapies to treat retinal abnormalities is becoming a likely possibility; therefore, identifying the key factors and the relevant mechanisms controlling optic vesicle morphogenesis and neuroretina (NR) differentiation is important. Recent advances in self-organizing, 3-dimensional (3D) tissue cultures of embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) provided a valuable in vitro model for characterizing regulatory cascades and signaling pathways controlling mammalian retinal development. Using Rx-GFP expressing ESCs and Six3/ iPSCs we identified R-spondin 2 (Rspo2)-mediated repression of Wnt signaling as a novel required step during optic vesicle morphogenesis and NR differentiation. Furthermore, we also show that transient ectopic expression of Rspo2 in the anterior neural plate of transgenic mouse embryos was sufficient to arrest NR differentiation. ChIP assays identified Six3-responsive elements in the Rspo2-promoter region, indicating that Six3-mediated repression of Rspo2 is required to restrict Wnt signaling in the developing anterior neuroectoderm and allow eye development to proceed.
Publication Title
An Eye Organoid Approach Identifies Six3 Suppression of R-spondin 2 as a Critical Step in Mouse Neuroretina Differentiation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 147 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Molecular signatures to improve diagnosis in PTCL and prognostication in angioimmunoblastic T-cell lymphoma (AITL). Gene expression profiling of PTCL patient samples was performed to investigate whether molecular signatures can be used to identify distinct entities of PTCL.
Publication Title
Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 60 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL.
Publication Title
Molecular and transcriptional characterization of 17p loss in B-cell chronic lymphocytic leukemia.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 60 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL.
Publication Title
Molecular and transcriptional characterization of 17p loss in B-cell chronic lymphocytic leukemia.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 229 Downloadable Samples
- 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
View Samples- Mus musculus
- 157 Downloadable Samples
- NextSeq 500
Description
Primary RNAseq data for 103 highly purified immunocyte populations representing all lineages and several differentiation cascades, profiled using the ImmGen ULI pipeline. Overall design: These RNAseq profiles were generated by ImmGen labs in a combined study associating RNAseq and ATACseq performed on cell populations sorted in parallel (companion ATACseq datasets are found in GSE100738). The 103 cell populations include all adaptive and innate lymphocytes (B, abT, gdT, Innate-Like Lymphocytes), myeloid cells (dendritic cells, macrophages, monocytes), mast cells and neutrophils. Most were prepared from baseline unchallenged mice, some after cell activation (LPS, anti-CD3, viral infection). For B and T lymphocytes, many successive steps of their known differentiation cascades in the thymus and bone marrow are included. ---------------------------------------- Immunological Genome Project Consortium
Publication Title
The cis-Regulatory Atlas of the Mouse Immune System.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples