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GSE54975
Homo sapiens
12 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Lipid-induced epigenomic changes in human macrophages identify a coronary artery disease-associated variant that regulates PPAP2B Expression through Altered C/EBP-beta binding.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The aim of the experiment was to determine the effects of 48 hours of treatment with oxidized low density lipoprotein (oxLDL) on gene expression in primary human monocyte-derived macrophages.
Publication Title
Lipid-induced epigenomic changes in human macrophages identify a coronary artery disease-associated variant that regulates PPAP2B Expression through Altered C/EBP-beta binding.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
Illumina HiSeq 2000
Description
We performed a systematic analysis of the coding and non-coding transcriptomes of human macrophages after stimulation with ligands to TLR2/6 (FSL), TLR 1/2 (Pam3CSK4), and TLR4 (LPS) Overall design: Transcriptome of THP1 derived macrophages without and with treatment with 3 different TLR ligands for 8hrs
Publication Title
The long noncoding RNA <i>ROCKI</i> regulates inflammatory gene expression.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Xenopus laevis
- 9 Downloadable Samples
- Affymetrix Xenopus laevis Genome Array (xenopuslaevis)
Description
ADAMs are transmembrane metalloproteases that control cell behavior by cleaving both cell adhesion and signaling molecules. The cytoplasmic domain of ADAMs can regulate the proteolytic activity by controlling the subcellular localization and/or the activation of the protease domain. Here we show that the cytoplasmic domain of ADAM13 is cleaved and translocates into the nucleus. Preventing this translocation renders the protein incapable of promoting cranial neural crest (CNC) cell migration in vivo, without affecting its proteolytic activity. In addition, the cytoplasmic domain of ADAM13 regulates the expression of multiple genes in the CNC. This study shows that the cytoplasmic domain of ADAM metalloproteases can perform essential functions in the nucleus of cells and may contribute substantially to the overall function of the protein.
Publication Title
Translocation of the cytoplasmic domain of ADAM13 to the nucleus is essential for Calpain8-a expression and cranial neural crest cell migration.
Sample Metadata Fields
Specimen part
View Samples- Zea mays
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
The maize Rough endosperm3 (Rgh3) gene encodes an ortholog of the human essential splicing factor, ZRSR2. To test whether a mutation in Rgh3 affects mRNA splicing, we compared rgh3 mutants and wild-type sibling transcriptomes in an RNA-seq experiment. Twelve libraries were constructed with mRNA extracted from the roots and shoots of three seedlings of each genotype. The libraries were multiplexed and sequenced on one lane of the HiSeq 2000 platform. The run produced 149 million paired-end 100 bp reads that mapped to 35,028 genes. Two approaches were used to analyze the dataset. In the first approach, Mosaik2, FreeBayes, GSNAP, and Cufflinks were used to identify differences in transcript isoform abundance in a SNP-tolerant fashion. During reverse-transcription PCR validation, six examples of intron retention were found to occur more frequently in rgh3 seedlings, and all six introns were members of a rare class of introns called U12-type introns. The second approach utilized a t-test to determine whether more reads were mapped to U12-type introns in rgh3 libraries relative to wild-type libraries. Out of all U12-type introns within genes that are expressed at a early seedling stage, 43% exhibit splicing defects in rgh3 mutants. These U12-type intron splicing defects include intron retention and cryptic splice site activation. We report that the rgh3 mutation specifically impairs the U12-type intron splicing. Overall design: Libraries were built from three replicates of each: wild-type roots, wild-type shoots, rgh3 roots, and rgh3 shoots
Publication Title
Aberrant splicing in maize <i>rough endosperm3</i> reveals a conserved role for U12 splicing in eukaryotic multicellular development.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of KLS cells purified from bone marrow of mice conditionally inactivated for TIF1 gene. TIF1 deletion results in multiple defects in adult hematopoiesis. Results provide insight into the role of TIF1 in hematopoietic stem cells functions.
Publication Title
Adult hematopoiesis is regulated by TIF1γ, a repressor of TAL1 and PU.1 transcriptional activity.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- NextSeq 500
Description
Rheumatoid arthritis is an inflammatory disease of the synovial joints that affects ~1% of the human population, with severe distress due to progressive joint inflammation and deformation. When addressing the links between specific components of the apoptotic cell clearance machinery and human disease, we noted a correlation between single nucleotide polymorphisms (SNPs) in ELMO1, DOCK2, and RAC1 genes and rheumatoid arthritis. ELMO1 is a cytoplasmic adapter protein that associates with DOCK2 and RAC1 to promote cytoskeletal reorganization needed for apoptotic cell uptake by phagocytes. We initially hypothesized that, since ELMO1 is linked to apoptotic cell clearance, loss of ELMO1 would lead to increased inflammation in arthritis. Contrary to the accumulation of apoptotic cells and greater disease severity that we predicted, we observed significantly reduced joint inflammation in two models of arthritis in mice lacking ELMO1. Using genetic and cell biological approaches in vivo and ex vivo, we determined that ELMO1 deficiency significantly reduces neutrophil recruitment to inflamed joints, but does not result in general inhibition of inflammatory responses. Through proteomic analyses, we find that ELMO1 protein associates with cellular receptors that contribute to neutrophil function in arthritis, and regulates C5a and LTB4 receptor-mediated activation and early neutrophil recruitment to the joints. Neutrophil-specific transcriptomics show that ELMO1 modulates neutrophil-specific gene expression that includes genes with known linkages to human arthritis. Finally, neutrophils from the peripheral blood of human donors that carry the SNP in ELMO1 associated with arthritis display increased migratory capacity, whereas ELMO1 knockdown reduces human neutrophil migration to LTB4. These data identify key 'non-canonical' roles for engulfment machinery components in arthritis, and ELMO1 as an important regulator of specific neutrophil receptors and signaling linked to arthritis. Overall design: The experiment consisted of two conditions: purified Ly6G+ bone marrow cells or peritoneal macrophages cultured overnight. Each condition consisted of four biological replicates.
Publication Title
A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Human regulatory T cells (TR) cells have potential for the treatment of immune mediated diseases, such as graft versus host disease, but the anergic phenotype of these cells makes them difficult to expand in vitro. We have examined the requirements for growth and cytokine expression from highly purified human TR cells, and correlated these findings with the signal transduction events of these cells. We demonstrate that these cells do not proliferate or secrete IL-10 even in the presence of high doses of IL-2. Stimulation with a superagonistic anti-CD28 antibody (clone 9D4) and IL-2 partially reversed the proliferative defect, and this correlated with reversal of the defective calcium mobilization in these cells. Dendritic cells were effective at promoting TR cell proliferation, and under these conditions the proliferative capacity of TR cells was comparable to conventional CD4 lymphocytes. Blocking TGF-beta activity abrogated IL-10 expression from these cells, while addition of TGF-beta resulted in IL-10 production. These data demonstrate the ability of dendritic cells to provide proper costimulation to overcome the anergic phenotype of TR cells. In addition, these data demonstrate for the first time that TGF-beta is critical to enable TR cells to express IL-10.
Publication Title
Requirements for growth and IL-10 expression of highly purified human T regulatory cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
GEP on Affymetrix U133+2.0 microarrays was performed on ex vivo cell-sorted Tfh from FL or TONS
Publication Title
CD10 delineates a subset of human IL-4 producing follicular helper T cells involved in the survival of follicular lymphoma B cells.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Macaca mulatta
- 6 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
The mucosa that lines the gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Epithelial barrier dysfunction during HIV infection has largely been attributed to the rapid and severe depletion of CD4 T cells in the gastrointestinal (GI) tract. In this study, the poential role of small non-coding microRNA (miRNA) to contribute to epithelial dysfunction was investigated in the non-human primate SIV model and microarrays were utilized to determine changes in mucosal gene expression (non-miRNA) that could be correlated to miRNA modulatiolns.
Publication Title
Intestinal epithelial barrier disruption through altered mucosal microRNA expression in human immunodeficiency virus and simian immunodeficiency virus infections.
Sample Metadata Fields
Specimen part
View Samples