Peripheral blood was collected from 18 Parkinson's Disease (PD) patients and 12 healthy controls (Ctrls). Total RNA was isolated and hybridized onto Affymetrix Exon_ST1 arrays to find in PDs versus controls: 1) genes that are differentiallly expressed and 2) genes with differential exonic expression (alternative splicing).
SRRM2, a potential blood biomarker revealing high alternative splicing in Parkinson's disease.
Sex, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice.
Specimen part, Treatment
View SamplesMiR-30e represses the osteogenic program in mesenchymal stem cells (MSCs) and smooth muscle cells (SMCs) by targeting IGF2, and drives their differentiation into adipogenic or smooth muscle lineage, respectively.
miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice.
Specimen part, Treatment
View SamplesMiR-30e represses the osteogenic program in mesenchymal stem cells (MSCs) and smooth muscle cells (SMCs) by targeting IGF2, and drives their differentiation into adipogenic or smooth muscle lineage, respectively.
miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice.
Specimen part, Treatment
View SamplesMiR-30e represses the osteogenic program in mesenchymal stem cells (MSCs) and smooth muscle cells (SMCs) by targeting IGF2, and drives their differentiation into adipogenic or smooth muscle lineage, respectively.
miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice.
Specimen part, Treatment
View SamplesWe used microarrays to detail the global program of gene expression underlying Parkinson's disease
A genomic pathway approach to a complex disease: axon guidance and Parkinson disease.
No sample metadata fields
View SamplesKidneys were snap frozen from 2 month old wild type, Col4a3-/-, or Col4a3-/-OPN-/- mice. RNA was isolated using Mirvana Paris kit.
Osteopontin deficiency ameliorates Alport pathology by preventing tubular metabolic deficits.
Specimen part
View SamplesExpression data from treatment of actinomycin D (2.5uM) and triptolide (500 nM) on MCF7 cells for 2, 4 and 6 hours.
Chemical genomics identifies small-molecule MCL1 repressors and BCL-xL as a predictor of MCL1 dependency.
Cell line, Compound, Time
View SamplesTo investigate whether and how expression of the oncogenic transcription factor EVI1 influences gene regulation by phorbol esters and vice versa, the human myeloid cell line U937 was transduced with an EVI1 expression vector or empty vector as a control. Cells were treated with 12-Otetradecanoylphorbol 13-acetate (TPA) or its solvent ethanol as a control. RNA was extracted and subjected to gene expression microarray analysis.
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Cell line
View SamplesThe product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARb gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well as biological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF-b superfamily of cytokines. In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects.
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Cell line
View Samples