In order to identify transcript changes in response to DEF , we used human macrophages with or without DEF treatment. In order to study the effect of iron chelation on LPS-polarized macrophage transcriptome, we exposed DEF-treated or control macrophages to short time exposure to LPS. We then performed whole-genome transcriptome sequencing by RNA-sequencing (RNA-seq). Overall design: Macrophages from 3 healthy donors were either treated with DEF (500 µM - designated as DEF) or left unstimulated (CONTROL). LPS treatment (100 ng/ml, 3 hours) was performed in cells with DEF (designated as LPS+DEF) or without (LPS). RNA-seq was performed on Illumina Hiseq 2500
Acute Iron Deprivation Reprograms Human Macrophage Metabolism and Reduces Inflammation In Vivo.
Specimen part, Treatment, Subject
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Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.
Specimen part
View SamplesThe cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.
Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.
Specimen part
View SamplesThe cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.
Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.
Specimen part
View SamplesGene expression profiling of normal hematopoietic cell subpopulations
Gene expression signatures in childhood acute leukemias are largely unique and distinct from those of normal tissues and other malignancies.
Specimen part
View SamplesTranscriptional expression data for bioactive small molecules for mechanism identification.
Identification of a novel topoisomerase inhibitor effective in cells overexpressing drug efflux transporters.
No sample metadata fields
View SamplesPIWI interacting RNAs (piRNAs) provide defense against transposable element (TE) expansion in the germline of metazoans. piRNAs are processed from the transcripts encoded by specialized heterochromatic clusters enriched in damaged copies of transposons. How these regions are recognized as a source of piRNAs is still elusive. The aim of this study is to determine how transgenes that contain a fragment of the LINE-like I transposon lead to an acquired TE resistance in Drosophila. We show that such transgenes, being inserted in unique euchromatic regions which normally do not produce small RNAs, become de novo bidirectional piRNA clusters that silence I-element activity in the germline. Strikingly, small RNAs of both polarities are generated from the entire transgene and flanking genomic sequences — not only from the transposon fragment. Chromatin immunoprecipitation analysis shows that in ovaries the trimethylated histone 3 lysine 9 (H3K9me3) mark associates with transgenes producing piRNAs. We show that transgene-derived hsp70 piRNAs stimulate in trans cleavage of cognate endogenous transcripts with subsequent processing of the non-homologous parts of these transcripts into piRNAs. Overall design: The fractions of small RNAs (19-29 nt) from ovaries of wild type and 11 transgenic lines of Drosophila melanogaster were sequenced using Illumina HiSeq 2000.
De novo piRNA cluster formation in the Drosophila germ line triggered by transgenes containing a transcribed transposon fragment.
Specimen part, Subject
View SamplesM21 or M21L cells were grown either in a 2-dimensional culture (on plastic) or in a 3-dimensional-collagen model.
Protein kinase Cα (PKCα) regulates p53 localization and melanoma cell survival downstream of integrin αv in three-dimensional collagen and in vivo.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular profiling uncovers a p53-associated role for microRNA-31 in inhibiting the proliferation of serous ovarian carcinomas and other cancers.
Disease, Disease stage, Cell line
View SamplesA variety of human cancers demonstrate alterations in microRNA expression. We hypothesized that regulatory defects in microRNAs play a central early role in organizing the molecular changes involved in ovarian cancer (OvCa). Using both gene arrays and deep sequencing, we comprehensively profiled mRNA and microRNA expression, respectively, in human serous epithelial OvCa cell lines, serous tumors, and short-term primary cultures of normal ovarian surface epithelium (NOSE). We expected that over-expression of a specific microRNA would lead to lower expression of its mRNA targets, and under-expression of a specific microRNA would lead to higher expression of its target genes. Using our expression data in conjunction with established in silico algorithms, we found putative microRNA:mRNA functional pairs.
Molecular profiling uncovers a p53-associated role for microRNA-31 in inhibiting the proliferation of serous ovarian carcinomas and other cancers.
Disease, Disease stage, Cell line
View Samples