Mass populations of thyrocytes stably expressing wild type RET/PTC1 oncogene or RET/PTC1 carrying Y451F mutation and parental thyrocytes were used for hybridization on Affymetrix HG-U133A and HG-U133B chips. For each cell condition were generated two different targets (indicated as two different samples in the database, i.e. "Parental Thyrocytes" and "Parental Thyrocytes bis")for a total number of six samples. For the data analysis the two samples from the same condition (i.e. Parental thyrocytes) were considered as duplicates.
Induction of a proinflammatory program in normal human thyrocytes by the RET/PTC1 oncogene.
Specimen part
View SamplesMicroarray was used to identify differential gene expression pattern in Barrett's esophagus (BE), compared to the normal adjacent epithelia gastric cardia (GC) and normal squamous esophagus (NE)
Evidence for a functional role of epigenetically regulated midcluster HOXB genes in the development of Barrett esophagus.
Specimen part
View SamplesHuntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. Striatal super-enhancers are enriched in binding motifs for Gata transcription factors, such as Gata2 regulating striatal identity genes. Thus, enhancer topography and transcription dynamics are major parameters determining the propensity of a gene to be deregulated in a neurodegenerative disease. Overall design: RNA profiles in Striatum of WT and R6/1 mice by deep sequencing using Illumina HiSeq 2000.
Altered enhancer transcription underlies Huntington's disease striatal transcriptional signature.
No sample metadata fields
View SamplesMacrophages and neutrophils are almost invariably the most abundant intratumoral immune cells, and recent studies have revealed a sinister role for these cells in limiting chemotherapy efficacy. However, how these tumor-educated myeloid cells influence chemotherapy response is incompletely understood. Targeting tumor-associated macrophages by CSF-1 receptor (CSF-1R) blockade in a pre-clinical transgenic mouse model for breast cancer improved the anti-cancer efficacy of cisplatin. Importantly, our findings reveal that macrophage blockade in combination with cisplatin treatment evokes a compensatory neutrophil response limiting the therapeutic synergy of this therapy combination. Here we characterize neutrophils and macrophages gene expression profile from the tumor of mice treated with anti-CSF-1R, Control antibody, Cisplatin/anti-CSF-1R or cisplatin/control ab. Overall design: Intervention studies combining anti-CSF1R and chemotherapy in a transgenic mouse model for breast cancer.
Therapeutic targeting of macrophages enhances chemotherapy efficacy by unleashing type I interferon response.
Specimen part, Cell line, Subject
View SamplesmRNA profiles of astrocytes infected with Borrelia burdorferi for 24 hours, 48 hours, and 24 hour uninfected controls were generated by deep sequencing, in triplicate, using Illumina HiSeq. Overall design: mRNA profiles of astrocytes infected with Borrelia burdorferi for 24 hours, 48 hours, and 24 hour uninfected controls were generated by deep sequencing, in triplicate, using Illumina HiSeq.
MicroRNA and mRNA Transcriptome Profiling in Primary Human Astrocytes Infected with Borrelia burgdorferi.
Specimen part, Subject, Time
View SamplesIn this study, murine primary aortic smooth muscle cells (SMCs) were transcriptionally profiled at baseline, after 3 d of cholesterol loading, and after 3 d of subsequent cholesterol unloading with HDL treatment, to identify vascular SMC genes that are transcripionally dysregulated in response to cholesterol loading and/or unloading.
Cholesterol loading reprograms the microRNA-143/145-myocardin axis to convert aortic smooth muscle cells to a dysfunctional macrophage-like phenotype.
Age, Specimen part
View SamplesComparison of emphysema vs non emphysema COPD lung tissue expression
Network Analysis of Lung Transcriptomics Reveals a Distinct B-Cell Signature in Emphysema.
Specimen part
View SamplesIn order to gain insight into the molecular pathogenesis of collagen VI defects we have performed gene expression microarray analysis of dermal fibroblasts. We have compared the transcriptome of fibroblasts, treated or untreated with ascorbic acid, from UCMD patients (n = 6) and aged-matched healthy children (n = 5).
Transcriptome Analysis of Ullrich Congenital Muscular Dystrophy Fibroblasts Reveals a Disease Extracellular Matrix Signature and Key Molecular Regulators.
Specimen part, Disease, Disease stage, Treatment
View SamplesWe have previously reported that elevated fibroblast growth factor-2 (FGF-2) expression is associated with tumor recurrence and reduced survival after surgical resection of esophageal cancer, and that these risks are reduced in tumors co-expressing an endogenous antisense (FGF-AS) RNA. In the present study we examined the role of the endogenous FGF-AS transcript in the regulation of FGF-2 expression in the human lung adenocarcinoma cell line, Seg-1. FGF-2 and FGF-AS were temporally and spatially co-localized in the cytoplasm of individual cells, and knock-down of either FGF-2 or FGF-AS by target specific siRNAs resulted in dose-dependent up-regulation of the complementary transcript and its encoded protein product. Using a luciferase reporter system we show that these effects are mediated by interaction of the endogenous antisense RNA with the 3UTR of the FGF-2 mRNA. Deletion mapping identified a 392 nt sequence in the 5823 nucleotide FGF-2 untranslated tail which is targeted by FGF-AS. siRNA-mediated knockdown of either FGF-AS or FGF-2 significantly increased the stability of the complementary partner mRNA, demonstrating that these mRNAs are mutually regulatory. Knockdown of FGF-AS also resulted in reduced expression of argonaute-2 (AGO-2) and a number of other elements of the endogenous microRNA/RNAi pathways. Conversely, siRNA-mediated knockdown of AGO-2 significantly increased the stability of the FGF-2 mRNA transcript, and the steady-state levels of both FGF-2 mRNA and protein, suggesting a role for AGO-2 in the regulation of FGF-2 expression.
Regulation of fibroblast growth factor-2 by an endogenous antisense RNA and by argonaute-2.
Specimen part, Cell line
View SamplesGene expression from cord blood stem cells and respective derived neuronal cells at different times point of differentiation:CD133+ cells;
Cord blood-derived neuronal cells by ectopic expression of Sox2 and c-Myc.
Specimen part, Time
View Samples