Transcription profiling by array of human prostate cancer samples in order to examine the changes in gene transcription underlying the aberrant citrate and choline metabolism
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ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: Flatberg Arnar
PROVIDER: E-MTAB-1041 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The mechanisms and molecular pathways underlying interstitial lung diseases (ILDs) are poorly understood. Systems biology approaches were used to identify perturbed networks in these disease states to gain a better understanding of the underlying mechanisms of disease. Through profiling genes and miRNAs, we found subsets of genes and miRNAs that distinguish different disease stages, ILDs from controls, and idiopathic pulmonary fibrosis (IPF) from non-specific interstitial pneumonitis (NSIP). Traditional pathway analysis revealed several disease-associated modules involving genes from the TGF-beta, Wnt, focal adhesion and smooth muscle actin pathways that may be involved in advancing fibrosis. A comprehensively integrative approach was used to construct a global gene regulatory network based on the perturbation of key regulatory elements, transcriptional factors and miRNAs. The data also demonstrated that several subnetworks were significantly associated with key molecules involved in the diseases. We present a broad overview of the disease at a molecular level and discuss several possibly key regulatory molecular circuits that could play central roles in facilitating the progression of ILDs. Lung tissue samples from 23 patients with IPF or related disorders were obtained from the Lung Tissue Research Consortium (www.ltrcpublic.org). 11 samples came from patients who had been diagnosed with usual interstitial pneumonia/ idiopathic pulmonary fibrosis (UIP/IPF), 5 samples came from patients with non-specific interstitial pneumonia (NSIP), the remaining from patients with uncharacterized fibrosis and from patients with other ILD variants. B. Biopsies from uninvolved lung tissue from lung cancer patients (5 samples) and from one lung transplant patient were used as controls for comparison with the ILD samples.
2011-03-24 | E-GEOD-21369 | biostudies-arrayexpress
Project description:In order to discover critical pathways /networks or therapeutic targets in pleural mesothelioma we profiled 55 tumors along with paired normal tissue (for 41 tumors) using Affymetrix U133 plus 2.0 chips RNA isolated from frozen resected tumor and normal tissues was hybridized to Affymetrix U133 plus 2.0 chips to discover genes upregulated/downregulated in mesothelioma tumors compared to paired normal non-tumor adjacent tissue as well as find differences between the different tumors
2014-08-31 | E-GEOD-51024 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE21369: Gene expression profiles of interstitial lung disease (ILD) patients GSE21394: MicroRNA expression profiles of interstitial lung disease (ILD) patients Refer to individual Series
2011-04-19 | E-GEOD-21411 | biostudies-arrayexpress
Project description:The limbus is a unique anatomic structure that is highly innervated and vascularized yet sets the boundary for the avascularized cornea. The corneal epithelial stem cells are believed to reside at the limbus. The intrinsic and external molecular signals that modulate the differentiation and proliferation of the limbal stems cells are still largely unidentified because of a lack of known specific markers. In this study, we used microarray technology to identify the unique gene expression profile in the limbus by comparing directly to that of its immediate adjacent structures, the cornea and conjunctiva, in the vervet monkey (Chlorocebus aethiops sabaeus). Many new genes were found to be preferentially expressed in the limbus, and two new biological pathways, melanin metabolism and apoptosis, were among other previously known processes identified in the limbus. These findings may shed light on the molecular components of limbal stem cells and their niche. Experiment Overall Design: The study consisted of gene expression profile comparisons across three anatomical structures of the eye. The parts of the eye compared included the cornea, the conjunctiva, and the limbus.
2008-04-06 | E-GEOD-10683 | biostudies-arrayexpress
Project description:Altered Ca2+ handling has both immediate physiological effects and long-term genomic effects on vascular smooth muscle function. Previously we have shown that elevation of cytoplasmic Ca2+ through voltage-dependent Ca2+ channels (VDCCs) or store-operated Ca2+ channels (SOCCs) results in phosphorylation of the Ca2+/cAMP response element binding protein (CREB) in cerebral arteries. Here we demonstrate that stimulation of these different Ca2+ influx pathways results in transcriptional activation of a distinct, yet overlapping set of genes, and that the induction of selected CRE-regulated genes is prevented by the addition of corresponding Ca2+ channel blockers. Using oligonucleotide array analysis, changes in mRNA levels were quantified following membrane depolarization with K+ or depletion of intracellular Ca2+ stores with thapsigargin in human cerebral vascular smooth muscle cells. Array results for differentially regulated genes containing a CRE were confirmed by quantitative RT-PCR, and corresponding changes in protein expression were shown by Western blot analysis and immunofluorescence. Membrane depolarization induced a transient increase in c-fos mRNA and a sustained increase in early growth response-1 (Egr-1) mRNA and protein that were inhibited by application of the VDCC blocker, nimodipine, and the SOCC inhibitor, 2-aminoethoxydiphenylborate (2-APB). Thapsigargin induced a sustained increase in c-fos mRNA and MAP kinase phosphatase-1 (MKP-1) mRNA and protein, and these effects were decreased by 2-APB but not by nimodipine. Our findings thus indicate that Ca2+ entry through VDCCs and SOCCs can differentially regulate CRE-containing genes in vascular smooth muscle and imply that signals involved in growth modulation are both temporally and spatially regulated by Ca2+. Experiment Overall Design: each of three experiments cell cultures were split three ways; one of the resulting samples was left untreated (C), another was treated with thapsigargin (TG), and the third was treated with elevated K+ (K). The resulting nine samples were used for triplicate estimates of the response of each gene to TG and K treatments. Experiment Overall Design: We tested the prospective hypothesis that genes having a CRE are differentially expressed after TG or K treatment using a permutation test: each of the 22,283 probe sets on the Affymetrix GeneChip was categorized two ways based on 1) whether or not it contains a CRE or not . Independence of CRE and threshold differential expression was rejected by Fisherâs exact test for both TG treatment ( ) and K treatment ( ). Target genes (c-fos, egr-1, and mkp-1 ) were identified based on ranking.
2009-04-29 | E-GEOD-2883 | biostudies-arrayexpress
Project description:Hox homeodomain transcription factors are key regulators of animal development. They specify the identity of segments along the anterior-posterior body axis in metazoans by controlling the expression of diverse downstream targets, including transcription factors and signaling pathway components. The Drosophila melanogaster Hox factor Ultrabithorax (Ubx) directs the development of thoracic and abdominal segments and appendages, and loss of Ubx function can lead for example to the transformation of third thoracic segment appendages (e.g. halters) into second thoracic segment appendages (e.g. wings), resulting in a characteristic four-wing phenotype. Here we present a Drosophila melanogaster strain with a V5-epitope tagged Ubx allele, which we employed to obtain a high quality genome-wide map of Ubx binding sites using ChIP-seq. We confirm the sensitivity of the V5 ChIP-seq by recovering 7/8 of well-studied Ubx-dependent cis-regulatory regions. Moreover, we show that Ubx binding is predictive of enhancer activity as suggested by comparison with a genome-scale resource of in vivo tested enhancer candidates. We observed densely clustered Ubx binding sites at 12 extended genomic loci that included ANTP-C, BX-C, Polycomb complex genes, and other regulators and the clustered binding sites were frequently active enhancers. Furthermore, Ubx binding was detected at known Polycomb response elements (PREs) and was associated with significant enrichments of Pc and Pho ChIP signals in contrast to binding sites of other developmental TFs. Together, our results show that Ubx targets developmental regulators via strongly clustered binding sites and allow us to hypothesize that regulation by Ubx might involve Polycomb group proteins to maintain specific regulatory states in cooperative or mutually exclusive fashion, an attractive model that combines two groups of proteins with prominent gene regulatory roles during animal development. Ubx was endogenously tagged with V5 epitope in Drosophila melanogaster (Ubx-V5). ChIP-seq was performed with chromatin from 0-16 hrs wild type and Ubx-V5 embryos. The samples were subjected to single-end sequencing in two replicates.
2016-07-03 | E-GEOD-64284 | biostudies-arrayexpress
Project description:Adult myogenic progenitor cells (activated satellite cells) express both HGF and its receptor cMet. Following muscle injury, autocrine HGF-Met stimulation plays a key role in promoting activation and early division of satellite cells. Magic-F1 (Met-Activating Genetically Improved Chimeric Factor-1) is an HGF-derived, engineered protein that contains two Met-binding domains that promotes muscle hypertrophy, protecting myogenic precursors against apoptosis, increasing their fusion ability and enhancing muscle differentiation. Hemizygous and homozygous Magic-F1 transgenic mice displayed constitutive muscle hypertrophy. We described here microarray analysis on Magic-F1 myogenic progenitor cells showing an altered gene signatures involving muscle hypertrophy and vasculogenesis compared to wild-type cells. In parallel, we performed a functional analysis on homozygous Magic-F1 transgenic mice versus control, demonstrating that Magic-F1+/+ mice display impairment on running performance. Finally, we show that induced muscle hypertrophy affects positively vascular network, increasing vessel number in fast twitch fibers. This is due to unique features of mammalian skeletal muscle and its remarkable ability to adapt promptly to different physiological demands by changing gene expression profile. Biological triplicates of Magic-F1+/+ and control satellite cells were used for microarray analysis.
2016-06-28 | E-GEOD-83771 | biostudies-arrayexpress
Project description:We produced RNA-Seq reads from messenger RNA isolated from root tissue for the 19 MAGIC founder accessions (inbred strains) of Arabidopsis thaliana (see Gan et al. 2011. Nature 477:419-23 for a description of the MAGIC genetic mapping resource). The read data was generated with biological replication (two replicates). The resulting RNA-Seq data provide a resource to assess root gene expression across different accessions of A. thaliana. Comparable RNA-Seq read data for the MAGIC founder accessions for aerial seedling tissue has previously been released under GEO series GSE30720 (Gan et al. 2011. Nature, 477:419-23).
2013-12-11 | GSE53198 | GEO
Project description:We produced RNA-Seq reads from messenger RNA isolated from seedling, root, and floral bud tissue for 17 MAGIC founder accessions (inbred strains) of Arabidopsis thaliana (see Gan et al. 2011. Nature, 477:419-23 for a description of the MAGIC genetic mapping resource). The resulting RNA-Seq data provide a resource to assess tissue-specific expression across different accessions of A. thaliana. Note that comparable read data for accessions Col-0 and Can-0, which are also founders of the MAGIC lines, has previously been released under GEO series GSE30795 (Gan et al. 2011. Nature, 477:419-23).
2013-12-11 | GSE53197 | GEO