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Accession Number: GSE64629 Platform: GPL16770: Agilent-031181 Unrestricted_Human_miRNA_V16.0_Microarray (miRBase release 16.0 miRNA ID version) Organism: Homo sapiens Published on 2018-01-02 Summary: Recent studies have revealed that microRNAs (miRNAs) participate in all steps of cancer initiation and progression by regulating protein coding genes at the post-transcriptional level. MiRNAs are in turn regulated by other genes, forming a complex regulatory network. The regulation networks between the p53 tumor suppressor and miRNAs in nasopharyngeal carcinoma (NPC) remain unclear. The aim of this study was to investigate the regulatory roles of the TP53 gene in regulating miRNA expression profiles in NPC cell line HNE2. Overall Design: p53 induced miRNAs expression in human nasopharyngeal carcinoma cell line HNE2 was measured at 0, 12, 24 and 48 hours after transfected by pCMV-p53 plasmid. Contact: Name: Wei Xiong Organization: Central South University Deparment: Cancer Research Institute Address: 110 Xiangya Road Changsha Hunan China Email: xiongwei@csu.edu.cn Organization: Agilent Technologies Address: Palo Alto CA 94304 USA Email: cag_sales-na@agilent.com Phone: 877-424-4536 Web-Link: www.agilent.com
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Accession Number: GSE107679 Platform: GPL15103: Illumina HiSeq 1000 (Mus musculus) Organism: Mus musculus Published on 2018-01-02 Summary: To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration. Overall Design: RNA-seq profilig of heart tissues from wild type mice on postanatal day 1, 7, and 28 (P1, P7, and P28), RNA-seq of hearts from control (Ctrl) and miR-128 overexpression transgenic mice (miR-128OE) at P7. Contact: Name: Mario Medvedovic Organization: University of Cincinnati Laboratory: Laboratory for Statistical Genomics and Systems Biology Deparment: Department of Environmental Health Address: 3223 Eden Av. ML 56 Cincinnati OH 45267-0056 USA Organization: GEO Address: USA
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Accession Number: GSE108000 Platform: GPL13497: Agilent-026652 Whole Human Genome Microarray 4x44K v2 (Probe Name version) Organism: Homo sapiens Published on 2018-01-01 Summary: In multiple sclerosis (MS), activated microglia and infiltrating macrophages phagocytose myelin focally in (chronic) active lesions. These demyelinating sites expand in time, but at some point turn inactive into a sclerotic scar. To identify molecular mechanisms underlying lesion activity and halt, we analyzed genome-wide gene expression in rim and peri-lesional regions of chronic active and inactive MS lesions, as well as in control tissue. Gene clustering revealed patterns of gene expression specifically associated with MS and with the presumed, subsequent stages of lesion development. Next to genes involved in immune functions, we found regulation of novel genes in and around the rim of chronic active lesions, such as NPY, KANK4, NCAN, TKTL1, and ANO4. Of note, the presence of many foamy macrophages in active rims was accompanied by a congruent upregulation of genes related to lipid binding, such as MSR1, CD68, CXCL16, and OLR1, and lipid uptake, such as CHIT1, GPNMB, and CCL18. Except CCL18, these genes were already upregulated in regions around active MS lesions, showing that such lesions are indeed expanding. In vitro downregulation of the scavenger receptors MSR1 and CXCL16 reduced myelin uptake. In conclusion, this study provides the gene expression profile of different aspects of MS pathology and indicates that early demyelination, mediated by scavenger receptors, is already present in regions around active MS lesions. Genes involved in early demyelination events in regions surrounding chronic active MS lesions might be promising therapeutic targets to stop lesion expansion. Overall Design: Microarray was performed on 7 chronic active MS lesions (PL-NAWM and RIM), 8 inactive MS lesions (PL-NAWM and RIM), and white matter (WM) of 10 control donors were included in this study. In total 40 samples were included. Experimental RNA and reference pool RNA input was used for linear amplification and fluorescent labeling Contact: Name: Inge Huitinga Organization: NIN Deparment: Neuroimmunology Address: meibergdreef 47 Amsterdam Netherlands Email: i.huitinga@nin.knaw.nl Organization: Agilent Technologies Address: Palo Alto CA 94304 USA Email: cag_sales-na@agilent.com Phone: 877-424-4536 Web-Link: www.agilent.com
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Accession Number: GSE89500 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-01 Summary: We performed whole genome expression analysis of Kit+ derived from wild type C57B/L6 Mouse bone marrow cells Trabsduced with control vector and CSF3R mutants by RNA seq. Overall Design: The experiment was designed to test the gene expression differences between leukemogenic (proximal and double muatnt) and non leukemogenic (truncation) mutants of CSF3R. Contact: Name: Mohammad Azam Organization: Cincinnati Childrens Hospital and Medical Center Deparment: Division of Experimental Hematology Address: 3333 Burnet Avenue Cincinnati OH 45229 USA Organization: GEO Address: USA
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Accession Number: GSE31700 Platform: GPL3209: SAGE:10:NlaIII:Danio rerio GPL13689: SAGE:16:NlaIII:Danio rerio GPL13690: SAGE:16:NlaIII:Oncorhynchus mykiss Organism: Danio rerio Published on 2018-01-01 Summary: Comparison of transcriptome data in fed and fasted conditions of zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss) anterior intestine using the serial analysis of gene expression (SAGE) method was done in a strategy to identify key regulated genes at the transcript level and to allow the identification of activated/deactivated pathways after feeding. Overall Design: For the fasted group of zebrafish, total RNAs from the anterior intestines of a pool of 6 animals were used to generate the SAGE library (14bp TAGs, including the 4-bp anchor enzyme site) using the I-SAGE kit (Invitrogen, Cergy Pointoise, France). For the fed group of zebrafish (pool of 6 animals), and the fed and fasted trout (pool of 8 animals each), total RNAs extracted from the anterior intestine were used to generate long-SAGE libraries (20pb TAGs, including the 4-bp anchor enzyme site) using the I-SAGE Long kit (Invitrogen, Cergy Pointoise, France). Contact: Name: Patrick J. BABIN Organization: Université Bordeaux Laboratory: Maladies Rares : Génétique et Métabolisme Deparment: UFR Biologie Address: Avenue des facultés Talence 33405 France Email: p.babin@gpp.u-bordeaux1.fr Phone: -33 540008776 Web-Link: http://www.u-bordeaux1.fr/gpp/ Organization: GEO Address: USA
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Accession Number: GSE92700 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-01 Summary: The accumulation of reactive oxygen species (ROS) is linked to several cardiovascular pathologies; it is also associated with cell cycle exit by nenonatal cardiomyocytes, a key limiting factor in the regenerative capacity of the adult mammalian heart. BMI1 is a component of the polycomb complex 1, which is linked to adult multipotent progenitors, and is also an important partner in DNA repair and redox regulation. Here we show that high BMI1 expression is associated with a cardiac Sca1+ progenitor subpopulation with low ROS levels. In homeostasis, BMI1 represses cell-fate genes, including a cardiogenic differentiation program. Persistent oxidative damage nonetheless modified BMI1 activity in vivo, by derepressing canonical target genes in favor of their antioxidant and anticlastogenic functions. This derepression induced cardiac progenitor proliferation and differentiation, and thus increased its contribution to mature cardiac progeny. This redox-mediated mechanism is not restricted to damage situations, and we report ROS-associated differentiation of cardiac progenitors in steady state. These findings demonstrate how redox status influences the adult cardiac progenitor response, and identifies a redox-mediated BMI1 function with potential implications in adult cardiac turnover. Overall Design: Examination of two different proteins (BMI1 and H2AK119ub) with two different treatments (Homeostasis and Damage) in Cardiac cells enriched in Sca1+CD45- from 6-8 weeks-old mice. Contact: Name: Monica Franch Organization: National Center for Biotechnology-CSIC Deparment: BioinfoGP Address: Darwin 3 Madrid 28049 Spain Organization: GEO Address: USA
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Accession Number: GSE101510 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-01 Summary: The purpose of this study is to identify expression differences between wild type CD8 T cells vs IRF4 knock out CD8 T cells. Overall Design: mRNA profiles were examed by Illumina Hiseq 2500 platform. Four samples were sequenced with two samples from wild type CD8 T cells and two samples from IRF4 knock-out CD8 T cells. Contact: Name: Yingjia Shen Organization: Xiamen University Deparment: Ecology Address: A316 Jingquan Building Xiamen Fujian China Email: shenyj@xmu.edu.cn Organization: GEO Address: USA
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Accession Number: GSE84820 Platform: GPL13112: Illumina HiSeq 2000 (Mus musculus) GPL19057: Illumina NextSeq 500 (Mus musculus) Organism: Mus musculus Published on 2018-01-01 Summary: During chronic stimulation T cells acquire an exhausted phenotype characterized by expression of multiple inhibitory receptors and down-modulation of effector function. While this is required for the protection of the organism from excessive immunopathology, it also prevents successful immunity against persistent viruses or tumor cells. Here we demonstrate that CD8+ T cell exhaustion is characterized by a progressive decline in cellular metabolism. Exhausted T cells exhibit reduced metabolic reserve, impaired fatty acid oxidation and production of mitochondrial reactive oxygen species (ROS). Blockade of inhibitory PD-1/PD-L1 signaling rescued mitochondrial biogenesis, oxidative phosphorylation and ROS production, which was required for efficient restoration of cellular expansion and effector function. Expression of inhibitory receptors and impaired metabolic function was fuled by high amounts of IRF4, BATF and NFAT, which formed a TCR-responsive transcriptional circuit that sustained the transcriptional network responsible for T cell exhaustion. Overall Design: Transcriptional profiling of T cells in mice with chronic and acute infections using RNA sequencing Contact: Name: Wei Shi Organization: The Walter and Eliza Hall Institute of Medical Research Address: 1G Royal Parade Parkville Victoria Australia Email: shi@wehi.edu.au Organization: GEO Address: USA
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Accession Number: GSE35530 Platform: GPL8786: [miRNA-1] Affymetrix Multispecies miRNA-1 Array Organism: synthetic construct Published on 2018-01-01 Summary: Dicer plays a key role in RNA silencing. By processing pre-miRNAs and dsRNAs, Dicer generates miRNAs and siRNAs that act as post-transcriptional regulators of gene expression. Dicer is also implicated in heterochromatin formation and toxic RNA degradation. Here we report that Dicer is controlled in cell cycle. The Dicer protein level drastically rises at late G1 phase and falls at early S phase. Interestingly, the protein stability of Dicer is decreased specifically at early S phase. MG132, an inhibitor of proteasome, increases Dicer protein level, suggesting that the stability of Dicer is controlled via ubiquitination-dependent proteasome pathway. Overall Design: Examination of small RNA regulation in the cell cycle Contact: Name: Hyeshik Chang Organization: Seoul National University Laboratory: Narry Kim Lab Deparment: School of Biological Sciences Address: Building 504 Room 501, School of Biological Sciences, Seoul National University, 599 Gwanangno, Gwanak-gu Seoul South Korea South Korea Email: hyeshik@snu.ac.kr Phone: +82-2-887-1343 Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: geo@ncbi.nlm.nih.gov, support@affymetrix.com Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.affx
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Accession Number: GSE93730 Platform: GPL13112: Illumina HiSeq 2000 (Mus musculus) GPL21103: Illumina HiSeq 4000 (Mus musculus) Organism: Mus musculus Published on 2018-01-01 Summary: This SuperSeries is composed of the SubSeries listed below. Overall Design: Refer to individual Series Contact: Name: Diane Dickel Organization: Lawrence Berkeley National Laboratory Laboratory: mammalian functional genomics laboratory Address: 1 Cyclotron Road Berkeley CA 94720 USA Organization: GEO Address: USA
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