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  • 1
    Publikationsdatum: 1999-03-26
    Beschreibung: Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeling, J M -- Miller, J R -- Gil, R -- Moon, R T -- White, R -- Virshup, D M -- 3P30CA42014/CA/NCI NIH HHS/ -- R01 CA71074/CA/NCI NIH HHS/ -- T32CA09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092233" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/genetics/*metabolism ; Down-Regulation ; Genes, Reporter ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/metabolism ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Phosphatase 2 ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; *Trans-Activators ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Wnt Proteins ; Xenopus ; Xenopus Proteins ; *Zebrafish Proteins ; beta Catenin
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2002-06-29
    Beschreibung: Myeloperoxidase (MPO) is an abundant mammalian phagocyte hemoprotein thought to primarily mediate host defense reactions. Although its microbicidal functions are well established in vitro, humans deficient in MPO are not at unusual risk of infection. MPO was observed herein to modulate the vascular signaling and vasodilatory functions of nitric oxide (NO) during acute inflammation. After leukocyte degranulation, MPO localized in and around vascular endothelial cells in a rodent model of acute endotoxemia and impaired endothelium-dependent relaxant responses, to which MPO-deficient mice were resistant. Altered vascular responsiveness was due to catalytic consumption of NO by substrate radicals generated by MPO. Thus MPO can directly modulate vascular inflammatory responses by regulating NO bioavailability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eiserich, Jason P -- Baldus, Stephan -- Brennan, Marie-Luise -- Ma, Wenxin -- Zhang, Chunxiang -- Tousson, Albert -- Castro, Laura -- Lusis, Aldons J -- Nauseef, William M -- White, C Roger -- Freeman, Bruce A -- I01 BX000513/BX/BLRD VA/ -- R01 HL067930/HL/NHLBI NIH HHS/ -- R03 TW005682/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 28;296(5577):2391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Division of Nephrology, University of California, Davis, CA 95616, USA. jpeiserich@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12089442" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aorta ; Catalysis ; Cattle ; Cells, Cultured ; Chromans/metabolism/pharmacology ; Coculture Techniques ; Cyclic GMP/metabolism ; Endothelium, Vascular/enzymology/*physiology ; Endotoxemia/enzymology ; Humans ; Hydrogen Peroxide/metabolism/pharmacology ; Inflammation/*enzymology/physiopathology ; Leukocytes/*enzymology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/metabolism ; Mutation ; Nitric Oxide/*metabolism ; Oxidation-Reduction ; Peroxidase/genetics/*metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Transfection ; Tumor Cells, Cultured ; *Vasodilation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2000-09-08
    Beschreibung: Myotonic dystrophy (DM), the most common form of muscular dystrophy in adult humans, results from expansion of a CTG repeat in the 3' untranslated region of the DMPK gene. The mutant DMPK messenger RNA (mRNA) contains an expanded CUG repeat and is retained in the nucleus. We have expressed an untranslated CUG repeat in an unrelated mRNA in transgenic mice. Mice that expressed expanded CUG repeats developed myotonia and myopathy, whereas mice expressing a nonexpanded repeat did not. Thus, transcripts with expanded CUG repeats are sufficient to generate a DM phenotype. This result supports a role for RNA gain of function in disease pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mankodi, A -- Logigian, E -- Callahan, L -- McClain, C -- White, R -- Henderson, D -- Krym, M -- Thornton, C A -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1769-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, School of Medicine and Dentistry, University of Rochester, Box 673, 601 Elmwood Avenue, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10976074" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions ; Actins/genetics ; Action Potentials ; Animals ; Cell Nucleus/metabolism/pathology ; Disease Models, Animal ; Humans ; In Situ Hybridization, Fluorescence ; Mice ; Mice, Transgenic ; Muscle, Skeletal/metabolism/pathology/physiopathology ; Myotonic Dystrophy/*genetics/metabolism/pathology/physiopathology ; Myotonin-Protein Kinase ; Phenotype ; Protein-Serine-Threonine Kinases/genetics ; RNA Splicing ; RNA, Messenger/*genetics/metabolism ; Transgenes ; *Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 1989-04-14
    Beschreibung: Previous studies have demonstrated that allelic deletions of the short arm of chromosome 17 occur in over 75% of colorectal carcinomas. Twenty chromosome 17p markers were used to localize the common region of deletion in these tumors to a region contained within bands 17p12 to 17p13.3. This region contains the gene for the transformation-associated protein p53. Southern and Northern blot hybridization experiments provided no evidence for gross alterations of the p53 gene or surrounding sequences. As a more rigorous test of the possibility that p53 was a target of the deletions, the p53 coding regions from two tumors were analyzed; these two tumors, like most colorectal carcinomas, had allelic deletions of chromosome 17p and expressed considerable amounts of p53 messenger RNA from the remaining allele. The remaining p53 allele was mutated in both tumors, with an alanine substituted for valine at codon 143 of one tumor and a histidine substituted for arginine at codon 175 of the second tumor. Both mutations occurred in a highly conserved region of the p53 gene that was previously found to be mutated in murine p53 oncogenes. The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, S J -- Fearon, E R -- Nigro, J M -- Hamilton, S R -- Preisinger, A C -- Jessup, J M -- vanTuinen, P -- Ledbetter, D H -- Barker, D F -- Nakamura, Y -- White, R -- Vogelstein, B -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- HD20619/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):217-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2649981" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; *Chromosome Deletion ; *Chromosomes, Human, Pair 17/ultrastructure ; Colorectal Neoplasms/*genetics ; Humans ; Mice ; Mice, Nude ; *Mutation ; Neoplasm Proteins/*genetics ; Nucleic Acid Hybridization ; Oncogenes ; Phosphoproteins/*genetics ; Suppression, Genetic ; Tumor Suppressor Protein p53
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Nature Publishing Group (NPG)
    Publikationsdatum: 2010-04-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, Craig R -- England -- Nature. 2010 Apr 1;464(7289):691-3. doi: 10.1038/464691a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360729" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Basal Metabolism/*physiology ; Body Size/*physiology ; Body Temperature/physiology ; Fractals ; History, 19th Century ; History, 20th Century ; Hot Temperature ; Mammals/*anatomy & histology/*physiology ; *Models, Biological
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 2008-02-22
    Beschreibung: The innate immune system recognizes nucleic acids during infection and tissue damage. Whereas viral RNA is detected by endosomal toll-like receptors (TLR3, TLR7, TLR8) and cytoplasmic RIG-I and MDA5, endosomal TLR9 and cytoplasmic DAI bind DNA, resulting in the activation of nuclear factor-kappaB and interferon regulatory factor transcription factors. However, viruses also trigger pro-inflammatory responses, which remain poorly defined. Here we show that internalized adenoviral DNA induces maturation of pro-interleukin-1beta in macrophages, which is dependent on NALP3 and ASC, components of the innate cytosolic molecular complex termed the inflammasome. Correspondingly, NALP3- and ASC-deficient mice display reduced innate inflammatory responses to adenovirus particles. Inflammasome activation also occurs as a result of transfected cytosolic bacterial, viral and mammalian (host) DNA, but in this case sensing is dependent on ASC but not NALP3. The DNA-sensing pro-inflammatory pathway functions independently of TLRs and interferon regulatory factors. Thus, in addition to viral and bacterial components or danger signals in general, inflammasomes sense potentially dangerous cytoplasmic DNA, strengthening their central role in innate immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muruve, Daniel A -- Petrilli, Virginie -- Zaiss, Anne K -- White, Lindsay R -- Clark, Sharon A -- Ross, P Joel -- Parks, Robin J -- Tschopp, Jurg -- England -- Nature. 2008 Mar 6;452(7183):103-7. doi: 10.1038/nature06664. Epub 2008 Feb 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Calgary, Alberta T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18288107" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenoviridae/genetics/immunology/physiology ; Animals ; Apoptosis Regulatory Proteins ; Carrier Proteins/genetics/*immunology ; Cell Line ; Cytoskeletal Proteins/deficiency/genetics/*immunology ; Cytosol/*metabolism/microbiology/*virology ; DNA/*immunology ; DNA, Viral/immunology ; Humans ; Immunity, Innate/*immunology ; Inflammation/*immunology/virology ; Interleukin-1beta/immunology/metabolism/secretion ; Macrophages, Peritoneal/immunology/metabolism ; Mice ; Mice, Inbred C57BL ; Protein Processing, Post-Translational
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Publikationsdatum: 1989-06-02
    Beschreibung: Balanced translocations, each involving chromosome 17q11.2, have been described in two patients with von Recklinghausen neurofibromatosis (NF1). To better localize the end points of these translocation events, and the NF1 gene (NF1) itself, human cosmids were isolated and mapped in the immediate vicinity of NF1. One cosmid probe, c11-1F10, demonstrated that both translocation breakpoints, and presumably NF1, are contained within a 600-kilobase Nru I fragment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connell, P -- Leach, R -- Cawthon, R M -- Culver, M -- Stevens, J -- Viskochil, D -- Fournier, R E -- Rich, D C -- Ledbetter, D H -- White, R -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1087-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Utah, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543077" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Cosmids ; DNA Restriction Enzymes ; Deoxyribonucleases, Type II Site-Specific ; Electrophoresis ; Genetic Linkage ; Humans ; Hybrid Cells ; Neurofibromatosis 1/*genetics ; Rats ; *Translocation, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Publikationsdatum: 2009-04-11
    Beschreibung: The nuclear factor kappaB (NF-kappaB) transcription factor regulates cellular stress responses and the immune response to infection. NF-kappaB activation results in oscillations in nuclear NF-kappaB abundance. To define the function of these oscillations, we treated cells with repeated short pulses of tumor necrosis factor-alpha at various intervals to mimic pulsatile inflammatory signals. At all pulse intervals that were analyzed, we observed synchronous cycles of NF-kappaB nuclear translocation. Lower frequency stimulations gave repeated full-amplitude translocations, whereas higher frequency pulses gave reduced translocation, indicating a failure to reset. Deterministic and stochastic mathematical models predicted how negative feedback loops regulate both the resetting of the system and cellular heterogeneity. Altering the stimulation intervals gave different patterns of NF-kappaB-dependent gene expression, which supports the idea that oscillation frequency has a functional role.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785900/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ashall, Louise -- Horton, Caroline A -- Nelson, David E -- Paszek, Pawel -- Harper, Claire V -- Sillitoe, Kate -- Ryan, Sheila -- Spiller, David G -- Unitt, John F -- Broomhead, David S -- Kell, Douglas B -- Rand, David A -- See, Violaine -- White, Michael R H -- BB/C007158/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C008219/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C520471/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D010748/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E004210/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E012965/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F005938/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0071581/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0082191/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC5204711/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBD0107481/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0059381/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500346/Medical Research Council/United Kingdom -- G0500346(73596)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):242-6. doi: 10.1126/science.1164860.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Imaging, School of Biological Sciences, Bioscience Research Building, Crown Street, Liverpool, L69 7ZB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359585" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression ; Humans ; I-kappa B Proteins/metabolism ; Mice ; Models, Biological ; Models, Statistical ; NF-kappa B/*metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Stochastic Processes ; Transcription Factor RelA/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Publikationsdatum: 2005-07-05
    Beschreibung: We report the genome sequence of Theileria parva, an apicomplexan pathogen causing economic losses to smallholder farmers in Africa. The parasite chromosomes exhibit limited conservation of gene synteny with Plasmodium falciparum, and its plastid-like genome represents the first example where all apicoplast genes are encoded on one DNA strand. We tentatively identify proteins that facilitate parasite segregation during host cell cytokinesis and contribute to persistent infection of transformed host cells. Several biosynthetic pathways are incomplete or absent, suggesting substantial metabolic dependence on the host cell. One protein family that may generate parasite antigenic diversity is not telomere-associated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gardner, Malcolm J -- Bishop, Richard -- Shah, Trushar -- de Villiers, Etienne P -- Carlton, Jane M -- Hall, Neil -- Ren, Qinghu -- Paulsen, Ian T -- Pain, Arnab -- Berriman, Matthew -- Wilson, Robert J M -- Sato, Shigeharu -- Ralph, Stuart A -- Mann, David J -- Xiong, Zikai -- Shallom, Shamira J -- Weidman, Janice -- Jiang, Lingxia -- Lynn, Jeffery -- Weaver, Bruce -- Shoaibi, Azadeh -- Domingo, Alexander R -- Wasawo, Delia -- Crabtree, Jonathan -- Wortman, Jennifer R -- Haas, Brian -- Angiuoli, Samuel V -- Creasy, Todd H -- Lu, Charles -- Suh, Bernard -- Silva, Joana C -- Utterback, Teresa R -- Feldblyum, Tamara V -- Pertea, Mihaela -- Allen, Jonathan -- Nierman, William C -- Taracha, Evans L N -- Salzberg, Steven L -- White, Owen R -- Fitzhugh, Henry A -- Morzaria, Subhash -- Venter, J Craig -- Fraser, Claire M -- Nene, Vishvanath -- New York, N.Y. -- Science. 2005 Jul 1;309(5731):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA. gardner@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15994558" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Animals ; Antigens, Protozoan/genetics ; Cattle ; Cell Proliferation ; Chromosomes/genetics ; Conserved Sequence ; Enzymes/genetics/metabolism ; Genes, Protozoan ; *Genome, Protozoan ; Lymphocytes/cytology/*parasitology ; Mitochondria/metabolism ; Molecular Sequence Data ; Organelles/genetics/physiology ; Plasmodium falciparum/genetics ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/*genetics/metabolism ; Sequence Analysis, DNA ; Synteny ; Telomere/genetics ; Theileria parva/*genetics/growth & development/pathogenicity/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 2011-03-25
    Beschreibung: Systematic annotation of gene regulatory elements is a major challenge in genome science. Direct mapping of chromatin modification marks and transcriptional factor binding sites genome-wide has successfully identified specific subtypes of regulatory elements. In Drosophila several pioneering studies have provided genome-wide identification of Polycomb response elements, chromatin states, transcription factor binding sites, RNA polymerase II regulation and insulator elements; however, comprehensive annotation of the regulatory genome remains a significant challenge. Here we describe results from the modENCODE cis-regulatory annotation project. We produced a map of the Drosophila melanogaster regulatory genome on the basis of more than 300 chromatin immunoprecipitation data sets for eight chromatin features, five histone deacetylases and thirty-eight site-specific transcription factors at different stages of development. Using these data we inferred more than 20,000 candidate regulatory elements and validated a subset of predictions for promoters, enhancers and insulators in vivo. We identified also nearly 2,000 genomic regions of dense transcription factor binding associated with chromatin activity and accessibility. We discovered hundreds of new transcription factor co-binding relationships and defined a transcription factor network with over 800 potential regulatory relationships.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179250/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Negre, Nicolas -- Brown, Christopher D -- Ma, Lijia -- Bristow, Christopher Aaron -- Miller, Steven W -- Wagner, Ulrich -- Kheradpour, Pouya -- Eaton, Matthew L -- Loriaux, Paul -- Sealfon, Rachel -- Li, Zirong -- Ishii, Haruhiko -- Spokony, Rebecca F -- Chen, Jia -- Hwang, Lindsay -- Cheng, Chao -- Auburn, Richard P -- Davis, Melissa B -- Domanus, Marc -- Shah, Parantu K -- Morrison, Carolyn A -- Zieba, Jennifer -- Suchy, Sarah -- Senderowicz, Lionel -- Victorsen, Alec -- Bild, Nicholas A -- Grundstad, A Jason -- Hanley, David -- MacAlpine, David M -- Mannervik, Mattias -- Venken, Koen -- Bellen, Hugo -- White, Robert -- Gerstein, Mark -- Russell, Steven -- Grossman, Robert L -- Ren, Bing -- Posakony, James W -- Kellis, Manolis -- White, Kevin P -- F32 GM074364/GM/NIGMS NIH HHS/ -- F32 GM074364-01/GM/NIGMS NIH HHS/ -- F32 GM074364-02/GM/NIGMS NIH HHS/ -- P50 GM081892/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-04/HG/NHGRI NIH HHS/ -- RC2 HG005639/HG/NHGRI NIH HHS/ -- RC2 HG005639-02/HG/NHGRI NIH HHS/ -- U01 HG004264/HG/NHGRI NIH HHS/ -- U01 HG004279/HG/NHGRI NIH HHS/ -- U01HG004264/HG/NHGRI NIH HHS/ -- England -- Nature. 2011 Mar 24;471(7339):527-31. doi: 10.1038/nature09990.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, Department of Human Genetics, The University of Chicago, 900 East 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430782" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Chromatin Immunoprecipitation ; Drosophila melanogaster/*genetics ; Enhancer Elements, Genetic/genetics ; Genome, Insect/*genetics ; Histone Deacetylases/metabolism ; Insulator Elements/genetics ; *Molecular Sequence Annotation ; Promoter Regions, Genetic/genetics ; Regulatory Sequences, Nucleic Acid/*genetics ; Reproducibility of Results ; Silencer Elements, Transcriptional/genetics ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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