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  • American Association for the Advancement of Science (AAAS)
  • 2000-2004  (6)
  • 1
    Publication Date: 2001-07-21
    Description: The 2,160,837-base pair genome sequence of an isolate of Streptococcus pneumoniae, a Gram-positive pathogen that causes pneumonia, bacteremia, meningitis, and otitis media, contains 2236 predicted coding regions; of these, 1440 (64%) were assigned a biological role. Approximately 5% of the genome is composed of insertion sequences that may contribute to genome rearrangements through uptake of foreign DNA. Extracellular enzyme systems for the metabolism of polysaccharides and hexosamines provide a substantial source of carbon and nitrogen for S. pneumoniae and also damage host tissues and facilitate colonization. A motif identified within the signal peptide of proteins is potentially involved in targeting these proteins to the cell surface of low-guanine/cytosine (GC) Gram-positive species. Several surface-exposed proteins that may serve as potential vaccine candidates were identified. Comparative genome hybridization with DNA arrays revealed strain differences in S. pneumoniae that could contribute to differences in virulence and antigenicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tettelin, H -- Nelson, K E -- Paulsen, I T -- Eisen, J A -- Read, T D -- Peterson, S -- Heidelberg, J -- DeBoy, R T -- Haft, D H -- Dodson, R J -- Durkin, A S -- Gwinn, M -- Kolonay, J F -- Nelson, W C -- Peterson, J D -- Umayam, L A -- White, O -- Salzberg, S L -- Lewis, M R -- Radune, D -- Holtzapple, E -- Khouri, H -- Wolf, A M -- Utterback, T R -- Hansen, C L -- McDonald, L A -- Feldblyum, T V -- Angiuoli, S -- Dickinson, T -- Hickey, E K -- Holt, I E -- Loftus, B J -- Yang, F -- Smith, H O -- Venter, J C -- Dougherty, B A -- Morrison, D A -- Hollingshead, S K -- Fraser, C M -- R01 AI40645-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 20;293(5529):498-506.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11463916" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Bacterial ; Bacterial Proteins/chemistry/genetics/immunology/metabolism ; Bacterial Vaccines ; Base Composition ; Carbohydrate Metabolism ; Carrier Proteins/genetics/metabolism ; Chromosomes, Bacterial/genetics ; Computational Biology ; DNA Transposable Elements ; DNA, Bacterial/chemistry/genetics ; Gene Duplication ; Genes, Bacterial ; *Genome, Bacterial ; Hexosamines/metabolism ; Oligonucleotide Array Sequence Analysis ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Species Specificity ; Streptococcus pneumoniae/*genetics/immunology/metabolism/*pathogenicity ; Virulence ; rRNA Operon
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-08-05
    Description: It has been assumed that the new members of the p53 protein family, p63 and p73, would have the same job as p53, namely, forcing cells to die if they or their DNA is damaged. Now, as Morrison and Kinoshita explain in their Perspective, one particular form of p73 has been found to be a survival factor rather than a death factor for sympathetic neurons during development (Pozniak et al.).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, R S -- Kinoshita, Y -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):257-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of Washington School of Medicine, Box 356470, Seattle, WA 98195-6470, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; DNA-Binding Proteins/genetics/*physiology ; Genes, Tumor Suppressor ; Mice ; Neurons/*physiology ; Nuclear Proteins/genetics/*physiology ; Sympathetic Nervous System/cytology/*growth & development/physiology ; Tumor Suppressor Protein p53/genetics/physiology ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2002-03-23
    Description: High-resolution transmission electron microscopy images of room-temperature fluid xenon in small faceted cavities in aluminum reveal the presence of three well-defined layers within the fluid at each facet. Such interfacial layering of simple liquids has been theoretically predicted, but observational evidence has been ambiguous. Molecular dynamics simulations indicate that the density variation induced by the layering will cause xenon, confined to an approximately cubic cavity of volume approximately 8 cubic nanometers, to condense into the body-centered cubic phase, differing from the face-centered cubic phase of both bulk solid xenon and solid xenon confined in somewhat larger (〉/=20 cubic nanometer) tetradecahedral cavities in face-centered cubic metals. Layering at the liquid-solid interface plays an important role in determining physical properties as diverse as the rheological behavior of two-dimensionally confined liquids and the dynamics of crystal growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donnelly, Stephen E -- Birtcher, Robert C -- Allen, Charles W -- Morrison, Ian -- Furuya, Kazuo -- Song, Minghui -- Mitsuishi, Kazutaka -- Dahmen, Ulrich -- New York, N.Y. -- Science. 2002 Apr 19;296(5567):507-10. Epub 2002 Mar 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joule Physics Laboratory, Institute for Materials Research, University of Salford, Manchester M5 4WT, UK. : s.e.donnelly@salford.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11910071" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2000-03-24
    Description: A comparative analysis of the genomes of Drosophila melanogaster, Caenorhabditis elegans, and Saccharomyces cerevisiae-and the proteins they are predicted to encode-was undertaken in the context of cellular, developmental, and evolutionary processes. The nonredundant protein sets of flies and worms are similar in size and are only twice that of yeast, but different gene families are expanded in each genome, and the multidomain proteins and signaling pathways of the fly and worm are far more complex than those of yeast. The fly has orthologs to 177 of the 289 human disease genes examined and provides the foundation for rapid analysis of some of the basic processes involved in human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754258/" 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/PMC2754258/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubin, G M -- Yandell, M D -- Wortman, J R -- Gabor Miklos, G L -- Nelson, C R -- Hariharan, I K -- Fortini, M E -- Li, P W -- Apweiler, R -- Fleischmann, W -- Cherry, J M -- Henikoff, S -- Skupski, M P -- Misra, S -- Ashburner, M -- Birney, E -- Boguski, M S -- Brody, T -- Brokstein, P -- Celniker, S E -- Chervitz, S A -- Coates, D -- Cravchik, A -- Gabrielian, A -- Galle, R F -- Gelbart, W M -- George, R A -- Goldstein, L S -- Gong, F -- Guan, P -- Harris, N L -- Hay, B A -- Hoskins, R A -- Li, J -- Li, Z -- Hynes, R O -- Jones, S J -- Kuehl, P M -- Lemaitre, B -- Littleton, J T -- Morrison, D K -- Mungall, C -- O'Farrell, P H -- Pickeral, O K -- Shue, C -- Vosshall, L B -- Zhang, J -- Zhao, Q -- Zheng, X H -- Lewis, S -- P4IHG00739/HG/NHGRI NIH HHS/ -- P50HG00750/HG/NHGRI NIH HHS/ -- R01 GM037193/GM/NIGMS NIH HHS/ -- R01 GM037193-14/GM/NIGMS NIH HHS/ -- R01 GM037193-15/GM/NIGMS NIH HHS/ -- R01 GM060988/GM/NIGMS NIH HHS/ -- R01 GM060988-01/GM/NIGMS NIH HHS/ -- R01 NS040296/NS/NINDS NIH HHS/ -- R01 NS040296-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2204-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cell Biology, Berkeley Drosophila Genome Project, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics ; Biological Evolution ; Caenorhabditis elegans/chemistry/*genetics/physiology ; Cell Adhesion/genetics ; Cell Cycle/genetics ; Drosophila melanogaster/chemistry/*genetics/physiology ; Fungal Proteins/chemistry/genetics ; Genes, Duplicate ; Genetic Diseases, Inborn/genetics ; Genetics, Medical ; *Genome ; Helminth Proteins/chemistry/genetics ; Humans ; Immunity/genetics ; Insect Proteins/chemistry/genetics ; Multigene Family ; Neoplasms/genetics ; Protein Structure, Tertiary ; *Proteome ; Saccharomyces cerevisiae/chemistry/*genetics/physiology ; Signal Transduction/genetics
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2003-08-16
    Description: Genes associated with Hirschsprung disease, a failure to form enteric ganglia in the hindgut, were highly up-regulated in gut neural crest stem cells relative to whole-fetus RNA. One of these genes, the glial cell line-derived neurotrophic factor (GDNF) receptor Ret, was necessary for neural crest stem cell migration in the gut. GDNF promoted the migration of neural crest stem cells in culture but did not affect their survival or proliferation. Gene expression profiling, combined with reverse genetics and analyses of stem cell function, suggests that Hirschsprung disease is caused by defects in neural crest stem cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614078/" 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/PMC2614078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashita, Toshihide -- Kruger, Genevieve M -- Pardal, Ricardo -- Kiel, Mark J -- Morrison, Sean J -- CA46592/CA/NCI NIH HHS/ -- DK58771/DK/NIDDK NIH HHS/ -- NIH5P60-DK20572/DK/NIDDK NIH HHS/ -- P30 AR48310/AR/NIAMS NIH HHS/ -- P60-AR20557/AR/NIAMS NIH HHS/ -- R01 NS040750/NS/NINDS NIH HHS/ -- R01 NS040750-01/NS/NINDS NIH HHS/ -- R01 NS40750-01/NS/NINDS NIH HHS/ -- R21 HD40760-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):972-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-0934, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Movement ; Cell Separation ; Cell Survival ; Cells, Cultured ; Digestive System/cytology/*embryology/innervation/metabolism ; Fetus/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Hirschsprung Disease/*etiology/genetics ; Mice ; Multipotent Stem Cells/*physiology ; Nerve Growth Factors/genetics/metabolism/pharmacology ; Neural Crest/*cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Up-Regulation
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2004-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deardorff, Don -- Dorhout, Peter -- Haegel, Nancy -- Iverson, Brent L -- Morrison, Michael -- Pladziewicz, Jack -- Selen, Mats -- Tullius, Thomas D -- Zwier, Timothy S -- New York, N.Y. -- Science. 2004 Nov 12;306(5699):1133.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539585" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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