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  • 1
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    Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: The functions of many open reading frames (ORFs) identified in genome-sequencing projects are unknown. New, whole-genome approaches are required to systematically determine their function. A total of 6925 Saccharomyces cerevisiae strains were constructed, by a high-throughput strategy, each with a precise deletion of one of 2026 ORFs (more than one-third of the ORFs in the genome). Of the deleted ORFs, 17 percent were essential for viability in rich medium. The phenotypes of more than 500 deletion strains were assayed in parallel. Of the deletion strains, 40 percent showed quantitative growth defects in either rich or minimal medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winzeler, E A -- Shoemaker, D D -- Astromoff, A -- Liang, H -- Anderson, K -- Andre, B -- Bangham, R -- Benito, R -- Boeke, J D -- Bussey, H -- Chu, A M -- Connelly, C -- Davis, K -- Dietrich, F -- Dow, S W -- El Bakkoury, M -- Foury, F -- Friend, S H -- Gentalen, E -- Giaever, G -- Hegemann, J H -- Jones, T -- Laub, M -- Liao, H -- Liebundguth, N -- Lockhart, D J -- Lucau-Danila, A -- Lussier, M -- M'Rabet, N -- Menard, P -- Mittmann, M -- Pai, C -- Rebischung, C -- Revuelta, J L -- Riles, L -- Roberts, C J -- Ross-MacDonald, P -- Scherens, B -- Snyder, M -- Sookhai-Mahadeo, S -- Storms, R K -- Veronneau, S -- Voet, M -- Volckaert, G -- Ward, T R -- Wysocki, R -- Yen, G S -- Yu, K -- Zimmermann, K -- Philippsen, P -- Johnston, M -- Davis, R W -- HG00185-02/HG/NHGRI NIH HHS/ -- HG01627/HG/NHGRI NIH HHS/ -- HG01633/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):901-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436161" target="_blank"〉PubMed〈/a〉
    Keywords: Culture Media ; *Gene Deletion ; Gene Expression Regulation, Fungal ; Gene Targeting ; *Genes, Essential ; Genes, Fungal ; *Genome, Fungal ; *Open Reading Frames ; Phenotype ; Polymerase Chain Reaction ; Recombination, Genetic ; Saccharomyces cerevisiae/*genetics/growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Selection forces and constraints on retroviral sequence variation (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-16
    Description: All retroviruses possess a highly error-prone reverse transcriptase, but the extent of the consequent sequence diversity and the rate of evolution differ greatly among retroviruses. Because of the high mutability of retroviruses, it is not the generation of new viral variants that limits the extent of diversity and the rate of evolution of retroviruses, but rather the selection forces that act on these variants. Here, we suggest that two selection forces--the immune response and the limited availability of appropriate target cells during transmission and persistence--are chiefly responsible for the observed sequence diversity in untreated retroviral infections. We illustrate these aspects of positive selection by reference to specific lentiviruses [human and simian immunodeficiency viruses (HIV and SIV)] and oncoviruses [feline leukemia virus (FeLV) and human T cell leukemia virus (HTLV)] that differ in their extent of variation and in disease outcomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Overbaugh, J -- Bangham, C R -- New York, N.Y. -- Science. 2001 May 11;292(5519):1106-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. joverbau@fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11352065" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Genetic Variation/*genetics ; HIV/genetics/immunology/physiology ; Human T-lymphotropic virus 1/genetics/immunology/physiology ; Humans ; Leukemia Virus, Feline/genetics/physiology ; Mutation/genetics ; Retroviridae/*genetics/immunology/physiology ; Retroviridae Infections/immunology/transmission/virology ; *Selection, Genetic ; Simian Immunodeficiency Virus/genetics/physiology ; Viral Vaccines/immunology
    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
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    Global analysis of protein activities using proteome chips (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-28
    Description: To facilitate studies of the yeast proteome, we cloned 5800 open reading frames and overexpressed and purified their corresponding proteins. The proteins were printed onto slides at high spatial density to form a yeast proteome microarray and screened for their ability to interact with proteins and phospholipids. We identified many new calmodulin- and phospholipid-interacting proteins; a common potential binding motif was identified for many of the calmodulin-binding proteins. Thus, microarrays of an entire eukaryotic proteome can be prepared and screened for diverse biochemical activities. The microarrays can also be used to screen protein-drug interactions and to detect posttranslational modifications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, H -- Bilgin, M -- Bangham, R -- Hall, D -- Casamayor, A -- Bertone, P -- Lan, N -- Jansen, R -- Bidlingmaier, S -- Houfek, T -- Mitchell, T -- Miller, P -- Dean, R A -- Gerstein, M -- Snyder, M -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2101-5. Epub 2001 Jul 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11474067" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Calmodulin/metabolism ; Calmodulin-Binding Proteins/metabolism ; Cell Membrane/metabolism ; Cloning, Molecular ; Fungal Proteins/chemistry/genetics/*metabolism ; Glucose/metabolism ; Liposomes/metabolism ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Open Reading Frames ; Peptide Library ; Phosphatidylcholines/metabolism ; Phosphatidylinositols/metabolism ; Phospholipids/metabolism ; Protein Binding ; *Proteome ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; Signal Transduction ; Streptavidin/metabolism
    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
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    Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-18
    Description: Cell contact is required for efficient transmission of human T cell leukemia virus- type 1 (HTLV-I) between cells and between individuals, because naturally infected lymphocytes produce virtually no cell-free infectious HTLV-I particles. However, the mechanism of cell-to-cell spread of HTLV-I is not understood. We show here that cell contact rapidly induces polarization of the cytoskeleton of the infected cell to the cell-cell junction. HTLV-I core (Gag protein) complexes and the HTLV-I genome accumulate at the cell-cell junction and are then transferred to the uninfected cell. Other lymphotropic viruses, such as HIV-1, may similarly subvert normal T cell physiology to allow efficient propagation between cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Igakura, Tadahiko -- Stinchcombe, Jane C -- Goon, Peter K C -- Taylor, Graham P -- Weber, Jonathan N -- Griffiths, Gillian M -- Tanaka, Yuetsu -- Osame, Mitsuhiro -- Bangham, Charles R M -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1713-6. Epub 2003 Feb 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Imperial College London, St. Mary's Campus, Norfolk Place, London W2 1PG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12589003" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/immunology/ultrastructure/virology ; CD8-Positive T-Lymphocytes/immunology/ultrastructure/virology ; Cell Adhesion Molecules/metabolism ; Cell Communication ; Cell Line ; *Cell Polarity ; Extracellular Space/virology ; Gene Products, env/metabolism ; Gene Products, gag/metabolism ; Genome, Viral ; HTLV-I Infections/virology ; Human T-lymphotropic virus 1/genetics/*physiology ; Humans ; In Situ Hybridization, Fluorescence ; Intercellular Junctions/*physiology/ultrastructure/virology ; Microscopy, Confocal ; Microtubule-Organizing Center/*physiology/ultrastructure ; Microtubules/physiology ; Nucleocapsid Proteins/metabolism ; Peptide Nucleic Acids ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology/*ultrastructure/*virology ; Talin/metabolism ; Virion/physiology
    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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  • 5
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    Population dynamics of immune responses to persistent viruses (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-05
    Description: Mathematical models, which are based on a firm understanding of biological interactions, can provide nonintuitive insights into the dynamics of host responses to infectious agents and can suggest new avenues for experimentation. Here, a simple mathematical approach is developed to explore the relation between antiviral immune responses, virus load, and virus diversity. The model results are compared to data on cytotoxic T cell responses and viral diversity in infections with the human T cell leukemia virus (HTLV-1) and the human immunodeficiency virus (HIV-1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, M A -- Bangham, C R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Apr 5;272(5258):74-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8600540" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/immunology ; Antigenic Variation ; Antigens, Viral/immunology ; Cytokines/immunology ; Cytotoxicity, Immunologic ; Epitopes/immunology ; Genetic Variation ; HIV Infections/immunology/virology ; HIV-1/immunology/physiology ; HTLV-I Infections/immunology/virology ; Human T-lymphotropic virus 1/genetics/immunology/physiology ; Humans ; *Models, Biological ; Mutation ; Population Dynamics ; T-Lymphocytes, Cytotoxic/*immunology ; Virus Diseases/*immunology/virology ; Virus Physiological Phenomena ; Virus Replication ; Viruses/genetics/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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