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  • 1
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    Emerging marine diseases--climate links and anthropogenic factors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997-98 is coincident with high El Nino temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harvell, C D -- Kim, K -- Burkholder, J M -- Colwell, R R -- Epstein, P R -- Grimes, D J -- Hofmann, E E -- Lipp, E K -- Osterhaus, A D -- Overstreet, R M -- Porter, J W -- Smith, G W -- Vasta, G R -- 1PO1 ES09563/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1505-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecology and Evolutionary Biology, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaculture ; *Climate ; Cnidaria ; *Disease Outbreaks/*veterinary ; Humans ; Infection/epidemiology/*etiology/transmission/*veterinary ; *Marine Biology ; Oceans and Seas ; Water Pollution
    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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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
    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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    Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: The transcription factor NF-AT responds to Ca2+-calcineurin signals by translocating to the nucleus, where it participates in the activation of early immune response genes. Calcineurin dephosphorylates conserved serine residues in the amino terminus of NF-AT, resulting in nuclear import. Purification of the NF-AT kinase revealed that it is composed of a priming kinase activity and glycogen synthase kinase-3 (GSK-3). GSK-3 phosphorylates conserved serines necessary for nuclear export, promotes nuclear exit, and thereby opposes Ca2+-calcineurin signaling. Because GSK-3 responds to signals initiated by Wnt and other ligands, NF-AT family members could be effectors of these pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beals, C R -- Sheridan, C M -- Turck, C W -- Gardner, P -- Crabtree, G R -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1930-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072970" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Brain/enzymology ; COS Cells ; Calcineurin ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Calmodulin-Binding Proteins/metabolism ; Cell Nucleus/*metabolism ; Cloning, Molecular ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Transfection
    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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    Defective TNF-alpha-induced apoptosis in STAT1-null cells due to low constitutive levels of caspases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Signal transducers and activators of transcription (STATs) enhance transcription of specific genes in response to cytokines and growth factors. STAT1 is also required for efficient constitutive expression of the caspases Ice, Cpp32, and Ich-1 in human fibroblasts. As a consequence, STAT1-null cells are resistant to apoptosis by tumor necrosis factor alpha (TNF-alpha). Reintroduction of STAT1alpha restored both TNF-alpha-induced apoptosis and the expression of Ice, Cpp32, and Ich-1. Variant STAT1 proteins carrying point mutations that inactivate domains required for STAT dimer formation nevertheless restored protease expression and sensitivity to apoptosis, indicating that the functions of STAT1 required for these activities are different from those that mediate induced gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, A -- Commane, M -- Flickinger, T W -- Horvath, C M -- Stark, G R -- P01 CA62220/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1630-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374464" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Caspase 1 ; Caspase 2 ; Caspase 3 ; *Caspases ; Cell Line ; Cysteine Endopeptidases/genetics/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dactinomycin/pharmacology ; Dimerization ; Gene Expression Regulation, Enzymologic ; Humans ; Interferon-gamma/pharmacology ; Phosphorylation ; Point Mutation ; Proteins/genetics/*metabolism ; STAT1 Transcription Factor ; Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
    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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    Bureaucrats save lives (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fink, G R -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638092" target="_blank"〉PubMed〈/a〉
    Keywords: *Administrative Personnel ; DNA, Recombinant ; Government Agencies/*organization & administration ; *Hepatitis B Vaccines ; Humans ; National Institutes of Health (U.S.) ; Research Support as Topic ; Saccharomyces cerevisiae/*genetics ; *Transformation, Genetic ; United States ; Vaccines, Synthetic
    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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  • 6
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    E5531, a pure endotoxin antagonist of high potency (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-07
    Description: Shock due to Gram-negative bacterial sepsis is a consequence of acute inflammatory response to lipopolysaccharide (LPS) or endotoxin released from bacteria. LPS is a major constituent of the outer membrane of Gram-negative bacteria, and its terminal disaccharide phospholipid (lipid A) portion contains the key structural features responsible for toxic activity. Based on the proposed structure of nontoxic Rhodobacter capsulatus lipid A, a fully stabilized endotoxin antagonist E5531 has been synthesized. In vitro, E5531 demonstrated potent antagonism of LPS-mediated cellular activation in a variety of systems. In vivo, E5531 protected mice from LPS-induced lethality and, in cooperation with an antibiotic, protected mice from a lethal infection of viable Escherichia coli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christ, W J -- Asano, O -- Robidoux, A L -- Perez, M -- Wang, Y -- Dubuc, G R -- Gavin, W E -- Hawkins, L D -- McGuinness, P D -- Mullarkey, M A -- New York, N.Y. -- Science. 1995 Apr 7;268(5207):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Elsai Research Institute, Andover, MA 01810-2441, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine/immunology ; Cytokines/secretion ; Drug Design ; Endotoxins/*antagonists & inhibitors ; Escherichia coli Infections/immunology ; Gram-Negative Bacteria/immunology ; Humans ; In Vitro Techniques ; Lipid A/*analogs & derivatives/chemical synthesis/chemistry/pharmacology ; Lipopolysaccharides/antagonists & inhibitors ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Moxalactam/pharmacology ; Nitric Oxide/metabolism ; Rhodobacter capsulatus/immunology ; Tumor Necrosis Factor-alpha/secretion
    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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  • 7
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    STATs find that hanging together can be stimulating (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, S -- Li, X -- Stark, G R -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):750-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701326" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Cytokines/*metabolism ; DNA-Binding Proteins/chemistry/metabolism ; Humans ; Interferon-alpha/metabolism ; Interferon-gamma/metabolism ; Phosphorylation ; Receptor, Interferon alpha-beta ; Receptors, Interferon/metabolism ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; src Homology Domains
    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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  • 8
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    The HUGO Mutation Database Initiative (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotton, R G -- McKusick, V -- Scriver, C R -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):10-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9441394" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Communication Networks ; *Databases, Factual ; *Genetics, Medical ; *Human Genome Project ; Humans ; *Mutation ; Terminology as Topic
    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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  • 9
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    Planting the seeds of new antimalarial drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridley, R G -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1502-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Drug Discovery Research and the New Medicines for Malaria Venture, Special Programme for Research and Training in Tropical Diseases, World Health Organization, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498534" target="_blank"〉PubMed〈/a〉
    Keywords: Aldose-Ketose Isomerases/*antagonists & inhibitors/genetics/metabolism ; Animals ; Antimalarials/pharmacokinetics/*pharmacology ; Drug Design ; Enzyme Inhibitors/pharmacology ; Fosfomycin/analogs & derivatives/pharmacokinetics/pharmacology ; *Hemiterpenes ; Humans ; Malaria/*drug therapy/parasitology ; Malaria, Falciparum/drug therapy ; Mice ; Multienzyme Complexes/*antagonists & inhibitors/genetics/metabolism ; Organelles/drug effects/metabolism ; Organophosphorus Compounds/metabolism ; Oxidoreductases/*antagonists & inhibitors/genetics/metabolism ; Plasmodium falciparum/*drug effects/metabolism ; Steroids/metabolism ; Transferases/antagonists & inhibitors/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    BRCA1 inhibition of estrogen receptor signaling in transfected cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, S -- Wang, J -- Yuan, R -- Ma, Y -- Meng, Q -- Erdos, M R -- Pestell, R G -- Yuan, F -- Auborn, K J -- Goldberg, I D -- Rosen, E M -- R01-CA75503/CA/NCI NIH HHS/ -- R01-ES09169/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, 270-05 76th Avenue, New Hyde Park, NY 11040, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334989" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*physiology ; Breast/cytology ; Breast Neoplasms/etiology ; Cell Division ; Enhancer Elements, Genetic ; Epithelial Cells/cytology ; Estradiol/metabolism ; Estrogen Receptor alpha ; Female ; Genes, BRCA1 ; Genes, Reporter ; Humans ; Ligands ; Male ; Receptors, Estrogen/*metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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