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  • Signal Transduction  (361)
  • Rats  (326)
  • American Association for the Advancement of Science (AAAS)  (655)
  • American Institute of Physics (AIP)
  • 1995-1999  (655)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (655)
  • American Institute of Physics (AIP)
  • Springer  (12)
  • Wiley-Blackwell  (1)
Years
Year
  • 1
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    Neurons and silicon get intimate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):578-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Electrodes ; Electrodes, Implanted ; *Electronics ; Electrophysiology ; Humans ; Nerve Net/*physiology ; Nervous System Diseases/*therapy ; Neurons/*physiology ; Rats ; Silicon ; *Transistors, Electronic
    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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    Stem cells. Rat spinal cord function partially restored (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1826-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Cell Differentiation ; Cell Survival ; Embryo, Mammalian ; Mice ; Neurons/cytology ; Oligodendroglia/cytology ; Rats ; Spinal Cord/cytology/*physiology ; Spinal Cord Injuries/*therapy ; *Stem Cell Transplantation ; Stem Cells/cytology
    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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    Key brain receptor gets an unusual regulator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1265-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*enzymology ; Brain/*enzymology ; Cloning, Molecular ; Glutamic Acid/metabolism ; Neurons/metabolism ; Racemases and Epimerases/*genetics/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Serine/*biosynthesis/metabolism ; Stereoisomerism ; Synapses/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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    Filling in the blanks of the GABAB receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/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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  • 5
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    Constitutive activation of toll-mediated antifungal defense in serpin-deficient Drosophila (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: The antifungal defense of Drosophila is controlled by the spaetzle/Toll/cactus gene cassette. Here, a loss-of-function mutation in the gene encoding a blood serine protease inhibitor, Spn43Ac, was shown to lead to constitutive expression of the antifungal peptide drosomycin, and this effect was mediated by the spaetzle and Toll gene products. Spaetzle was cleaved by proteolytic enzymes to its active ligand form shortly after immune challenge, and cleaved Spaetzle was constitutively present in Spn43Ac-deficient flies. Hence, Spn43Ac negatively regulates the Toll signaling pathway, and Toll does not function as a pattern recognition receptor in the Drosophila host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levashina, E A -- Langley, E -- Green, C -- Gubb, D -- Ashburner, M -- Hoffmann, J A -- Reichhart, J M -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1917-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UPR 9022 CNRS, Institut de Biologie Moleculaire et Cellulaire, 15 Rue Rene Descartes, Strasbourg 67084, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antifungal Agents/*metabolism ; *Antimicrobial Cationic Peptides ; Body Patterning ; Drosophila/embryology/genetics/*immunology ; *Drosophila Proteins ; Escherichia coli/genetics/immunology ; Genes, Insect ; Hemolymph/metabolism ; Insect Proteins/*biosynthesis/genetics/metabolism/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Micrococcus luteus/immunology ; Molecular Sequence Data ; Mutagenesis ; Peptides/genetics/metabolism ; *Receptors, Cell Surface ; Recombinant Fusion Proteins/genetics/metabolism ; Serine Proteinase Inhibitors/genetics/*metabolism ; Serpins/genetics/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Up-Regulation
    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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    Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: To monitor changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor distribution in living neurons, the AMPA receptor subunit GluR1 was tagged with green fluorescent protein (GFP). This protein (GluR1-GFP) was functional and was transiently expressed in hippocampal CA1 neurons. In dendrites visualized with two-photon laser scanning microscopy or electron microscopy, most of the GluR1-GFP was intracellular, mimicking endogenous GluR1 distribution. Tetanic synaptic stimulation induced a rapid delivery of tagged receptors into dendritic spines as well as clusters in dendrites. These postsynaptic trafficking events required synaptic N-methyl-D-aspartate (NMDA) receptor activation and may contribute to the enhanced AMPA receptor-mediatedtransmission observed during long-term potentiation and activity-dependent synaptic maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, S H -- Hayashi, Y -- Petralia, R S -- Zaman, S H -- Wenthold, R J -- Svoboda, K -- Malinow, R -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1811-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/*metabolism/ultrastructure ; Electric Stimulation ; Hippocampus/cytology/physiology ; Humans ; Long-Term Potentiation ; *Neuronal Plasticity ; Neurons/*physiology ; Organ Culture Techniques ; Rats ; Receptor Aggregation ; Receptors, AMPA/*metabolism ; Receptors, N-Methyl-D-Aspartate/*physiology ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Tetany
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    A tobacco syntaxin with a role in hormonal control of guard cell ion channels (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: The plant hormone abscisic acid (ABA) regulates potassium and chloride ion channels at the plasma membrane of guard cells, leading to stomatal closure that reduces transpirational water loss from the leaf. The tobacco Nt-SYR1 gene encodes a syntaxin that is associated with the plasma membrane. Syntaxins and related SNARE proteins aid intracellular vesicle trafficking, fusion, and secretion. Disrupting Nt-Syr1 function by cleavage with Clostridium botulinum type C toxin or competition with a soluble fragment of Nt-Syr1 prevents potassium and chloride ion channel response to ABA in guard cells and implicates Nt-Syr1 in an ABA-signaling cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leyman, B -- Geelen, D -- Quintero, F J -- Blatt, M R -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):537-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Plant Physiology and Biophysics, University of London, Wye College, Wye, Kent TN25 5AH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915701" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Animals ; Botulinum Toxins/metabolism ; Cell Membrane/physiology ; Chloride Channels/*physiology ; Genes, Plant ; Genetic Complementation Test ; Ion Channel Gating/drug effects ; Membrane Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Oocytes ; Patch-Clamp Techniques ; Plant Growth Regulators/*pharmacology ; Plant Leaves/*physiology ; *Plants, Toxic ; Potassium Channels/*physiology ; Qa-SNARE Proteins ; Saccharomyces cerevisiae/genetics/growth & development ; Signal Transduction ; Tobacco/genetics/*physiology ; Xenopus
    Print ISSN: 0036-8075
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  • 8
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    Calmodulin dependence of presynaptic metabotropic glutamate receptor signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Glutamatergic neurotransmission is controlled by presynaptic metabotropic glutamate receptors (mGluRs). A subdomain in the intracellular carboxyl-terminal tail of group III mGluRs binds calmodulin and heterotrimeric guanosine triphosphate-binding protein (G protein) betagamma subunits in a mutually exclusive manner. Mutations interfering with calmodulin binding and calmodulin antagonists inhibit G protein-mediated modulation of ionic currents by mGluR 7. Calmodulin antagonists also prevent inhibition of excitatory neurotransmission via presynaptic mGluRs. These results reveal a novel mechanism of presynaptic modulation in which Ca(2+)-calmodulin is required to release G protein betagamma subunits from the C-tail of group III mGluRs in order to mediate glutamatergic autoinhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, V -- El Far, O -- Bofill-Cardona, E -- Nanoff, C -- Freissmuth, M -- Karschin, A -- Airas, J M -- Betz, H -- Boehm, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1180-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calmodulin/antagonists & inhibitors/*metabolism ; Cells, Cultured ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*metabolism ; Glutamic Acid/*metabolism ; Hippocampus/cytology/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Presynaptic Terminals/metabolism ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sesterterpenes ; Signal Transduction ; Swine ; *Synaptic Transmission ; Terpenes/pharmacology
    Print ISSN: 0036-8075
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  • 9
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    Defective angiogenesis in mice lacking endoglin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-29
    Description: Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, D Y -- Sorensen, L K -- Brooke, B S -- Urness, L D -- Davis, E C -- Taylor, D G -- Boak, B B -- Wendel, D P -- K08 HL03490-03/HL/NHLBI NIH HHS/ -- T35 HL07744-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 28;284(5419):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD31/analysis ; Blood Vessels/cytology/*embryology/metabolism ; Cell Differentiation ; Crosses, Genetic ; Endothelium, Vascular/cytology/*embryology/metabolism ; Female ; Gene Targeting ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Muscle, Smooth, Vascular/cytology/*embryology ; *Neovascularization, Physiologic ; Receptors, Cell Surface ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Vascular Cell Adhesion Molecule-1/genetics/*physiology ; Yolk Sac/ultrastructure
    Print ISSN: 0036-8075
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  • 10
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    AP-2 recruitment to synaptotagmin stimulated by tyrosine-based endocytic motifs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Clathrin-mediated endocytosis is initiated by the recruitment of the clathrin adaptor protein AP-2 to the plasma membrane where the membrane protein synaptotagmin is thought to act as a docking site. AP-2 also interacts with endocytic motifs present in other cargo proteins. Peptides with a tyrosine-based endocytic motif stimulated binding of AP-2 to synaptotagmin and enhanced AP-2 recruitment to the plasma membrane of neuronal and non-neuronal cells. This suggests a mechanism by which nucleation of clathrin-coated pits is stimulated by the loading of cargo proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haucke, V -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36252/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455054" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Proteins, Vesicular Transport ; Animals ; Binding Sites ; CHO Cells ; *Calcium-Binding Proteins ; Cattle ; Cell Membrane/metabolism ; Clathrin/*metabolism ; Coated Pits, Cell-Membrane/*metabolism ; Cricetinae ; *Endocytosis ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/metabolism ; Oligopeptides/chemistry/metabolism/*pharmacology ; Phospholipase D/metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; Synaptic Membranes/*metabolism ; Synaptotagmins ; Tyrosine/chemistry
    Print ISSN: 0036-8075
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  • 11
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    An activating immunoreceptor complex formed by NKG2D and DAP10 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Many immune receptors are composed of separate ligand-binding and signal-transducing subunits. In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA. Within the DAP10 cytoplasmic domain, an Src homology 2 (SH2) domain-binding site was capable of recruiting the p85 subunit of the phosphatidylinositol 3-kinase (PI 3-kinase), providing for NKG2D-dependent signal transduction. Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Song, Y -- Bakker, A B -- Bauer, S -- Spies, T -- Lanier, L L -- Phillips, J H -- AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):730-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; NK Cell Lectin-Like Receptor Subfamily K ; Neoplasms/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Immunologic/chemistry/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Cells, Cultured ; src Homology Domains
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  • 12
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    Positive selection of natural autoreactive B cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Lymphocyte development is critically influenced by self-antigens. T cells are subject to both positive and negative selection, depending on their degree of self-reactivity. Although B cells are subject to negative selection, it has been difficult to test whether self-antigen plays any positive role in B cell development. A murine model system of naturally generated autoreactive B cells with a germ line gene-encoded specificity for the Thy-1 (CD90) glycoprotein was developed, in which the presence of self-antigen promotes B cell accumulation and serum autoantibody secretion. Thus, B cells can be subject to positive selection, generated, and maintained on the basis of their autoreactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayakawa, K -- Asano, M -- Shinton, S A -- Gui, M -- Allman, D -- Stewart, C L -- Silver, J -- Hardy, R R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA. K_Hayakawa@fccc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390361" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Animals ; Antigens, CD5/analysis ; Antigens, Thy-1/*immunology ; Autoantibodies/*biosynthesis/blood/immunology ; Autoantigens/*immunology ; B-Lymphocyte Subsets/*immunology ; Genes, Immunoglobulin ; Hybridomas ; Immunity, Innate ; Immunologic Surveillance ; Mice ; Mice, SCID ; Mice, Transgenic ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction ; T-Lymphocytes/immunology
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  • 13
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    Severe liver degeneration in mice lacking the IkappaB kinase 2 gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Phosphorylation of inhibitor of kappa B (IkappaB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-kappaB) and requires two IkappaB kinases, IKK1 (IKKalpha) and IKK2 (IKKbeta). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2-/- embryos showed a marked reduction in tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enhanced apoptosis in response to TNF-alpha. IKK1 associated with NF-kappaB essential modulator (IKKgamma/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Q -- Van Antwerp, D -- Mercurio, F -- Lee, K F -- Verma, I M -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA. Signal Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Liver/cytology/*embryology ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factor RelA ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
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  • 14
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    Techsigting. Neural regeneration. Some nerve! (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Separation ; Chick Embryo ; Neural Crest/*cytology/embryology ; Neuroglia/*cytology ; Neurons/*cytology ; Rats ; Regeneration ; Sciatic Nerve/*cytology/embryology ; Stem Cells/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Role of DNA 5-methylcytosine transferase in cell transformation by fos (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The Fos and Jun oncoproteins form dimeric complexes that stimulate transcription of genes containing activator protein-1 regulatory elements. We found, by representational difference analysis, that expression of DNA 5-methylcytosine transferase (dnmt1) in fos-transformed cells is three times the expression in normal fibroblasts and that fos-transformed cells contain about 20 percent more 5-methylcytosine than normal fibroblasts. Transfection of the gene encoding Dnmt1 induced morphological transformation, whereas inhibition of dnmt1 expression or activity resulted in reversion of fos transformation. Inhibition of histone deacetylase, which associates with methylated DNA, also caused reversion. These results suggest that fos may transform cells through alterations in DNA methylation and in histone deacetylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakin, A V -- Curran, T -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888853" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Acetylation ; Animals ; Cell Size ; *Cell Transformation, Neoplastic ; Cytosine/analogs & derivatives/metabolism ; DNA (Cytosine-5-)-Methyltransferase/genetics/*metabolism ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Neoplastic ; *Genes, fos ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; Proto-Oncogene Proteins c-fos/*metabolism ; Rats ; Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Pigment epithelium-derived factor: a potent inhibitor of angiogenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: In the absence of disease, the vasculature of the mammalian eye is quiescent, in part because of the action of angiogenic inhibitors that prevent vessels from invading the cornea and vitreous. Here, an inhibitor responsible for the avascularity of these ocular compartments is identified as pigment epithelium-derived factor (PEDF), a protein previously shown to have neurotrophic activity. The amount of inhibitory PEDF produced by retinal cells was positively correlated with oxygen concentrations, suggesting that its loss plays a permissive role in ischemia-driven retinal neovascularization. These results suggest that PEDF may be of therapeutic use, especially in retinopathies where pathological neovascularization compromises vision and leads to blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, D W -- Volpert, O V -- Gillis, P -- Crawford, S E -- Xu, H -- Benedict, W -- Bouck, N P -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Department of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies/immunology ; Cattle ; Cells, Cultured ; Chemotaxis/drug effects ; Culture Media, Conditioned ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/cytology/drug effects/physiology ; Eye/blood supply ; *Eye Proteins ; Humans ; Lymphokines/metabolism ; Mice ; Neovascularization, Pathologic/*drug therapy/metabolism/pathology ; Neovascularization, Physiologic/*drug effects ; *Nerve Growth Factors ; Oxygen/physiology ; Proteins/genetics/immunology/*pharmacology/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/*metabolism/pathology ; Retinal Neovascularization/*drug therapy ; Retinal Vessels/growth & development ; Serpins/genetics/immunology/*pharmacology/*physiology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 17
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    Plant paralog to viral movement protein that potentiates transport of mRNA into the phloem (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: CmPP16 from Cucurbita maxima was cloned and the protein was shown to possess properties similar to those of viral movement proteins. CmPP16 messenger RNA (mRNA) is present in phloem tissue, whereas protein appears confined to sieve elements (SE). Microinjection and grafting studies revealed that CmPP16 moves from cell to cell, mediates the transport of sense and antisense RNA, and moves together with its mRNA into the SE of scion tissue. CmPP16 possesses the characteristics that are likely required to mediate RNA delivery into the long-distance translocation stream. Thus, RNA may move within the phloem as a component of a plant information superhighway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xoconostle-Cazares, B -- Xiang, Y -- Ruiz-Medrano, R -- Wang, H L -- Monzer, J -- Yoo, B C -- McFarland, K C -- Franceschi, V R -- Lucas, W J -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):94-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Plant Biology, Division of Biological Sciences, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872750" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Transport ; Cloning, Molecular ; Cucumis sativus ; Cucurbitaceae/genetics/*metabolism ; Microinjections ; Molecular Sequence Data ; Plant Leaves/metabolism ; Plant Proteins/chemistry/genetics/*metabolism ; Plant Roots/metabolism ; Plant Stems/metabolism ; Plant Viral Movement Proteins ; RNA, Antisense/metabolism ; RNA, Messenger/*metabolism ; RNA, Plant/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Viral Proteins/chemistry/metabolism
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  • 18
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    Unlimited mileage from telomerase? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- DePinho, R A -- CA76027/CA/NCI NIH HHS/ -- HD 348880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Aging ; *Cell Division ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Neoplasms/enzymology/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; ras Proteins/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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  • 19
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    Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanagisawa, J -- Yanagi, Y -- Masuhiro, Y -- Suzawa, M -- Watanabe, M -- Kashiwagi, K -- Toriyabe, T -- Kawabata, M -- Miyazono, K -- Kato, S -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1317-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/pharmacology ; COS Cells ; Calcitriol/*metabolism/pharmacology ; Cell Nucleus/metabolism ; DNA-Binding Proteins/*metabolism ; Histone Acetyltransferases ; Ligands ; Nuclear Receptor Coactivator 1 ; Phosphorylation ; Receptor Cross-Talk ; Receptors, Calcitriol/*metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Receptors, Retinoic Acid/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Smad3 Protein ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism
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  • 20
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    Requirement for B cell linker protein (BLNK) in B cell development (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Linker proteins function as molecular scaffolds to localize enzymes with substrates. In B cells, B cell linker protein (BLNK) links the B cell receptor (BCR)-activated Syk kinase to the phosphoinositide and mitogen-activated kinase pathways. To examine the in vivo role of BLNK, mice deficient in BLNK were generated. B cell development in BLNK-/- mice was blocked at the transition from B220+CD43+ progenitor B to B220+CD43- precursor B cells. Only a small percentage of immunoglobulin M++ (IgM++), but not mature IgMloIgDhi, B cells were detected in the periphery. Hence, BLNK is an essential component of BCR signaling pathways and is required to promote B cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pappu, R -- Cheng, A M -- Li, B -- Gong, Q -- Chiu, C -- Griffin, N -- White, M -- Sleckman, B P -- Chan, A C -- AI42787/AI/NIAID NIH HHS/ -- CA71516/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1949-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Division of Rheumatology, Department of Medicine, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583957" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Aging ; Animals ; B-Lymphocyte Subsets/cytology/immunology ; B-Lymphocytes/*cytology/immunology/*metabolism ; Bone Marrow Cells/cytology/immunology ; Carrier Proteins/genetics/*physiology ; Cell Count ; Cell Differentiation ; Cell Separation ; Cell Size ; Flow Cytometry ; Gene Targeting ; Hematopoietic Stem Cells/*cytology/metabolism ; Immunoglobulin M/analysis ; Leukopoiesis ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; *Phosphoproteins ; Receptors, Antigen, B-Cell/*metabolism ; Second Messenger Systems ; Signal Transduction
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  • 21
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    Focal adhesion motility revealed in stationary fibroblasts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Focal adhesions (FAs) are clustered integrins and associated proteins that mediate cell adhesion and signaling. A green fluorescent protein-beta1 integrin chimera was used to label FAs in living cells. In stationary cells, FAs were highly motile, moving linearly for several plaque lengths toward the cell center. FA motility was independent of cell density and resulted from contraction of associated actin fibers. In migrating cells, FAs were stationary and only moved in the tail. FA motility in stationary cells suggests that cell movement may be regulated by a clutch-like mechanism by which the affinity of integrins to substrate may be altered in response to migratory cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smilenov, L B -- Mikhailov, A -- Pelham, R J -- Marcantonio, E E -- Gundersen, G G -- GM42026/GM/NIGMS NIH HHS/ -- GM44585/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1172-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/physiology ; Animals ; Antigens, CD29/*metabolism ; *Cell Adhesion ; Cell Count ; Cell Line ; *Cell Movement ; Fibroblasts/*cytology/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins ; Mice ; Microscopy, Interference ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 22
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    Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elchebly, M -- Payette, P -- Michaliszyn, E -- Cromlish, W -- Collins, S -- Loy, A L -- Normandin, D -- Cheng, A -- Himms-Hagen, J -- Chan, C C -- Ramachandran, C -- Gresser, M J -- Tremblay, M L -- Kennedy, B P -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1544-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada, H3G 1Y6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dietary Fats/administration & dosage ; Gene Targeting ; Glucose Tolerance Test ; Insulin/blood/*metabolism/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; Obesity/*metabolism/therapy ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatases/*genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
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  • 23
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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  • 24
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    Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bosch, F -- Miksa, M -- Bittigau, P -- Vockler, J -- Dikranian, K -- Tenkova, T I -- Stefovska, V -- Turski, L -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):70-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/*cytology/drug effects/embryology/growth & development ; Calcium Channel Blockers/pharmacology ; Dizocilpine Maleate/pharmacology ; Dopamine Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Fetus ; Haloperidol/pharmacology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Electron ; Muscarinic Antagonists/pharmacology ; *Nerve Degeneration ; Neurons/*cytology/drug effects/metabolism ; Quinoxalines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/metabolism ; Scopolamine Hydrobromide/pharmacology
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  • 25
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    The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Ubiquitination of receptor protein-tyrosine kinases (RPTKs) terminates signaling by marking active receptors for degradation. c-Cbl, an adapter protein for RPTKs, positively regulates RPTK ubiquitination in a manner dependent on its variant SRC homology 2 (SH2) and RING finger domains. Ubiquitin-protein ligases (or E3s) are the components of ubiquitination pathways that recognize target substrates and promote their ligation to ubiquitin. The c-Cbl protein acted as an E3 that can recognize tyrosine-phosphorylated substrates, such as the activated platelet-derived growth factor receptor, through its SH2 domain and that recruits and allosterically activates an E2 ubiquitin-conjugating enzyme through its RING domain. These results reveal an SH2-containing protein that functions as a ubiquitin-protein ligase and thus provide a distinct mechanism for substrate targeting in the ubiquitin system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joazeiro, C A -- Wing, S S -- Huang, H -- Leverson, J D -- Hunter, T -- Liu, Y C -- CA39780/CA/NCI NIH HHS/ -- R01 DK56558/DK/NIDDK NIH HHS/ -- T32CA09523/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute, Molecular Biology and Virology Laboratory, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Humans ; Ligases/chemistry/*metabolism ; Molecular Sequence Data ; Phosphotyrosine/metabolism ; Point Mutation ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Alignment ; Signal Transduction ; *Ubiquitin-Conjugating Enzymes ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism ; src Homology Domains
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  • 26
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    Building neural representations of habits (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Memories for habits and skills ("implicit or procedural memory") and memories for facts ("explicit or episodic memory") are built up in different brain systems and are vulnerable to different neurodegenerative disorders in humans. So that the striatum-based mechanisms underlying habit formation could be studied, chronic recordings from ensembles of striatal neurons were made with multiple tetrodes as rats learned a T-maze procedural task. Large and widely distributed changes in the neuronal activity patterns occurred in the sensorimotor striatum during behavioral acquisition, culminating in task-related activity emphasizing the beginning and end of the automatized procedure. The new ensemble patterns remained stable during weeks of subsequent performance of the same task. These results suggest that the encoding of action in the sensorimotor striatum undergoes dynamic reorganization as habit learning proceeds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jog, M S -- Kubota, Y -- Connolly, C I -- Hillegaart, V -- Graybiel, A M -- R03 MH57878/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1745-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London Health Sciences Center, London, Ontario N6A 5A5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576743" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal ; Brain Mapping ; Corpus Striatum/*physiology ; Electrodes, Implanted ; Evoked Potentials ; *Habits ; Locomotion ; *Maze Learning ; Memory/physiology ; Motor Activity ; Neurons/physiology ; Rats ; Reaction Time
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    Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: A mechanism by which the Ras-mitogen-activated protein kinase (MAPK) signaling pathway mediates growth factor-dependent cell survival was characterized. The MAPK-activated kinases, the Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro and in vivo. The Rsk-induced phosphorylation of BAD at serine 112 suppressed BAD-mediated apoptosis in neurons. Rsks also are known to phosphorylate the transcription factor CREB (cAMP response element-binding protein) at serine 133. Activated CREB promoted cell survival, and inhibition of CREB phosphorylation at serine 133 triggered apoptosis. These findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Brunet, A -- West, A E -- Datta, S R -- Takasu, M A -- Greenberg, M E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 HD 24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1358-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain-Derived Neurotrophic Factor/pharmacology ; Carrier Proteins/genetics/metabolism ; *Cell Survival ; Cells, Cultured ; Cerebellum/cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Kinase 1 ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Mutation ; Neurons/*cytology/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; *Protein-Serine-Threonine Kinases ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; bcl-Associated Death Protein ; ras Proteins/metabolism
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    Gating of BDNF-induced synaptic potentiation by cAMP (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulanger, L -- Poo, M M -- NS 37831/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1982-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*pharmacology ; *Carbazoles ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cycloleucine/analogs & derivatives/pharmacology ; *Excitatory Postsynaptic Potentials/drug effects ; Indoles/pharmacology ; Nerve Growth Factors/pharmacology ; Neuronal Plasticity ; Neurons/cytology/physiology ; Neurotrophin 3 ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Pyrroles/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; Xenopus
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    Dissecting dendrite dynamics (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, S J -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1860-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. sjsmith@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206891" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Action Potentials ; Animals ; Dendrites/*physiology/ultrastructure ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Microscopy, Fluorescence ; Neurons/physiology/ultrastructure ; Pseudopodia/*physiology/ultrastructure ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology/ultrastructure ; Synaptic Membranes/physiology
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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    Precisely localized LTD in the neocortex revealed by infrared-guided laser stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: In a direct approach to elucidate the origin of long-term depression (LTD), glutamate was applied onto dendrites of neurons in rat neocortical slices. An infrared-guided laser stimulation was used to release glutamate from caged glutamate in the focal spot of an ultraviolet laser. A burst of light flashes caused an LTD-like depression of glutamate receptor responses, which was highly confined to the region of "tetanic" stimulation (〈10 micrometers). A similar depression of glutamate receptor responses was observed during LTD of synaptic transmission. A spatially highly specific postsynaptic mechanism can account for the LTD induced by glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodt, H -- Eder, M -- Frick, A -- Zieglgansberger, W -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, 80804 Munich, Germany. dodt@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamates/pharmacology ; Glutamic Acid/metabolism ; In Vitro Techniques ; Infrared Rays ; Lasers ; Microscopy, Video ; Neocortex/cytology/*physiology ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Photolysis ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/*metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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    RNA, whither goest thou? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tiedge, H -- Bloom, F E -- Richter, D -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):186-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, State Univeristy of New York Health Science Center at Brooklyn, Brooklyn, NY 11203, USA. tiedge@hscbklyn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Biological Transport ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dendrites/*metabolism ; Gene Expression Regulation ; *Neuronal Plasticity ; Protein Biosynthesis ; RNA, Messenger/chemistry/genetics/*metabolism ; Ribonucleoproteins/metabolism ; Signal Transduction ; Synapses/metabolism/*physiology
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    Key molecular signals identified in plants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206881" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/*genetics/growth & development/metabolism ; *Arabidopsis Proteins ; *Genes, Plant ; Ligands ; Meristem/growth & development ; Phosphotransferases/genetics/metabolism ; Plant Proteins/chemistry/*genetics/metabolism/physiology ; Signal Transduction
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    Requirement of type III TGF-beta receptor for endocardial cell transformation in the heart (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Transforming growth factor-beta (TGF-beta) signaling is mediated by a complex of type I (TBRI) and type II (TBRII) receptors. The type III receptor (TBRIII) lacks a recognizable signaling domain and has no clearly defined role in TGF-beta signaling. Cardiac endothelial cells that undergo epithelial-mesenchymal transformation express TBRIII, and here TBRIII-specific antisera were found to inhibit mesenchyme formation and migration in atrioventricular cushion explants. Misexpression of TBRIII in nontransforming ventricular endothelial cells conferred transformation in response to TGF-beta2. These results support a model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, C B -- Boyer, A S -- Runyan, R B -- Barnett, J V -- 38649/PHS HHS/ -- 42266/PHS HHS/ -- HL52922/HL/NHLBI NIH HHS/ -- R01 HL052922/HL/NHLBI NIH HHS/ -- R01 HL052922-05/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2080-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN 37232-6600, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092230" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Chick Embryo ; Culture Techniques ; Endocardium/cytology/*embryology/metabolism ; Endothelium/*cytology/embryology/metabolism ; Genetic Vectors ; Heart/*embryology ; Heart Atria/cytology/embryology ; Heart Ventricles/cytology/embryology/virology ; Immune Sera ; Ligands ; Mesoderm/*cytology/metabolism ; Myocardium/cytology/metabolism ; Protein-Serine-Threonine Kinases ; Proteoglycans/immunology/*physiology ; Receptors, Transforming Growth Factor beta/immunology/*physiology ; Retroviridae/genetics/physiology ; Signal Transduction ; Transforming Growth Factor beta/*metabolism/pharmacology
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    Structural basis of Smad2 recognition by the Smad anchor for receptor activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: The Smad proteins mediate transforming growth factor-beta (TGFbeta) signaling from the transmembrane serine-threonine receptor kinases to the nucleus. The Smad anchor for receptor activation (SARA) recruits Smad2 to the TGFbeta receptors for phosphorylation. The crystal structure of a Smad2 MH2 domain in complex with the Smad-binding domain (SBD) of SARA has been determined at 2.2 angstrom resolution. SARA SBD, in an extended conformation comprising a rigid coil, an alpha helix, and a beta strand, interacts with the beta sheet and the three-helix bundle of Smad2. Recognition between the SARA rigid coil and the Smad2 beta sheet is essential for specificity, whereas interactions between the SARA beta strand and the Smad2 three-helix bundle contribute significantly to binding affinity. Comparison of the structures between Smad2 and a comediator Smad suggests a model for how receptor-regulated Smads are recognized by the type I receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, G -- Chen, Y G -- Ozdamar, B -- Gyuricza, C A -- Chong, P A -- Wrana, J L -- Massague, J -- Shi, Y -- CA85171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):92-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615055" target="_blank"〉PubMed〈/a〉
    Keywords: *Activin Receptors, Type I ; Amino Acid Sequence ; Binding Sites ; Carrier Proteins/*chemistry/*metabolism ; Crystallography, X-Ray ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Point Mutation ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction ; Smad2 Protein ; Trans-Activators/*chemistry/genetics/*metabolism ; Zinc Fingers
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    Transmission of chronic nociception by spinal neurons expressing the substance P receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Substance P receptor (SPR)-expressing spinal neurons were ablated with the selective cytotoxin substance P-saporin. Loss of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated with persistent neuropathic and inflammatory pain states. This loss appeared to be permanent. Responses to mildly painful stimuli and morphine analgesia were unaffected by this treatment. These results identify a target for treating persistent pain and suggest that the small population of SPR-expressing neurons in the dorsal horn of the spinal cord plays a pivotal role in the generation and maintenance of chronic neuropathic and inflammatory pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nichols, M L -- Allen, B J -- Rogers, S D -- Ghilardi, J R -- Honore, P -- Luger, N M -- Finke, M P -- Li, J -- Lappi, D A -- Simone, D A -- Mantyh, P W -- 23970/PHS HHS/ -- 31223/PHS HHS/ -- DEO 7288/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preventive Sciences, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Ganglia, Spinal/drug effects/physiology ; *Immunotoxins ; Inflammation/physiopathology ; Ligation ; *N-Glycosyl Hydrolases ; Neuralgia/drug therapy/physiopathology ; Pain/*drug therapy/*physiopathology ; Plant Proteins/administration & dosage/*pharmacology ; Posterior Horn Cells/drug effects/*physiology ; Rats ; Receptors, Neurokinin-1/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Spinal Nerves ; Substance P/administration & dosage/*pharmacology ; Time Factors
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    Contact-dependent inhibition of cortical neurite growth mediated by notch signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: The exuberant growth of neurites during development becomes markedly reduced as cortical neurons mature. In vitro studies of neurons from mouse cerebral cortex revealed that contact-mediated Notch signaling regulates the capacity of neurons to extend and elaborate neurites. Up-regulation of Notch activity was concomitant with an increase in the number of interneuronal contacts and cessation of neurite growth. In neurons with low Notch activity, which readily extend neurites, up-regulation of Notch activity either inhibited extension or caused retraction of neurites. Conversely, in more mature neurons that had ceased their growth after establishing numerous connections and displayed high Notch activity, inhibition of Notch signaling promoted neurite extension. Thus, the formation of neuronal contacts results in activation of Notch receptors, leading to restriction of neuronal growth and a subsequent arrest in maturity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sestan, N -- Artavanis-Tsakonas, S -- Rakic, P -- NS14841/NS/NINDS NIH HHS/ -- NS26084/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):741-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Count ; Cell Differentiation ; Cell Movement ; Cell Nucleus/metabolism ; Cell Size ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Contact Inhibition ; Humans ; Ligands ; Membrane Proteins/*metabolism ; Mice ; Mitosis ; Neurites/chemistry/*physiology ; Neurons/*cytology/metabolism ; Protein Structure, Tertiary ; Receptor, Notch1 ; Receptor, Notch2 ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; *Transcription Factors ; Transcriptional Activation ; Up-Regulation
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    Perspectives: cell biology. All creatures great and small (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leevers, S J -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2082-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, London, UK. sallyl@ludwig.ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Constitution ; Carrier Proteins/genetics/metabolism ; Cell Count ; Cell Division ; Cell Size ; Drosophila/*enzymology/genetics/*growth & development ; *Drosophila Proteins ; Genes, Insect ; Insect Proteins/biosynthesis/genetics/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins ; *Intracellular Signaling Peptides and Proteins ; Mutation ; Phosphatidylinositol 3-Kinases/genetics/metabolism ; *Protein-Serine-Threonine Kinases ; Protein-Tyrosine Kinases/genetics/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-akt ; *Receptor Protein-Tyrosine Kinases ; Receptor, Insulin/genetics/metabolism ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; Signal Transduction
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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
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    Stem cells as potential nerve therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):650-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Diffuse Cerebral Sclerosis of Schilder/*therapy ; Embryo, Mammalian/cytology ; Financing, Government ; Germany ; Humans ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/physiology/transplantation ; Rats ; Research Support as Topic ; Spinal Cord ; Stem Cells/*cytology/physiology
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    A phospholipase C-dependent inositol polyphosphate kinase pathway required for efficient messenger RNA export (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: In order to identify additional factors required for nuclear export of messenger RNA, a genetic screen was conducted with a yeast mutant deficient in a factor Gle1p, which associates with the nuclear pore complex (NPC). The three genes identified encode phospholipase C and two potential inositol polyphosphate kinases. Together, these constitute a signaling pathway from phosphatidylinositol 4, 5-bisphosphate to inositol hexakisphosphate (IP6). The common downstream effects of mutations in each component were deficiencies in IP6 synthesis and messenger RNA export, indicating a role for IP6 in GLE1 function and messenger RNA export.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉York, J D -- Odom, A R -- Murphy, R -- Ives, E B -- Wente, S R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):96-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, DUMC 3813, Durham, NC 27710, USA. yorkj@acpub.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390371" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Transport ; Carrier Proteins/genetics/*metabolism ; Genes, Fungal ; Genetic Complementation Test ; Inositol Phosphates/metabolism ; Mutation ; Nuclear Envelope/*metabolism ; Nuclear Pore Complex Proteins ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Phytic Acid/metabolism ; RNA, Fungal/metabolism ; RNA, Messenger/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Type C Phospholipases/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    PEG antibodies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorsky, R -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites, Antibody ; Biological Availability ; Half-Life ; Immunoglobulin Fab Fragments/*immunology/*metabolism ; Male ; Polyethylene Glycols/*metabolism ; Rats ; Rats, Wistar
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    The structural era of endocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: Endocytosis is crucial for an array of cellular functions and can occur through several distinct mechanisms with the capacity to internalize anything from small molecules to entire cells. The clathrin-mediated endocytic pathway has recently received considerable attention because of (i) the identification of an array of molecules that orchestrate the assembly of clathrin-coated vesicles and the selection of the vesicle cargo and (ii) the resolution of structures for a number of these proteins. Together, these data provide an initial three-dimensional framework for understanding the clathrin endocytic machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, M -- McMahon, H T -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):215-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK. m.marsh@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Calcium-Binding Proteins/chemistry/physiology ; Cell Membrane/ultrastructure ; Clathrin/chemistry/*physiology ; Coated Pits, Cell-Membrane/physiology/ultrastructure ; Coated Vesicles/physiology/ultrastructure ; Dynamins ; *Endocytosis ; GTP Phosphohydrolases/chemistry/physiology ; Membrane Proteins/chemistry/physiology ; Nerve Tissue Proteins/chemistry/physiology ; Phosphoproteins/chemistry/physiology ; Signal Transduction
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    Regulation of neurotrophin-3 expression by epithelial-mesenchymal interactions: the role of Wnt factors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: Neurotrophins regulate survival, axonal growth, and target innervation of sensory and other neurons. Neurotrophin-3 (NT-3) is expressed specifically in cells adjacent to extending axons of dorsal root ganglia neurons, and its absence results in loss of most of these neurons before their axons reach their targets. However, axons are not required for NT-3 expression in limbs; instead, local signals from ectoderm induce NT-3 expression in adjacent mesenchyme. Wnt factors expressed in limb ectoderm induce NT-3 in the underlying mesenchyme. Thus, epithelial-mesenchymal interactions mediated by Wnt factors control NT-3 expression and may regulate axonal growth and guidance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710127/" 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/PMC2710127/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patapoutian, A -- Backus, C -- Kispert, A -- Reichardt, L F -- MH48200/MH/NIMH NIH HHS/ -- P01 NS016033/NS/NINDS NIH HHS/ -- P01 NS016033-190014/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1180-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143-0723, USA. ardem@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024246" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Coculture Techniques ; Ectoderm/metabolism/*physiology ; Embryo, Mammalian/metabolism ; Epithelium/metabolism ; Extremities/embryology/innervation ; Ganglia, Spinal/physiology ; *Gene Expression Regulation, Developmental ; *Glycoproteins ; Mesoderm/*metabolism ; Mice ; Motor Neurons/physiology ; Nerve Growth Factors/biosynthesis/*genetics ; Neurons, Afferent/physiology ; Neurotrophin 3 ; Organ Culture Techniques ; Proto-Oncogene Proteins/*physiology ; Signal Transduction ; Wnt Proteins ; Wnt4 Protein
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    New online tools for scholars: 3 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, F E -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577220" target="_blank"〉PubMed〈/a〉
    Keywords: Databases, Factual ; *Internet ; Medline ; National Library of Medicine (U.S.) ; *Online Systems ; *Periodicals as Topic ; *Publishing ; Signal Transduction ; United States
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    Regulation of myosin phosphatase by a specific interaction with cGMP- dependent protein kinase Ialpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Contraction and relaxation of smooth muscle are regulated by myosin light-chain kinase and myosin phosphatase through phosphorylation and dephosphorylation of myosin light chains. Cyclic guanosine monophosphate (cGMP)-dependent protein kinase Ialpha (cGKIalpha) mediates physiologic relaxation of vascular smooth muscle in response to nitric oxide and cGMP. It is shown here that cGKIalpha is targeted to the smooth muscle cell contractile apparatus by a leucine zipper interaction with the myosin-binding subunit (MBS) of myosin phosphatase. Uncoupling of the cGKIalpha-MBS interaction prevents cGMP-dependent dephosphorylation of myosin light chain, demonstrating that this interaction is essential to the regulation of vascular smooth muscle cell tone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surks, H K -- Mochizuki, N -- Kasai, Y -- Georgescu, S P -- Tang, K M -- Ito, M -- Lincoln, T M -- Mendelsohn, M E -- HL09330/HL/NHLBI NIH HHS/ -- HL55309/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1583-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Research Institute and Cardiology Division, Department of Medicine, Tufts University School of Medicine and New England Medical Center, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567269" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/genetics/*metabolism ; Histones/metabolism ; Humans ; Isoenzymes/chemistry/metabolism ; Leucine Zippers ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular/*enzymology/physiology ; Mutagenesis, Site-Directed ; Myosin Light Chains/*metabolism ; Myosin-Light-Chain Phosphatase ; Phosphoprotein Phosphatases/chemistry/*metabolism ; Phosphorylation ; Precipitin Tests ; Rats ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Transfection ; Two-Hybrid System Techniques
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    A symphony of bacterial voices (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 May 21;284(5418):1302-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383312" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/physiology ; Acylation ; Bacterial Infections/*microbiology ; Colony Count, Microbial ; Fungi/physiology ; Gene Expression Regulation, Bacterial ; Gram-Negative Bacteria/genetics/pathogenicity/*physiology ; Gram-Positive Bacteria/genetics/pathogenicity/*physiology ; Humans ; Luminescent Measurements ; Peptides/*physiology ; Plants/microbiology ; Signal Transduction ; Virulence
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    The role of CCR7 in TH1 and TH2 cell localization and delivery of B cell help in vivo (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Subsets of murine CD4+ T cells localize to different areas of the spleen after adoptive transfer. Naive and T helper 1 (TH1) cells, which express the chemokine receptor CCR7, are home to the periarteriolar lymphoid sheath, whereas activated TH2 cells, which lack CCR7, form rings at the periphery of the T cell zones near B cell follicles. Retroviral transduction of TH2 cells with CCR7 forces them to localize in a TH1-like pattern and inhibits their participation in B cell help in vivo but not in vitro. Thus, differential expression of chemokine receptors results in unique cellular migration patterns that are important for effective immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randolph, D A -- Huang, G -- Carruthers, C J -- Bromley, L E -- Chaplin, D D -- AI34580/AI/NIAID NIH HHS/ -- T32 GM07200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2159-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Allergy and Immunology, Department of Internal Medicine, Center for Immunology, Washington University School of Medicine. Howard Hughes Medical Institute, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591648" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/*immunology ; Calcium/metabolism ; Cell Movement ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, CCR7 ; Receptors, Chemokine/*immunology/metabolism ; Signal Transduction ; Spleen/*immunology ; Th1 Cells/*immunology/metabolism ; Th2 Cells/*immunology/metabolism ; Transfection
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    Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play a central role in neuronal degeneration. CD40 expression was increased on cultured microglia treated with freshly solublized amyloid-beta (Abeta, 500 nanomolar) and on microglia from a transgenic murine model of AD (Tg APPsw). Increased tumor necrosis factor alpha production and induction of neuronal injury occurred when Abeta-stimulated microglia were treated with CD40 ligand (CD40L). Microglia from Tg APPsw mice deficient for CD40L demonstrated reduction in activation, suggesting that the CD40-CD40L interaction is necessary for Abeta-induced microglial activation. Finally, abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J -- Town, T -- Paris, D -- Mori, T -- Suo, Z -- Crawford, F -- Mattson, M P -- Flavell, R A -- Mullan, M -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Roskamp Institute, University of South Florida, 3515 East Fletcher Avenue, Tampa, FL 33613, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600748" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Antigens, CD40/biosynthesis/*metabolism ; CD40 Ligand ; Cell Death ; Cells, Cultured ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Ligands ; Membrane Glycoproteins/*metabolism/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/immunology/*metabolism ; Neurons/cytology ; Peptide Fragments/pharmacology ; Phosphorylation ; Signal Transduction ; Tumor Necrosis Factor-alpha/biosynthesis/pharmacology ; tau Proteins/metabolism
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    Discovery of a small molecule insulin mimetic with antidiabetic activity in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Insulin elicits a spectrum of biological responses by binding to its cell surface receptor. In a screen for small molecules that activate the human insulin receptor tyrosine kinase, a nonpeptidyl fungal metabolite (L-783,281) was identified that acted as an insulin mimetic in several biochemical and cellular assays. The compound was selective for insulin receptor versus insulin-like growth factor I (IGFI) receptor and other receptor tyrosine kinases. Oral administration of L-783,281 to two mouse models of diabetes resulted in significant lowering in blood glucose levels. These results demonstrate the feasibility of discovering novel insulin receptor activators that may lead to new therapies for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, B -- Salituro, G -- Szalkowski, D -- Li, Z -- Zhang, Y -- Royo, I -- Vilella, D -- Diez, M T -- Pelaez, F -- Ruby, C -- Kendall, R L -- Mao, X -- Griffin, P -- Calaycay, J -- Zierath, J R -- Heck, J V -- Smith, R G -- Moller, D E -- New York, N.Y. -- Science. 1999 May 7;284(5416):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Endocrinology, Merck Research Laboratories, R80W250, Post Office Box 2000, Rahway, NJ 07065, USA. bei_zhang@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320380" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Ascomycota/*metabolism ; Binding Sites ; Blood Glucose/metabolism ; CHO Cells ; Cricetinae ; Diabetes Mellitus, Type 2/*drug therapy ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Enzyme Activation ; Glucose Tolerance Test ; Hyperglycemia/drug therapy ; Hypoglycemic Agents/chemistry/metabolism/*pharmacology/therapeutic use ; Indoles/chemistry/metabolism/*pharmacology/therapeutic use ; Insulin/blood/metabolism/*pharmacology ; Insulin Receptor Substrate Proteins ; Mice ; Mice, Mutant Strains ; Mice, Obese ; Molecular Mimicry ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Conformation/drug effects ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/chemistry/*metabolism ; Signal Transduction
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    Potential target found for antimetastasis drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Cloning, Molecular ; *Glucuronidase ; Glycoside Hydrolases/*antagonists & inhibitors/*genetics/isolation & ; purification/metabolism ; Humans ; Mice ; Neoplasm Metastasis/*prevention & control ; Rats ; Tumor Cells, Cultured
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    Mapping smells in the brain (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):508.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Diagnostic Imaging ; Light ; Mice ; *Odors ; Olfactory Bulb/*physiology ; Olfactory Receptor Neurons/physiology ; Rats ; Receptors, Odorant/*physiology ; Smell/*physiology
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    Two-metal-Ion catalysis in adenylyl cyclase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Adenylyl cyclase (AC) converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate, a ubiquitous second messenger that regulates many cellular functions. Recent structural studies have revealed much about the structure and function of mammalian AC but have not fully defined its active site or catalytic mechanism. Four crystal structures were determined of the catalytic domains of AC in complex with two different ATP analogs and various divalent metal ions. These structures provide a model for the enzyme-substrate complex and conclusively demonstrate that two metal ions bind in the active site. The similarity of the active site of AC to those of DNA polymerases suggests that the enzymes catalyze phosphoryl transfer by the same two-metal-ion mechanism and likely have evolved from a common ancestor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tesmer, J J -- Sunahara, R K -- Johnson, R A -- Gosselin, G -- Gilman, A G -- Sprang, S R -- DK38828/DK/NIDDK NIH HHS/ -- DK46371/DK/NIDDK NIH HHS/ -- GM34497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):756-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427002" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/chemistry/genetics/*metabolism ; Animals ; Aspartic Acid/metabolism ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Deoxyadenine Nucleotides/metabolism/pharmacology ; Dideoxynucleotides ; Dimerization ; Enzyme Inhibitors/metabolism ; Hydrogen Bonding ; Ligands ; Magnesium/*metabolism ; Manganese/*metabolism ; Models, Molecular ; Mutation ; Protein Conformation ; Protein Folding ; Rats ; Thionucleotides/metabolism/pharmacology ; Zinc/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Apoptosis can be triggered by members of the Bcl-2 protein family, such as Bim, that share only the BH3 domain with this family. Gene targeting in mice revealed important physiological roles for Bim. Lymphoid and myeloid cells accumulated, T cell development was perturbed, and most older mice accumulated plasma cells and succumbed to autoimmune kidney disease. Lymphocytes were refractory to apoptotic stimuli such as cytokine deprivation, calcium ion flux, and microtubule perturbation but not to others. Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouillet, P -- Metcalf, D -- Huang, D C -- Tarlinton, D M -- Kay, T W -- Kontgen, F -- Adams, J M -- Strasser, A -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Autoimmune Diseases/etiology ; *Autoimmunity ; B-Lymphocytes/physiology ; Carrier Proteins/*physiology ; Cells, Cultured ; Crosses, Genetic ; Female ; Gene Targeting ; Glomerulonephritis/etiology ; Hematopoietic Stem Cells/physiology ; Homeostasis ; Leukocyte Count ; Leukocytes/*physiology ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; T-Lymphocyte Subsets/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holash, J -- Maisonpierre, P C -- Compton, D -- Boland, P -- Alexander, C R -- Zagzag, D -- Yancopoulos, G D -- Wiegand, S J -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1994-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/blood supply/pathology ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/pathology ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/pathology/physiology ; Glioblastoma/blood supply/pathology ; Glioma/blood supply/pathology ; In Situ Hybridization ; Lymphokines/genetics/*physiology ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/pathology/physiology ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*pathology ; *Neovascularization, Pathologic ; Proteins/genetics/*physiology ; Rats ; Rats, Sprague-Dawley ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Initiation of mammalian liver development from endoderm by fibroblast growth factors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: The signaling molecules that elicit embryonic induction of the liver from the mammalian gut endoderm or induction of other gut-derived organs are unknown. Close proximity of cardiac mesoderm, which expresses fibroblast growth factors (FGFs) 1, 2, and 8, causes the foregut endoderm to develop into the liver. Treatment of isolated foregut endoderm from mouse embryos with FGF1 or FGF2, but not FGF8, was sufficient to replace cardiac mesoderm as an inducer of the liver gene expression program, the latter being the first step of hepatogenesis. The hepatogenic response was restricted to endoderm tissue, which selectively coexpresses FGF receptors 1 and 4. Further studies with FGFs and their specific inhibitors showed that FGF8 contributes to the morphogenetic outgrowth of the hepatic endoderm. Thus, different FGF signals appear to initiate distinct phases of liver development during mammalian organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jung, J -- Zheng, M -- Goldfarb, M -- Zaret, K S -- GM36477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1998-2003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Box G-J363, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culture Techniques ; Digestive System/embryology ; *Embryonic Induction ; Endoderm/metabolism/*physiology ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/genetics/pharmacology/physiology ; Fibroblast Growth Factor 8 ; Fibroblast Growth Factors/genetics/pharmacology/*physiology ; Gene Expression ; Heart/embryology ; Heparitin Sulfate/pharmacology ; Liver/*embryology/metabolism ; Mesoderm/metabolism ; Mice ; Mice, Inbred C3H ; Morphogenesis ; Organ Specificity ; Prealbumin/genetics ; Receptors, Fibroblast Growth Factor/physiology ; Recombinant Fusion Proteins ; Serum Albumin/genetics ; Signal Transduction ; alpha-Fetoproteins/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    New clues to how neurons strengthen their connections (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1755-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10391789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/physiology ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Glutamic Acid/*physiology ; Long-Term Potentiation/*physiology ; Mice ; Neurons/physiology ; Rats ; Receptors, AMPA/*physiology ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology
    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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    Odor response properties of rat olfactory receptor neurons (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-06-26
    Description: Molecular biology studies of olfaction have identified a multigene family of molecular receptors that are likely to be involved in odor transduction mechanisms. However, because previous functional data on peripheral coding were mainly collected from inferior vertebrates, it has been difficult to document the degree of specificity of odor interaction mechanisms. As a matter of fact, studies of the functional expression of olfactory receptors have not demonstrated the low or high specificity of olfactory receptors. In this study, the selectivity of olfactory receptor neurons was investigated in the rat at the cellular level under physiological conditions by unitary extracellular recordings. Individual olfactory receptor neurons were broadly responsive to qualitatively distinct odor compounds. We conclude that peripheral coding is based on activated arrays of olfactory receptor cells with overlapping tuning profiles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duchamp-Viret, P -- Chaput, M A -- Duchamp, A -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Neurosciences et Systemes Sensoriels, CNRS, UMR, Universite Claude Bernard, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne cedex, France. pduchamp@olfac.univ-lyon1.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381881" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones ; Action Potentials ; Animals ; Anisoles ; Benzaldehydes ; Camphor ; Cyclohexenes ; *Odors ; Olfactory Receptor Neurons/*physiology ; Pentanols ; Rats ; Rats, Wistar ; Receptors, Odorant/genetics/*physiology ; Terpenes
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    Role of the S. typhimurium actin-binding protein SipA in bacterial internalization (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Entry of the bacterium Salmonella typhimurium into host cells requires membrane ruffling and rearrangement of the actin cytoskeleton. Here, it is shown that the bacterial protein SipA plays a critical role in this process. SipA binds directly to actin, decreases its critical concentration, and inhibits depolymerization of actin filaments. These activities result in the spatial localization and more pronounced outward extension of the Salmonella-induced membrane ruffles, thereby facilitating bacterial uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, D -- Mooseker, M S -- Galan, J E -- AI30492/AI/NIAID NIH HHS/ -- DK25387/DK/NIDDK NIH HHS/ -- GM52543/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2092-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale School of Medicine, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092234" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/genetics/*metabolism ; Antigens, Bacterial/metabolism ; Bacterial Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Biopolymers ; Cell Membrane/ultrastructure ; HeLa Cells ; Humans ; *Microfilament Proteins ; Microscopy, Fluorescence ; Mutation ; Recombinant Fusion Proteins/metabolism ; Salmonella typhimurium/genetics/metabolism/*pathogenicity ; Signal Transduction ; Vinculin/metabolism
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    IkappaB kinases: kinsmen with different crafts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉May, M J -- Ghosh, S -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):271-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232975" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/enzymology/genetics ; Animals ; Bone Development ; DNA-Binding Proteins/metabolism ; Dimerization ; *Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Mice ; Morphogenesis ; NF-kappa B/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Signal Transduction ; Skin/embryology ; Tumor Necrosis Factor-alpha/pharmacology
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    Dual function of the selenoprotein PHGPx during sperm maturation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: The selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) changes its physical characteristics and biological functions during sperm maturation. PHGPx exists as a soluble peroxidase in spermatids but persists in mature spermatozoa as an enzymatically inactive, oxidatively cross-linked, insoluble protein. In the midpiece of mature spermatozoa, PHGPx protein represents at least 50 percent of the capsule material that embeds the helix of mitochondria. The role of PHGPx as a structural protein may explain the mechanical instability of the mitochondrial midpiece that is observed in selenium deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ursini, F -- Heim, S -- Kiess, M -- Maiorino, M -- Roveri, A -- Wissing, J -- Flohe, L -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1393-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartmento di Chimica Biologica, Universita di Padova, Viale G. Colombo 3, I-35121 Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophoresis, Gel, Two-Dimensional ; Electrophoresis, Polyacrylamide Gel ; Glutathione Peroxidase/chemistry/isolation & purification/*physiology ; Infertility, Male/metabolism ; Male ; Mitochondria/chemistry/enzymology ; Oxidation-Reduction ; Proteins/chemistry/isolation & purification/*physiology ; Rats ; Rats, Wistar ; Selenium/deficiency/*physiology ; Selenoproteins ; Solubility ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Spermatids/chemistry/enzymology ; *Spermatogenesis ; Spermatozoa/chemistry/enzymology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Extracellular signals often result in simultaneous activation of both the Raf-MEK-ERK and PI3K-Akt pathways (where ERK is extracellular-regulated kinase, MEK is mitogen-activated protein kinase or ERK kinase, and PI3K is phosphatidylinositol 3-kinase). However, these two signaling pathways were shown to exert opposing effects on muscle cell hypertrophy. Furthermore, the PI3K-Akt pathway was shown to inhibit the Raf-MEK-ERK pathway; this cross-regulation depended on the differentiation state of the cell: Akt activation inhibited the Raf-MEK-ERK pathway in differentiated myotubes, but not in their myoblast precursors. The stage-specific inhibitory action of Akt correlated with its stage-specific ability to form a complex with Raf, suggesting the existence of differentially expressed mediators of an inhibitory Akt-Raf complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rommel, C -- Clarke, B A -- Zimmermann, S -- Nunez, L -- Rossman, R -- Reid, K -- Moelling, K -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Signaling System/drug effects ; Mice ; Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism ; Muscle, Skeletal/*cytology/*metabolism ; Myogenin/genetics ; Phenotype ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-raf/*antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection ; Transgenes
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    Activation tagging of the floral inducer FT (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-12-03
    Description: FLOWERING LOCUS T (FT), which acts in parallel with the meristem-identity gene LEAFY (LFY) to induce flowering of Arabidopsis, was isolated by activation tagging. Like LFY, FT acts partially downstream of CONSTANS (CO), which promotes flowering in response to long days. Unlike many other floral regulators, the deduced sequence of the FT protein does not suggest that it directly controls transcription or transcript processing. Instead, it is similar to the sequence of TERMINAL FLOWER 1 (TFL1), an inhibitor of flowering that also shares sequence similarity with membrane-associated mammalian proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kardailsky, I -- Shukla, V K -- Ahn, J H -- Dagenais, N -- Christensen, S K -- Nguyen, J T -- Chory, J -- Harrison, M J -- Weigel, D -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1962-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583961" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/*genetics/*growth & development ; *Arabidopsis Proteins ; DNA-Binding Proteins/chemistry/*genetics/*physiology ; Gene Expression Regulation, Plant ; Genes, Plant ; Genetic Complementation Test ; MADS Domain Proteins ; Meristem/growth & development/metabolism ; Mutation ; Phenotype ; Plant Proteins/*genetics/physiology ; Plant Structures/growth & development ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; Signal Transduction ; Transcription Factors/chemistry/*genetics/*physiology
    Print ISSN: 0036-8075
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    UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Modification of cell surface molecules with sialic acid is crucial for their function in many biological processes, including cell adhesion and signal transduction. Uridine diphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase) is an enzyme that catalyzes an early, rate-limiting step in the sialic acid biosynthetic pathway. UDP-GlcNAc 2-epimerase was found to be a major determinant of cell surface sialylation in human hematopoietic cell lines and a critical regulator of the function of specific cell surface adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keppler, O T -- Hinderlich, S -- Langner, J -- Schwartz-Albiez, R -- Reutter, W -- Pawlita, M -- New York, N.Y. -- Science. 1999 May 21;284(5418):1372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Tumor Virology Program, Tumor Immunology Program, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, CD14/biosynthesis ; Antigens, CD15/biosynthesis ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Carbohydrate Epimerases/genetics/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Culture Media ; *Escherichia coli Proteins ; Glycoconjugates/*metabolism ; HL-60 Cells ; Histocompatibility Antigens Class I/biosynthesis ; Humans ; Lectins/metabolism ; Oligosaccharides/biosynthesis ; Rats ; Sialic Acid Binding Ig-like Lectin 2 ; Sialic Acids/*biosynthesis ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    A nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Many human diseases are associated with the overproduction of oxygen free radicals that inflict cell damage. A manganese(II) complex with a bis(cyclohexylpyridine)-substituted macrocyclic ligand (M40403) was designed to be a functional mimic of the superoxide dismutase (SOD) enzymes that normally remove these radicals. M40403 had high catalytic SOD activity and was chemically and biologically stable in vivo. Injection of M40403 into rat models of inflammation and ischemia-reperfusion injury protected the animals against tissue damage. Such mimics may result in better clinical therapies for diseases mediated by superoxide radicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salvemini, D -- Wang, Z Q -- Zweier, J L -- Samouilov, A -- Macarthur, H -- Misko, T P -- Currie, M G -- Cuzzocrea, S -- Sikorski, J A -- Riley, D P -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MetaPhore Pharmaceuticals, 1910 Innerbelt Business Center Drive, St. Louis, MO 63114, USA. dsalvemini@metaphore.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/metabolism/*therapeutic use ; Cytoprotection ; Dinoprostone/metabolism ; Dose-Response Relationship, Drug ; Drug Design ; Drug Stability ; Inflammation/*drug therapy ; Interleukin-1/metabolism ; L-Lactate Dehydrogenase/metabolism ; Male ; Manganese ; Molecular Mimicry ; Neutrophils/drug effects ; Organometallic Compounds/chemical synthesis/chemistry/metabolism/*toxicity ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/*drug therapy ; Splanchnic Circulation ; *Superoxide Dismutase/metabolism ; Superoxides/*metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/metabolism
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    Cholesterol-lowering drugs may boost bones (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticholesteremic Agents/*pharmacology ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis ; Clinical Trials as Topic ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology ; Lovastatin/*pharmacology ; Mice ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Rats ; Simvastatin/pharmacology ; *Transforming Growth Factor beta
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    Many of modes of transport for an embryo's signals (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1003, 1005.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10475837" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Biological Transport ; Body Patterning ; Cytoskeletal Proteins/metabolism ; Diffusion ; Embryo, Nonmammalian/*metabolism/ultrastructure ; Embryonic Development ; Insect Proteins/metabolism ; Microtubules/*metabolism ; Phosphoproteins/metabolism ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; *Trans-Activators ; Wings, Animal/embryology/metabolism ; beta Catenin
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    The vomeronasal organ (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: The vomeronasal organ (VNO) is a chemoreceptor organ enclosed in a cartilaginous capsule and separated from the main olfactory epithelium. The vomeronasal neurons have two distinct types of receptor that differ from each other and from the large family of odorant receptors. The VNO receptors are seven-transmembrane receptors coupled to GTP-binding protein, but appear to activate inositol 1,4,5-trisphosphate signaling as opposed to cyclic adenosine monophosphate. The nature of stimulus access suggests that the VNO responds to nonvolatile cues, leading to activation of the hypothalamus by way of the accessory olfactory bulb and amygdala. The areas of hypothalamus innervated regulate reproductive, defensive, and ingestive behavior as well as neuroendocrine secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keverne, E B -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):716-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sub-Department of Animal Behaviour, University of Cambridge, Madingley, Cambridge CB3 8AA, UK. ebk10@cus.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531049" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Afferent Pathways ; Animals ; Behavior, Animal ; Chemoreceptor Cells/chemistry/*physiology ; Female ; GTP-Binding Proteins/metabolism ; Humans ; Hypothalamus/physiology ; Male ; Neurons, Afferent/*physiology ; Olfactory Bulb/physiology ; Pheromones/physiology ; Receptors, Cell Surface/chemistry/genetics/*physiology ; Signal Transduction ; Vomeronasal Organ/anatomy & histology/innervation/*physiology
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    A pair of related genes with antagonistic roles in mediating flowering signals (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Flowering in Arabidopsis is promoted via several interacting pathways. A photoperiod-dependent pathway relays signals from photoreceptors to a transcription factor gene, CONSTANS (CO), which activates downstream meristem identity genes such as LEAFY (LFY). FT, together with LFY, promotes flowering and is positively regulated by CO. Loss of FT causes delay in flowering, whereas overexpression of FT results in precocious flowering independent of CO or photoperiod. FT acts in part downstream of CO and mediates signals for flowering in an antagonistic manner with its homologous gene, TERMINAL FLOWER1 (TFL1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Y -- Kaya, H -- Goto, K -- Iwabuchi, M -- Araki, T -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1960-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583960" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/*genetics/*growth & development ; *Arabidopsis Proteins ; DNA-Binding Proteins/chemistry/*genetics/physiology ; *Gene Expression Regulation, Plant ; Genes, Plant ; MADS Domain Proteins ; Molecular Sequence Data ; Phenotype ; Photoperiod ; Plant Proteins/chemistry/*genetics/physiology ; Plant Structures/growth & development ; Plants, Genetically Modified ; Signal Transduction ; Transcription Factors/chemistry/*genetics/physiology ; Up-Regulation
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    Modulation of respiratory frequency by peptidergic input to rhythmogenic neurons in the preBotzinger complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Neurokinin-1 receptor (NK1R) and mu-opioid receptor (muOR) agonists affected respiratory rhythm when injected directly into the preBotzinger Complex (preBotC), the hypothesized site for respiratory rhythmogenesis in mammals. These effects were mediated by actions on preBotC rhythmogenic neurons. The distribution of NK1R+ neurons anatomically defined the preBotC. Type 1 neurons in the preBotC, which have rhythmogenic properties, expressed both NK1Rs and muORs, whereas type 2 neurons expressed only NK1Rs. These findings suggest that the preBotC is a definable anatomic structure with unique physiological function and that a subpopulation of neurons expressing both NK1Rs and muORs generate respiratory rhythm and modulate respiratory frequency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" 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/PMC2811082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, P A -- Rekling, J C -- Bocchiaro, C M -- Feldman, J L -- HL37941/HL/NHLBI NIH HHS/ -- HL40959/HL/NHLBI NIH HHS/ -- R01 HL040959/HL/NHLBI NIH HHS/ -- R01 HL040959-12/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of California Los Angeles, Box 951763, Los Angeles, CA 90095-1763, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Female ; In Vitro Techniques ; Medulla Oblongata/cytology/drug effects/*physiology ; Mice ; Mice, Inbred BALB C ; Neurons/chemistry/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/analysis/physiology ; Receptors, Neurokinin-1/agonists/analysis/*physiology ; Receptors, Opioid, mu/agonists/analysis/*physiology ; Respiratory Mechanics/drug effects/*physiology ; Substance P/pharmacology ; Synaptic Transmission/drug effects
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    Two distinct cytokines released from a human aminoacyl-tRNA synthetase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Aminoacyl-tRNA synthetases catalyze aminoacylation of transfer RNAs (tRNAs). It is shown that human tyrosyl-tRNA synthetase can be split into two fragments with distinct cytokine activities. The endothelial monocyte-activating polypeptide II-like carboxy-terminal domain has potent leukocyte and monocyte chemotaxis activity and stimulates production of myeloperoxidase, tumor necrosis factor-alpha, and tissue factor. The catalytic amino-terminal domain binds to the interleukin-8 type A receptor and functions as an interleukin-8-like cytokine. Under apoptotic conditions in cell culture, the full-length enzyme is secreted, and the two cytokine activities can be generated by leukocyte elastase, an extracellular protease. Secretion of this tRNA synthetase may contribute to apoptosis both by arresting translation and producing needed cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakasugi, K -- Schimmel, P -- GM23562/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):147-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology, The Scripps Research Institute, Beckman Center, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102815" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD/metabolism ; Apoptosis ; Binding, Competitive ; Catalytic Domain ; Chemotaxis, Leukocyte ; *Cytokines ; Humans ; Interleukin-8/*metabolism/pharmacology ; Leukocyte Elastase/metabolism ; Molecular Sequence Data ; Monocytes/physiology ; Neoplasm Proteins/*metabolism/pharmacology ; Neutrophils/metabolism/physiology ; RNA-Binding Proteins/*metabolism/pharmacology ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-8A ; Recombinant Proteins/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine-tRNA Ligase/chemistry/*metabolism/pharmacology
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    Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H G -- Pathan, N -- Ethell, I M -- Krajewski, S -- Yamaguchi, Y -- Shibasaki, F -- McKeon, F -- Bobo, T -- Franke, T F -- Reed, J C -- AG-1593/AG/NIA NIH HHS/ -- CA-69381/CA/NCI NIH HHS/ -- HD25938/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195903" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; *Apoptosis ; Calcineurin/genetics/*metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism/pharmacology ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Dimerization ; Enzyme Inhibitors/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology ; Humans ; Mitochondria/metabolism ; Neurons/cytology/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Transfection ; *Tyrosine 3-Monooxygenase ; bcl-Associated Death Protein ; bcl-X Protein
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    Stimulation of bone formation in vitro and in rodents by statins (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-12-03
    Description: Osteoporosis and other diseases of bone loss are a major public health problem. Here it is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents. This effect was associated with increased expression of the bone morphogenetic protein-2 (BMP-2) gene in bone cells. Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats. Thus, in appropriate doses, statins may have therapeutic applications for the treatment of osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mundy, G -- Garrett, R -- Harris, S -- Chan, J -- Chen, D -- Rossini, G -- Boyce, B -- Zhao, M -- Gutierrez, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉OsteoScreen, 2040 Babcock Road, San Antonio, TX 78229, USA. mundy@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis/genetics/pharmacology ; Cell Line ; Female ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/*pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Organ Culture Techniques ; Osteoblasts/*drug effects/metabolism ; Osteoclasts/drug effects ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Promoter Regions, Genetic/drug effects ; Rats ; Recombinant Proteins/pharmacology ; Simvastatin/*pharmacology ; Skull ; Transfection ; *Transforming Growth Factor beta
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    Olfactory reception in invertebrates (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Recent progress in understanding the principles and mechanisms in olfaction is the result of multidisciplinary research efforts that explored chemosensation by using a variety of model organisms. Studies on invertebrates, notably nematodes, insects, and crustaceans, to which diverse experimental approaches can be applied, have greatly helped elucidate various aspects of olfactory signaling. From the converging results of genetic, molecular, and physiological studies, a common set of chemosensory mechanisms emerges. Recognition and discrimination of odorants as well as chemo-electrical transduction and processing of olfactory signals appear to be mediated by fundamentally similar mechanisms in phylogenetically diverse animals. The common challenge of organisms to decipher the world of odors was apparently met by a phylogenetically conserved strategy. Thus, comparative studies should continue to provide important contributions toward an understanding of the sense of smell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krieger, J -- Breer, H -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):720-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Stuttgart-Hohenheim, Institute of Physiology, Garbenstrasse 30, 70599 Stuttgart, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531050" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; GTP-Binding Proteins/metabolism ; Invertebrates/anatomy & histology/*physiology ; Ion Channels/physiology ; Membrane Proteins/chemistry/genetics/physiology ; Odors ; Olfactory Receptor Neurons/*physiology ; Receptors, Odorant/chemistry/genetics/metabolism/*physiology ; Second Messenger Systems ; Signal Transduction ; Smell/*physiology
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    The presenilins in Alzheimer's disease--proteolysis holds the key (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Alzheimer's disease (AD) research has shown that patients with an inherited form of the disease carry mutations in the presenilin proteins or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (the primary component of the amyloid deposits found in AD brains). However, it is not clear how the presenilins contribute to this increase. New findings now show that the presenilins affect APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is known that the presenilins are involved in the cleavage of the Notch receptor, hinting that they either directly regulate gamma-secretase activity or themselves are protease enzymes. These findings suggest that the presenilins may prove to be valuable molecular targets for the development of drugs to combat AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haass, C -- De Strooper, B -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Adolf-Butenandt-Institute, Department of Biochemistry, Ludwig-Maximilians University Munich, Germany. chaass@pbm.med.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10542139" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/enzymology/*metabolism ; Amyloid Precursor Protein Secretases ; Amyloid beta-Protein Precursor/*metabolism ; Animals ; Aspartic Acid Endopeptidases ; Endopeptidases/*metabolism ; Humans ; Membrane Proteins/*metabolism ; Protease Inhibitors/therapeutic use ; Protein Processing, Post-Translational ; Receptors, Notch ; Signal Transduction
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    Role of heteromer formation in GABAB receptor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
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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)
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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    STAT5 interaction with the T cell receptor complex and stimulation of T cell proliferation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: The role of STAT (signal transducer and activator of transcription) proteins in T cell receptor (TCR) signaling was analyzed. STAT5 became immediately and transiently phosphorylated on tyrosine 694 in response to TCR stimulation. Expression of the protein tyrosine kinase Lck, a key signaling protein in the TCR complex, activated DNA binding of transfected STAT5A and STAT5B to specific STAT inducible elements. The role of Lck in STAT5 activation was confirmed in a Lck-deficient T cell line in which the activation of STAT5 by TCR stimulation was abolished. Expression of Lck induced specific interaction of STAT5 with the subunits of the TCR, indicating that STAT5 may be directly involved in TCR signaling. Stimulation of T cell clones and primary T cell lines also induced the association of STAT5 with the TCR complex. Inhibition of STAT5 function by expression of a dominant negative mutant STAT5 reduced antigen-stimulated proliferation of T cells. Thus, TCR stimulation appears to directly activate STAT5, which may participate in the regulation of gene transcription and T cell proliferation during immunological responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welte, T -- Leitenberg, D -- Dittel, B N -- al-Ramadi, B K -- Xie, B -- Chin, Y E -- Janeway, C A Jr -- Bothwell, A L -- Bottomly, K -- Fu, X Y -- AI34522/AI/NIAID NIH HHS/ -- GM46367/GM/NIGMS NIH HHS/ -- GM55590/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):222-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigen-Presenting Cells/immunology ; Antigens/immunology ; Cell Division ; Cell Line ; DNA-Binding Proteins/genetics/*metabolism ; Interferon-gamma/pharmacology ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/genetics/immunology/metabolism ; Mice ; Mice, Transgenic ; *Milk Proteins ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Antigen, T-Cell/genetics/immunology/*metabolism ; STAT5 Transcription Factor ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology/metabolism ; Th2 Cells/immunology/metabolism ; Trans-Activators/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 79
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    Probing alcoholism's 'dark side' (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1473.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498528" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/cerebrospinal fluid/*metabolism ; Animals ; Brain/*metabolism ; Corticotropin-Releasing Hormone/cerebrospinal fluid/*metabolism ; Dopamine/metabolism ; Humans ; Rats ; Substance Withdrawal Syndrome/metabolism/prevention & control
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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    Meeting. American Chemical Society. Raising a glass to health and nanotubes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2053, 2055.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523196" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/*metabolism ; Animals ; Carbon ; Electronics ; Ethanol/metabolism ; Glucose/chemistry/metabolism ; Glycosylation End Products, Advanced/*metabolism ; Hemoglobin A, Glycosylated/chemistry ; Humans ; Rats
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  • 81
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    Long-term depression in hippocampal interneurons: joint requirement for pre- and postsynaptic events (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: Long-term depression (LTD) is a well-known form of synaptic plasticity of principal neurons in the mammalian brain. Whether such changes occur in interneurons is still controversial. CA3 hippocampal interneurons expressing Ca2+-permeable AMPA receptors exhibited LTD after tetanic stimulation of CA3 excitatory inputs. LTD was independent of NMDA receptors and required both Ca2+ influx through postsynaptic AMPA receptors and activation of presynaptic mGluR7-like receptors. These results point to the capability of interneurons to undergo plastic changes of synaptic strength through joint activation of pre- and postsynaptic glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laezza, F -- Doherty, J J -- Dingledine, R -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1411-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/*physiology ; Male ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/drug effects/*metabolism ; Receptors, Metabotropic Glutamate/drug effects/*metabolism ; Synapses/*physiology ; Synaptic Transmission ; Tetany
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  • 82
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    Modulation of brain reward circuitry by leptin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Leptin, a hormone secreted by fat cells, suppresses food intake and promotes weight loss. To assess the action of this hormone on brain reward circuitry, changes in the rewarding effect of lateral hypothalamic stimulation were measured after leptin administration. At five stimulation sites near the fornix, the effectiveness of the rewarding electrical stimulation was enhanced by chronic food restriction and attenuated by intracerebroventricular infusion of leptin. In contrast, the rewarding effect of stimulating neighboring sites was insensitive to chronic food restriction and was enhanced by leptin in three of four cases. These opposing effects of leptin may mirror complementary changes in the rewarding effects of feeding and of competing behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fulton, S -- Woodside, B -- Shizgal, P -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Studies in Behavioural Neurobiology, Concordia University, Montreal, QC, H3G 1M8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Energy Metabolism ; Feeding Behavior ; Food Deprivation/*physiology ; Hypothalamic Area, Lateral/drug effects/*physiology ; Injections, Intraventricular ; Leptin/administration & dosage/*pharmacology ; Male ; Neurons/physiology ; Neuropeptides/physiology ; Rats ; Rats, Long-Evans ; Recombinant Proteins/administration & dosage/pharmacology ; *Reward ; Self Stimulation/physiology ; Time Factors
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  • 83
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    Regulation of NMDA receptors by an associated phosphatase-kinase signaling complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Regulation of N-methyl-D-aspartate (NMDA) receptor activity by kinases and phosphatases contributes to the modulation of synaptic transmission. Targeting of these enzymes near the substrate is proposed to enhance phosphorylation-dependent modulation. Yotiao, an NMDA receptor-associated protein, bound the type I protein phosphatase (PP1) and the adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (PKA) holoenzyme. Anchored PP1 was active, limiting channel activity, whereas PKA activation overcame constitutive PP1 activity and conferred rapid enhancement of NMDA receptor currents. Hence, yotiao is a scaffold protein that physically attaches PP1 and PKA to NMDA receptors to regulate channel activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westphal, R S -- Tavalin, S J -- Lin, J W -- Alto, N M -- Fraser, I D -- Langeberg, L K -- Sheng, M -- Scott, J D -- F32 NS010202/NS/NINDS NIH HHS/ -- GM 48231/GM/NIGMS NIH HHS/ -- NS10202/NS/NINDS NIH HHS/ -- NS10543/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):93-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Vollum Institute, Oregon Health Sciences University, 3181 S.W. Sam Jackson Road, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390370" target="_blank"〉PubMed〈/a〉
    Keywords: A Kinase Anchor Proteins ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; Cyclic AMP/analogs & derivatives/pharmacology ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Cytoskeletal Proteins/*metabolism ; Enzyme Inhibitors/pharmacology ; Holoenzymes/metabolism ; Humans ; Molecular Sequence Data ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thionucleotides/pharmacology ; Transfection
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  • 84
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    American Chemical Society. Chemists mix it up in California (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):243-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biocompatible Materials ; *Biomedical Engineering ; Brain/*drug effects/metabolism ; Caffeine/administration & dosage/adverse effects/*pharmacology ; Catalysis ; Genetic Engineering ; Genetic Therapy/*methods ; Humans ; Polycarboxylate Cement/chemical synthesis ; Polymers/chemical synthesis ; Rats ; Substance-Related Disorders/*etiology
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  • 85
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    Dancing the immunological two-step (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malissen, B -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie INSERM-CNRS de Marseille-Luminy, Marseille, France. bernardm@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD/metabolism ; Antigens, CD80/metabolism ; Histocompatibility Antigens/*metabolism ; Histocompatibility Antigens Class I/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Models, Immunological ; Peptides/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Time Factors
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  • 86
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    Enhanced cortical dopamine output and antipsychotic-like effects of raclopride by alpha2 adrenoceptor blockade (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Clozapine exerts superior clinical efficacy and markedly enhances cortical dopamine output compared with classical antipsychotic drugs. Here the alpha2 adrenoceptor antagonist idazoxan was administered to rats alone or in combination with the D2/3 dopamine receptor antagonist raclopride. Dopamine efflux in the medial prefrontal cortex and conditioned avoidance responding were analyzed. Idazoxan selectively potentiated the cortical output of dopamine and augmented the suppression of conditioned avoidance responding induced by raclopride. These results challenge basic assumptions underlying the dopamine hypothesis of schizophrenia and provide insight into clozapine's mode of action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hertel, P -- Fagerquist, M V -- Svensson, T H -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):105-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, Section of Neuropsychopharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506554" target="_blank"〉PubMed〈/a〉
    Keywords: *Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Antipsychotic Agents/*pharmacology ; Avoidance Learning/drug effects ; Catalepsy/chemically induced ; Conditioning (Psychology) ; Corpus Striatum/drug effects/metabolism ; Dopamine/*metabolism ; Dopamine Antagonists/*pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Idazoxan/*pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Prefrontal Cortex/*drug effects/metabolism ; Raclopride ; Rats ; Receptors, Adrenergic, alpha-2/metabolism ; Salicylamides/*pharmacology ; Schizophrenia/drug therapy/metabolism
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  • 87
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    Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, S -- Groh, V -- Wu, J -- Steinle, A -- Phillips, J H -- Lanier, L L -- Spies, T -- P01 CA18221/CA/NCI NIH HHS/ -- R01 AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):727-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426993" target="_blank"〉PubMed〈/a〉
    Keywords: Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology/metabolism ; Humans ; Jurkat Cells ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Lymphocyte Subsets/immunology ; Membrane Proteins/metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Immunologic/chemistry/genetics/*immunology/metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; Tumor Cells, Cultured
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  • 88
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    Neuronal activity-dependent cell survival mediated by transcription factor MEF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: During mammalian development, electrical activity promotes the calcium-dependent survival of neurons that have made appropriate synaptic connections. However, the mechanisms by which calcium mediates neuronal survival during development are not well characterized. A transcription-dependent mechanism was identified by which calcium influx into neurons promoted cell survival. The transcription factor MEF2 was selectively expressed in newly generated postmitotic neurons and was required for the survival of these neurons. Calcium influx into cerebellar granule neurons led to activation of p38 mitogen-activated protein kinase-dependent phosphorylation and activation of MEF2. Once activated, MEF2 regulated neuronal survival by stimulating MEF2-dependent gene transcription. These findings demonstrate that MEF2 is a calcium-regulated transcription factor and define a function for MEF2 during nervous system development that is distinct from previously well-characterized functions of MEF2 during muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Z -- Bonni, A -- Xia, F -- Nadal-Vicens, M -- Greenberg, M E -- 5T32NS07112/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):785-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Department of Neurology, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/embryology/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dimerization ; Immunohistochemistry ; MEF2 Transcription Factors ; Mitogen-Activated Protein Kinases/metabolism ; Mitosis ; Mutation ; Myogenic Regulatory Factors ; Neurons/*cytology/*metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; p38 Mitogen-Activated Protein Kinases
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  • 89
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    Unexpected modes of PDZ domain scaffolding revealed by structure of nNOS-syntrophin complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: The PDZ protein interaction domain of neuronal nitric oxide synthase (nNOS) can heterodimerize with the PDZ domains of postsynaptic density protein 95 and syntrophin through interactions that are not mediated by recognition of a typical carboxyl-terminal motif. The nNOS-syntrophin PDZ complex structure revealed that the domains interact in an unusual linear head-to-tail arrangement. The nNOS PDZ domain has two opposite interaction surfaces-one face has the canonical peptide binding groove, whereas the other has a beta-hairpin "finger." This nNOS beta finger docks in the syntrophin peptide binding groove, mimicking a peptide ligand, except that a sharp beta turn replaces the normally required carboxyl terminus. This structure explains how PDZ domains can participate in diverse interaction modes to assemble protein networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hillier, B J -- Christopherson, K S -- Prehoda, K E -- Bredt, D S -- Lim, W A -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221915" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Crystallography, X-Ray ; Dimerization ; *Dystrophin-Associated Proteins ; Ligands ; Membrane Proteins/*chemistry/metabolism ; Molecular Sequence Data ; Muscle Proteins/*chemistry/metabolism ; Nitric Oxide Synthase/*chemistry/metabolism ; Nitric Oxide Synthase Type I ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Signal Transduction
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    Preliminary data touch off genetic food fight (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1094-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Crops, Agricultural/*adverse effects ; Digestive System/pathology ; Food Technology ; Great Britain ; *Growth ; *Immunity ; Infection/pathology ; Lectins/genetics ; Plant Lectins ; Plants, Genetically Modified/*adverse effects ; Rats ; Solanum tuberosum/adverse effects/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    Dracula's wish (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1999 May 21;284(5418):1294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticoagulants/*chemical synthesis/chemistry/pharmacology ; Antithrombins/metabolism ; Bleeding Time ; Heparin/chemistry/metabolism/*pharmacology ; Humans ; Molecular Mimicry ; Platelet Activation/drug effects ; Polysaccharides/*chemical synthesis/chemistry/pharmacology ; Rats ; Thrombin/*antagonists & inhibitors/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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  • 92
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    Bone marrow as a potential source of hepatic oval cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Bone marrow stem cells develop into hematopoietic and mesenchymal lineages but have not been known to participate in production of hepatocytes, biliary cells, or oval cells during liver regeneration. Cross-sex or cross-strain bone marrow and whole liver transplantation were used to trace the origin of the repopulating liver cells. Transplanted rats were treated with 2-acetylaminofluorene, to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation. Markers for Y chromosome, dipeptidyl peptidase IV enzyme, and L21-6 antigen were used to identify liver cells of bone marrow origin. From these cells, a proportion of the regenerated hepatic cells were shown to be donor-derived. Thus, a stem cell associated with the bone marrow has epithelial cell lineage capability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, B E -- Bowen, W C -- Patrene, K D -- Mars, W M -- Sullivan, A K -- Murase, N -- Boggs, S S -- Greenberger, J S -- Goff, J P -- New York, N.Y. -- Science. 1999 May 14;284(5417):1168-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA. bryon+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325227" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/pharmacology ; Animals ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carbon Tetrachloride/pharmacology ; Cell Differentiation ; Cell Division ; DNA-Binding Proteins/genetics ; Dipeptidyl Peptidase 4/metabolism ; Epithelial Cells/cytology ; Female ; Hematopoietic Stem Cells/cytology ; In Situ Hybridization ; Liver/*cytology/drug effects/physiology ; *Liver Regeneration ; Liver Transplantation ; Male ; *Nuclear Proteins ; Polymerase Chain Reaction ; Rats ; Rats, Inbred F344 ; Rats, Inbred Lew ; Sex-Determining Region Y Protein ; Stem Cells/*cytology ; *Transcription Factors ; Y Chromosome
    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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  • 93
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    Redefining rats, mice, and birds. AAA (American Association of Anatomists) Public Affairs Committee (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besharse, J C -- Carlson, B M -- Jenkins, D P -- Lester, D S -- Olds, J L -- Satir, P -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10215528" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Rights/*legislation & jurisprudence ; Animal Welfare/*legislation & jurisprudence ; Animals ; *Animals, Laboratory ; Birds ; Mice ; Rats ; Research ; Societies, Scientific ; United States ; United States Department of Agriculture/legislation & jurisprudence
    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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  • 94
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    Xid-like immunodeficiency in mice with disruption of the p85alpha subunit of phosphoinositide 3-kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Mice with a targeted gene disruption of p85alpha, a regulatory subunit of phosphoinositide 3-kinase, had impaired B cell development at the pro-B cell stage, reduced numbers of mature B cells and peritoneal CD5+ Ly-1 B cells, reduced B cell proliferative responses, and no T cell-independent antibody production. These phenotypes are nearly identical to those of Btk-/- or xid (X-linked immunodeficiency) mice. These results provide evidence that p85alpha is functionally linked to the Btk pathway in antigen receptor-mediated signal transduction and is pivotal in B cell development and functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, H -- Terauchi, Y -- Fujiwara, M -- Aizawa, S -- Yazaki, Y -- Kadowaki, T -- Koyasu, S -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):390-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Antigens, CD5/analysis ; Antigens, Ly/analysis ; Antigens, T-Independent/immunology ; B-Lymphocyte Subsets/cytology/immunology ; B-Lymphocytes/cytology/*immunology ; Bone Marrow/immunology ; Cell Survival ; Gene Targeting ; Genetic Linkage ; Immunologic Deficiency Syndromes/*enzymology/genetics/immunology ; Lymphocyte Count ; Lymphoid Tissue/immunology ; Mice ; Mutation ; Phenotype ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; X Chromosome
    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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  • 95
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    Turning thoughts into actions (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):888-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Computer Systems ; Cybernetics ; Electrodes, Implanted ; Electroencephalography ; Female ; Humans ; Male ; Models, Neurological ; Motivation ; Motor Cortex/physiology ; Paralysis/*rehabilitation ; Prostheses and Implants ; Psychomotor Performance/*physiology ; Rats ; *Robotics
    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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  • 96
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    Learning visualised, on the double (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1661.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology/*ultrastructure ; Calcium/metabolism ; Image Processing, Computer-Assisted ; In Vitro Techniques ; Learning/*physiology ; *Long-Term Potentiation ; Microscopy, Electron ; Rats ; Synapses/*ultrastructure ; Synaptic Transmission
    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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  • 97
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    Processing of the notch ligand delta by the metalloprotease Kuzbanian (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Signaling by the Notch surface receptor controls cell fate determination in a broad spectrum of tissues. This signaling is triggered by the interaction of the Notch protein with what, so far, have been thought to be transmembrane ligands expressed on adjacent cells. Here biochemical and genetic analyses show that the ligand Delta is cleaved on the surface, releasing an extracellular fragment capable of binding to Notch and acting as an agonist of Notch activity. The ADAM disintegrin metalloprotease Kuzbanian is required for this processing event. These observations raise the possibility that Notch signaling in vivo is modulated by soluble forms of the Notch ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qi, H -- Rand, M D -- Wu, X -- Sestan, N -- Wang, W -- Rakic, P -- Xu, T -- Artavanis-Tsakonas, S -- NS14841/NS/NINDS NIH HHS/ -- NS26084/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):91-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536-0812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872749" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Disintegrins/genetics/*metabolism ; Drosophila/embryology/genetics/metabolism ; *Drosophila Proteins ; Female ; Intracellular Signaling Peptides and Proteins ; Ligands ; Male ; Membrane Proteins/genetics/*metabolism ; Metalloendopeptidases/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Neurons/cytology ; Protein Processing, Post-Translational ; Receptors, Notch ; Signal Transduction ; Transfection
    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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  • 98
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    New clues found to diabetes and obesity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1423, 1425.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus/drug therapy/*metabolism ; Diabetes Mellitus, Type 2/drug therapy/*metabolism ; Humans ; Insulin/*metabolism ; Mice ; Mice, Knockout ; Mutation ; Obesity/drug therapy/*metabolism ; Phosphates/metabolism ; Protein Tyrosine Phosphatases/antagonists & inhibitors/genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
    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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  • 99
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    Leaves in the dark see the light (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foyer, C H -- Noctor, G -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):599-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Physiology, IACR-Rothamsted, Harpenden, Herts AL5 2JQ, UK. christine.foyer@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328743" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Arabidopsis/genetics/*metabolism ; Ascorbate Peroxidases ; Chloroplasts/metabolism ; Electron Transport ; *Gene Expression Regulation, Plant ; Hydrogen Peroxide/metabolism ; *Light ; Oxidation-Reduction ; Peroxidases/genetics ; Photosynthesis ; Plant Leaves/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction
    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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  • 100
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; 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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