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  • Signal Transduction  (80)
  • *Biological Evolution  (56)
  • American Association for the Advancement of Science (AAAS)  (136)
  • Wiley
  • 1995-1999  (136)
  • 1999  (136)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (136)
  • Wiley
Years
  • 1995-1999  (136)
Year
  • 1
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    The handy-dandy kitchen device (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abramson, P R -- Pinkerton, S D -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):1993-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura/*genetics/physiology ; *Biological Evolution ; Male ; Selection, Genetic ; *Sexual Behavior, Animal ; *Vocalization, Animal
    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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    Diminishing returns from mutation supply rate in asexual populations (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Mutator genotypes with increased mutation rates may be especially important in microbial evolution if genetic adaptation is generally limited by the supply of mutations. In experimental populations of the bacterium Escherichia coli, the rate of evolutionary adaptation was proportional to the mutation supply rate only in particular circumstances of small or initially well-adapted populations. These experiments also demonstrate a "speed limit" on adaptive evolution in asexual populations, one that is independent of the mutation supply rate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arjan, J A -- Visser, M -- Zeyl, C W -- Gerrish, P J -- Blanchard, J L -- Lenski, R E -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):404-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Microbial Ecology, Michigan State University, East Lansing, MI 48824, USA. arjan.devisser@algemeen.micr.wau.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888858" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Biological Evolution ; Escherichia coli/*genetics/physiology ; Genetics, Population ; Genotype ; Linear Models ; *Models, Biological ; *Mutation
    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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    Test tube evolution catches time in a bottle (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Appenzeller, T -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2108-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409068" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; *Biological Evolution ; Culture Media ; *Ecosystem ; Escherichia coli/*genetics/physiology ; Glucose/metabolism ; Maltose/metabolism ; *Mutation ; Pseudomonas fluorescens/*genetics/physiology ; Selection, Genetic
    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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    Science and scripture (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitehead, F -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):681.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577223" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Education/legislation & jurisprudence/standards ; Kansas ; *Politics ; Religion and Science ; Science/*education
    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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  • 5
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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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  • 6
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    A new human ancestor? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):572-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Ethiopia ; Facial Bones/anatomy & histology ; *Fossils ; History, Ancient ; *Hominidae/anatomy & histology/classification ; Humans ; Paleodontology ; Skull/anatomy & histology ; Tooth/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    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
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  • 8
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    Population biology, evolution, and infectious disease: convergence and synthesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-05
    Description: Traditionally, the interest of population and evolutionary biologists in infectious diseases has been almost exclusively in their role as agents of natural selection in higher organisms. Recently, this interest has expanded to include the genetic structure and evolution of microparasite populations, the mechanisms of pathogenesis and the immune response, and the population biology, ecology, and evolutionary consequences of medical and public health interventions. This article describes recent work in these areas, emphasizing the ways in which quantitative, population-biological approaches have been contributing to the understanding of infectious disease and the design and evaluation of interventions for their treatment and prevention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levin, B R -- Lipsitch, M -- Bonhoeffer, S -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Emory University, 1510 Clifton Road, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Physiological Phenomena ; *Biological Evolution ; Drug Resistance, Microbial ; Humans ; Infection/immunology/*microbiology ; Molecular Epidemiology ; Parasites/genetics/physiology ; Parasitic Diseases/immunology/*parasitology ; Population Dynamics ; Vaccination ; Virus Physiological Phenomena
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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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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  • 10
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    Science and "truth" (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wojcik, J F -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):663.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454918" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Humans ; *Religion and Science
    Print ISSN: 0036-8075
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  • 11
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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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  • 12
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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
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  • 13
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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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  • 14
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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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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    Kansas evolution ruling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1849.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515786" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Biology/education ; Kansas ; Science/*education ; Universities/standards
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
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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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    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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  • 22
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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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  • 23
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    Complexity, pattern, and evolutionary trade-offs in animal aggregation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: One of the most striking patterns in biology is the formation of animal aggregations. Classically, aggregation has been viewed as an evolutionarily advantageous state, in which members derive the benefits of protection, mate choice, and centralized information, balanced by the costs of limiting resources. Consisting of individual members, aggregations nevertheless function as an integrated whole, displaying a complex set of behaviors not possible at the level of the individual organism. Complexity theory indicates that large populations of units can self-organize into aggregations that generate pattern, store information, and engage in collective decision-making. This begs the question, are all emergent properties of animal aggregations functional or are some simply pattern? Solutions to this dilemma will necessitate a closer marriage of theoretical and modeling studies linked to empirical work addressing the choices, and trajectories, of individuals constrained by membership in the group.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parrish, J K -- Edelstein-Keshet, L -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoology Department, University of Washington, Seattle, WA 98195, USA. jparrish@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; *Biological Evolution ; *Cooperative Behavior ; Mathematics ; Models, Biological
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  • 24
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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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  • 25
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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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  • 26
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    The evolution of species interactions (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-06-26
    Description: Interactions between species are as evolutionarily malleable as the species themselves and have played a central role in the diversification and organization of life. This malleability creates complex geographic mosaics in interspecific interactions that can evolve rapidly over decades, blurring the distinction between evolutionary time and ecological time and making the study of coevolution crucial for human health and welfare.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, J N -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2116-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Botany and Zoology, Washington State University, Pullman, WA 99164, USA. jnt@wsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drug Resistance, Microbial ; *Ecosystem ; Humans ; Models, Biological ; Parasites/pathogenicity ; *Selection, Genetic ; Virulence/genetics
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  • 27
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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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  • 28
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    RNA, whither goest thou? (1999)
    American Association for the Advancement of Science (AAAS)
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    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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  • 29
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genomes reveal kin connections for whales and pumas (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2081.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Artiodactyla/*genetics ; *Biological Evolution ; Carnivora/classification/*genetics ; Short Interspersed Nucleotide Elements ; Whales/*genetics
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    Evolution flies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dusenbery, D B -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):413-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Genetic Variation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Paleoanthropology. Kenyan skeleton shakes ape family tree (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, C -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1335, 1337.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490402" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones/anatomy & histology ; *Fossils ; History, Ancient ; Hominidae/anatomy & histology/*classification ; Humans ; Kenya ; Paleodontology ; Skeleton ; Terminology as Topic
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    Is it time to uproot the tree of life? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 May 21;284(5418):1305-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383313" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/classification/*genetics ; Bacteria/classification/*genetics ; *Biological Evolution ; *Eukaryotic Cells ; Evolution, Molecular ; Genes, rRNA ; *Genome ; *Phylogeny ; Recombination, Genetic
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    From embryos and fossils, new clues to vertebrate evolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):575, 577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Fishes/anatomy & histology ; *Fossils ; Jaw/*anatomy & histology ; Neural Crest/cytology/physiology ; *Vertebrates/anatomy & histology
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  • 35
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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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    Neandertals: not so fast (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolpoff, M H -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):1991.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; DNA, Mitochondrial/*genetics ; Evolution, Molecular ; Gene Frequency ; Hominidae/*genetics ; Humans ; Mutation ; Phylogeny ; Selection, Genetic
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  • 38
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Fending off furtive strategists (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanson, R B -- Bloom, F -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1847.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515785" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Kansas ; Politics ; Religion and Science ; Science/*education
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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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  • 41
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    Genetic study shakes up out of Africa theory (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1828.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206882" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Biological Evolution ; Evolution, Molecular ; Haplotypes ; *Hominidae/genetics ; Humans ; Mutation ; *Pyruvate Dehydrogenase (Lipoamide) ; Pyruvate Dehydrogenase Complex/genetics ; X Chromosome
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  • 42
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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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    The structural era of endocytosis (1999)
    American Association for the Advancement of Science (AAAS)
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    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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  • 44
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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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    The future of the fossil record (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: The fossil record provides a powerful basis for analyzing the controlling factors and impact of biological evolution over a wide range of temporal and spatial scales and in the context of an evolving Earth. An increasingly interdisciplinary paleontology has begun to formulate the next generation of questions, drawing on a wealth of new data, and on methodological advances ranging from high-resolution geochronology to simulation of morphological evolution. Key issues related to evolutionary biology include the biotic and physical factors that govern biodiversity dynamics, the developmental and ecological basis for the nonrandom introduction of evolutionary innovations in time and space, rules of biotic response to environmental perturbations, and the dynamic feedbacks between life and the Earth's surface processes. The sensitivity of evolutionary processes to rates, magnitudes, and spatial scales of change in the physical and biotic environment will be important in all these areas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jablonski, D -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2114-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geophysical Sciences, University of Chicago 5734 South Ellis Avenue Chicago, IL 60637, USA. djablons@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Ecosystem ; *Fossils ; *Paleontology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Silent scientists (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pruett, S B -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):902-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577240" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Curriculum ; Kansas ; *Religion and Science ; Science/*education ; Teaching
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Phylogenetic classification and the universal tree (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: From comparative analyses of the nucleotide sequences of genes encoding ribosomal RNAs and several proteins, molecular phylogeneticists have constructed a "universal tree of life," taking it as the basis for a "natural" hierarchical classification of all living things. Although confidence in some of the tree's early branches has recently been shaken, new approaches could still resolve many methodological uncertainties. More challenging is evidence that most archaeal and bacterial genomes (and the inferred ancestral eukaryotic nuclear genome) contain genes from multiple sources. If "chimerism" or "lateral gene transfer" cannot be dismissed as trivial in extent or limited to special categories of genes, then no hierarchical universal classification can be taken as natural. Molecular phylogeneticists will have failed to find the "true tree," not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree. However, taxonomies based on molecular sequences will remain indispensable, and understanding of the evolutionary process will ultimately be enriched, not impoverished.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doolittle, W F -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2124-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Canadian Institute for Advanced Research, Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. ford@is.dal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaea/*classification/genetics ; Bacteria/*classification/genetics ; *Biological Evolution ; Eukaryotic Cells/*classification ; Genes, rRNA ; Genome ; *Phylogeny ; RNA, Ribosomal/chemistry/genetics ; *Recombination, Genetic
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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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    Gaining new insight into the molecular basis of evolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):654-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454913" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; *Biological Evolution ; *Evolution, Molecular ; Fishes/*genetics/physiology ; Mutation ; Rhodopsin/chemistry/*genetics/physiology ; *Selection, Genetic ; Vision, Ocular
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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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    Development shapes evolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):518-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cervical Vertebrae/*anatomy & histology ; Cockroaches/genetics/*physiology ; Genes, Homeobox ; Humans ; Mammals/*anatomy & histology/embryology ; Mutation ; Neoplasms/genetics ; *Parthenogenesis ; Reactive Oxygen Species
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    Evolving smarts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duke, J A -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):589.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328736" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Brain ; Cooking ; Estrogens, Non-Steroidal/*analysis ; Female ; *Hominidae ; Humans ; *Isoflavones ; Male ; Phytoestrogens ; Plant Preparations ; *Vegetables/chemistry
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    Kansas dumps Darwin, raises alarm across the United States (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1186-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484724" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Curriculum ; Kansas ; Religion and Science ; Science/*education ; United States
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    DNA and field data help plumb evolution's secrets (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):192-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Female ; Genes, Recessive ; Genetic Variation ; Inbreeding ; Male ; Moths/genetics/physiology ; Plants/genetics ; Songbirds/genetics/physiology
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    Science and "truth" (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Touryan, K J -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):663.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Humans ; *Science
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
    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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    Archean molecular fossils and the early rise of eukaryotes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: Molecular fossils of biological lipids are preserved in 2700-million-year-old shales from the Pilbara Craton, Australia. Sequential extraction of adjacent samples shows that these hydrocarbon biomarkers are indigenous and syngenetic to the Archean shales, greatly extending the known geological range of such molecules. The presence of abundant 2alpha-methylhopanes, which are characteristic of cyanobacteria, indicates that oxygenic photosynthesis evolved well before the atmosphere became oxidizing. The presence of steranes, particularly cholestane and its 28- to 30-carbon analogs, provides persuasive evidence for the existence of eukaryotes 500 million to 1 billion years before the extant fossil record indicates that the lineage arose.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brocks, J J -- Logan, G A -- Buick, R -- Summons, R E -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1033-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geosciences, University of Sydney, Sydney, NSW 2006, Australia. jochen.brocks@agso.gov.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10446042" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere ; Australia ; *Biological Evolution ; Biomarkers/analysis ; Cholestanes/analysis ; Cyanobacteria/physiology ; Eukaryotic Cells/*physiology ; Fossils ; Geologic Sediments/*chemistry ; Hydrocarbons/*analysis ; Lipids/*analysis ; Paleontology ; Photosynthesis ; Steroids/*analysis ; Triterpenes/*analysis
    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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    Turtle origins (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rieppel, O -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):945-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology, The Foeld Museum, Chicago, IL 60605-2496, USA. rieppel@fmppr.fmnh.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075558" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; DNA/genetics ; Phylogeny ; Reptiles/anatomy & histology/classification/genetics ; Turtles/anatomy & histology/*classification/*genetics
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    Science and scripture (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brosnan-Watters, G -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):681.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577221" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Kansas ; *Religion and Science ; Science/*education
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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)
    Details
    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
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    Clonal interference and the evolution of RNA viruses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: In asexual populations, beneficial mutations that occur in different lineages compete with one another. This phenomenon, known as clonal interference, ensures that those beneficial mutations that do achieve fixation are of large effect. Clonal interference also increases the time between fixations, thereby slowing the adaptation of asexual populations. The effects of clonal interference were measured in the asexual RNA virus vesicular stomatitis virus; rates and average effects of beneficial mutations were quantified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miralles, R -- Gerrish, P J -- Moya, A -- Elena, S F -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1745-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Cavanilles de Biodiversitat i Biologia Evolutiva and Departament de Genetica, Universitat de Valencia, Apartado 22085, 46071 Valencia, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481012" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; *Biological Evolution ; Cell Line ; Confidence Intervals ; Cricetinae ; Gene Frequency ; Genes, Viral ; Likelihood Functions ; Models, Biological ; Models, Statistical ; *Mutation ; Vesicular stomatitis Indiana virus/genetics/*physiology ; Virus Replication
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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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    Going beyond appearances to find life's history (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2112-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409070" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacteria ; *Biological Evolution ; *Eukaryotic Cells ; *Fossils ; Geologic Sediments/*microbiology ; Hydrocarbons/analysis ; Isotopes ; Magnetic Resonance Spectroscopy ; X-Rays
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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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    Science and scripture (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, J W -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):681.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577222" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Kansas ; *Politics ; *Religion and Science ; Science/*education
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    Mitochondrial evolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: The serial endosymbiosis theory is a favored model for explaining the origin of mitochondria, a defining event in the evolution of eukaryotic cells. As usually described, this theory posits that mitochondria are the direct descendants of a bacterial endosymbiont that became established at an early stage in a nucleus-containing (but amitochondriate) host cell. Gene sequence data strongly support a monophyletic origin of the mitochondrion from a eubacterial ancestor shared with a subgroup of the alpha-Proteobacteria. However, recent studies of unicellular eukaryotes (protists), some of them little known, have provided insights that challenge the traditional serial endosymbiosis-based view of how the eukaryotic cell and its mitochondrion came to be. These data indicate that the mitochondrion arose in a common ancestor of all extant eukaryotes and raise the possibility that this organelle originated at essentially the same time as the nuclear component of the eukaryotic cell rather than in a separate, subsequent event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, M W -- Burger, G -- Lang, B F -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1476-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. M.W.Gray@Dal.Ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066161" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaea/genetics ; Bacteria/genetics ; *Biological Evolution ; DNA, Mitochondrial/chemistry/*genetics ; *Eukaryotic Cells/physiology/ultrastructure ; Evolution, Molecular ; Genes ; Mitochondria/*genetics ; Models, Biological ; Phylogeny ; Symbiosis
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    Evolution flies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schall, J J -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):414.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577202" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila/genetics ; Periodicals as Topic ; Publishing
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Two distinct cytokines released from a human aminoacyl-tRNA synthetase (1999)
    American Association for the Advancement of Science (AAAS)
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    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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    Evolution flies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregory, T R -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):414.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila/genetics ; Selection, Genetic
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    Documenting speciation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knox, J S -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):684.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asteraceae/genetics ; *Biological Evolution ; Phylogeny ; *Poaceae/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Highly visible, curiously intangible (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, G A -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2029, 2031-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Arizona State University, Tempe, AZ 85287-2402, USA. gaclark@asu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206911" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Archaeology ; *Biological Evolution ; Europe ; History, Ancient ; *Hominidae ; Humans ; Models, Biological ; *Paleontology
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  • 80
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    Forming the robust australopithecine face (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232966" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Biological Evolution ; Face/anatomy & histology ; Facial Bones/*anatomy & histology ; History, Ancient ; Hominidae/*anatomy & histology ; Humans ; Molar/anatomy & histology ; Paleodontology ; Paleontology ; Phylogeny
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  • 81
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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
    Print ISSN: 0036-8075
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  • 82
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    The evolution of dinosaurs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: The ascendancy of dinosaurs on land near the close of the Triassic now appears to have been as accidental and opportunistic as their demise and replacement by therian mammals at the end of the Cretaceous. The dinosaurian radiation, launched by 1-meter-long bipeds, was slower in tempo and more restricted in adaptive scope than that of therian mammals. A notable exception was the evolution of birds from small-bodied predatory dinosaurs, which involved a dramatic decrease in body size. Recurring phylogenetic trends among dinosaurs include, to the contrary, increase in body size. There is no evidence for co-evolution between predators and prey or between herbivores and flowering plants. As the major land masses drifted apart, dinosaurian biogeography was molded more by regional extinction and intercontinental dispersal than by the breakup sequence of Pangaea.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sereno, P C -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2137-47.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismal Biology and Anatomy, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/anatomy & histology/physiology ; Body Constitution ; Feathers ; Flight, Animal ; Fossils ; Locomotion ; *Paleontology ; Phylogeny ; *Reptiles/anatomy & histology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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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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  • 86
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    Keeping calm about Kansas (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allison, M L -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):411.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577198" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Biology/*education ; Curriculum ; Kansas ; Science/*education
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  • 87
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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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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  • 89
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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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    Perspectives: evolutionary biology. The evolutionary synthesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenseth, N C -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1490.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Oslo, Oslo, Norway. n.c.stenseth@bio.uio.no〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610549" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes ; *Awards and Prizes ; *Biological Evolution ; England ; History, 20th Century ; Selection, Genetic ; Sweden ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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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
    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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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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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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  • 95
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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
    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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    A barely tested hypothesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hogg, D W -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610561" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomical Phenomena ; Astronomy ; *Biological Evolution ; Selection, Genetic
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Science and "truth" (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hogg, D W -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):663.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Science ; *Selection, Genetic
    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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  • 98
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Fossil offers a glimpse into mammals' past (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, C -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):1989-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206896" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; China ; *Fossils ; *Mammals/anatomy & histology ; Paleodontology ; Paleontology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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