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  • Male  (612)
  • Signal Transduction  (361)
  • Models, Molecular  (269)
  • American Association for the Advancement of Science (AAAS)  (1,200)
  • American Institute of Physics (AIP)
  • Emerald
  • Oxford University Press
  • 1995-1999  (1,200)
Collection
Keywords
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  • American Association for the Advancement of Science (AAAS)  (1,200)
  • American Institute of Physics (AIP)
  • Emerald
  • Oxford University Press
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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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    Heat shock protein mutes genetic changes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1796.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874626" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Drosophila/*genetics ; Female ; *Genes, Insect ; HSP90 Heat-Shock Proteins/genetics/*physiology ; Insect Proteins/genetics/physiology ; Male ; *Mutation ; Temperature
    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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  • 3
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    Postdoctoral patterns, career advancement, and problems (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Postdoctoral appointments can have different functions and meanings, depending on the field and whether the postdoc is a man or a woman. The Ph.D.'s-Ten Years Later study confirmed that in biochemistry, the postdoc, not the Ph.D., has become the general proving ground for excellence both in academia and industry. Because they spent a longer time in these "mandatory" postdocs, biochemists had the largest proportion of untenured faculty 10 to 13 years after the Ph. D. In mathematics, where substantially fewer postdoctoral positions are available, Ph.D.'s taking postdocs are more likely to obtain faculty positions, but this is true only for men. University administrators should be accountable for monitoring the total time spent in these positions and should provide administrative assistance for skills training, career growth, and the job search. In addition, creative solutions concerning the dual-career couple phenomenon are necessary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nerad, M -- Cerny, J -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1533-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Division, University of California, Berkeley, 424 Sproul Hall, Berkeley, CA 94720-5900, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477510" target="_blank"〉PubMed〈/a〉
    Keywords: *Biochemistry/education ; *Career Mobility ; *Education, Graduate ; Employment ; Faculty ; *Fellowships and Scholarships ; Female ; Humans ; Male ; *Mathematics ; Salaries and Fringe Benefits ; Societies, Scientific ; Time Factors ; United States ; Universities
    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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  • 4
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    Evolution of a protein fold in vitro (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: A "switch" mutant of the Arc repressor homodimer was constructed by interchanging the sequence positions of a hydrophobic core residue, leucine 12, and an adjacent surface polar residue, asparagine 11, in each strand of an intersubunit beta sheet. The mutant protein adopts a fold in which each beta strand is replaced by a right-handed helix and side chains in this region undergo significant repacking. The observed structural changes allow the protein to maintain solvent exposure of polar side chains and optimal burial of hydrophobic side chains. These results suggest that new protein folds can evolve from existing folds without drastic or large-scale mutagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cordes, M H -- Walsh, N P -- McKnight, C J -- Sauer, R T -- AI-15706/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):325-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195898" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Asparagine/chemistry ; Circular Dichroism ; Hydrogen Bonding ; Leucine/chemistry ; Models, Molecular ; Molecular Sequence Data ; Mutagenesis, Insertional ; Nuclear Magnetic Resonance, Biomolecular ; Protein Conformation ; *Protein Folding ; *Protein Structure, Secondary ; Protein Structure, Tertiary ; Repressor Proteins/*chemistry ; Viral Proteins/*chemistry ; Viral Regulatory and Accessory Proteins
    Print ISSN: 0036-8075
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  • 5
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    Crystal structure of invasin: a bacterial integrin-binding protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: The Yersinia pseudotuberculosis invasin protein promotes bacterial entry by binding to host cell integrins with higher affinity than natural substrates such as fibronectin. The 2.3 angstrom crystal structure of the invasin extracellular region reveals five domains that form a 180 angstrom rod with structural similarities to tandem fibronectin type III domains. The integrin-binding surfaces of invasin and fibronectin include similarly located key residues, but in the context of different folds and surface shapes. The structures of invasin and fibronectin provide an example of convergent evolution, in which invasin presents an optimized surface for integrin binding, in comparison with host substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamburger, Z A -- Brown, M S -- Isberg, R R -- Bjorkman, P J -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):291-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 156-29, Howard Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514372" target="_blank"〉PubMed〈/a〉
    Keywords: *Adhesins, Bacterial ; Amino Acid Sequence ; Bacterial Proteins/*chemistry/metabolism ; Binding Sites ; Crystallography, X-Ray ; Evolution, Molecular ; Fibronectins/chemistry/metabolism ; Hydrogen Bonding ; Integrins/*metabolism ; Ligands ; Models, Molecular ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Yersinia pseudotuberculosis/*chemistry/metabolism
    Print ISSN: 0036-8075
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  • 6
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    Unmasking a cheating gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crow, J F -- New York, N.Y. -- Science. 1999 Mar 12;283(5408):1651-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, University of Wisconsin, Madison, WI 53706, USA. jfcrow@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10189318" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics/physiology ; Cell Nucleus/metabolism ; Cloning, Molecular ; Drosophila/*genetics/physiology ; *Drosophila Proteins ; *GTPase-Activating Proteins ; *Genes, Insect ; Male ; *Meiosis ; Nuclear Proteins/*genetics/physiology ; Sperm Maturation ; Spermatozoa/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Stimulation of microtubule aster formation and spindle assembly by the small GTPase Ran (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Ran, a small guanosine triphosphatase, is suggested to have additional functions beyond its well-characterized role in nuclear trafficking. Guanosine triphosphate-bound Ran, but not guanosine diphosphate-bound Ran, stimulated polymerization of astral microtubules from centrosomes assembled on Xenopus sperm. Moreover, a Ran allele with a mutation in the effector domain (RanL43E) induced the formation of microtubule asters and spindle assembly, in the absence of sperm nuclei, in a gammaTuRC (gamma-tubulin ring complex)- and XMAP215 (Xenopus microtubule associated protein)-dependent manner. Therefore, Ran could be a key signaling molecule regulating microtubule polymerization during mitosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilde, A -- Zheng, Y -- GM56312-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1359-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Extracts ; Cell Nucleus/metabolism ; Centrosome/physiology ; Dimethyl Sulfoxide/pharmacology ; Dyneins/physiology ; GTP Phosphohydrolases/genetics/*metabolism ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/*metabolism ; Male ; Microtubule-Associated Proteins/metabolism ; Microtubules/*metabolism/ultrastructure ; Mutation ; Nuclear Proteins/analysis/genetics/*metabolism/pharmacology ; Ovum ; Recombinant Fusion Proteins/metabolism/pharmacology ; Sperm Head/physiology ; Spindle Apparatus/chemistry/*metabolism/ultrastructure ; Tubulin/analysis/metabolism ; Xenopus ; *Xenopus Proteins ; ran GTP-Binding Protein
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  • 8
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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
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  • 9
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    Regulation of intestinal alpha-defensin activation by the metalloproteinase matrilysin in innate host defense (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Precursors of alpha-defensin peptides require activation for bactericidal activity. In mouse small intestine, matrilysin colocalized with alpha-defensins (cryptdins) in Paneth cell granules, and in vitro it cleaved the pro segment from cryptdin precursors. Matrilysin-deficient (MAT-/-) mice lacked mature cryptdins and accumulated precursor molecules. Intestinal peptide preparations from MAT-/- mice had decreased antimicrobial activity. Orally administered bacteria survived in greater numbers and were more virulent in MAT-/- mice than in MAT+/+ mice. Thus, matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, C L -- Ouellette, A J -- Satchell, D P -- Ayabe, T -- Lopez-Boado, Y S -- Stratman, J L -- Hultgren, S J -- Matrisian, L M -- Parks, W C -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):113-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Division of Allergy and Pulmonary Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. wilson_c@kids.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Catalysis ; Cytoplasmic Granules/enzymology ; Escherichia coli/growth & development ; Escherichia coli Infections/immunology/microbiology ; Female ; Humans ; *Immunity, Innate ; *Immunity, Mucosal ; Intestinal Mucosa/enzymology/immunology/microbiology ; Intestine, Small/enzymology/*immunology/microbiology ; Male ; Matrix Metalloproteinase 7 ; Metalloendopeptidases/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Paneth Cells/enzymology ; Protein Precursors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Salmonella typhimurium/growth & development/pathogenicity ; Tissue Extracts/pharmacology
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  • 10
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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
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  • 11
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    Perspectives: protein structure. Class-conscious TCR? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, I A -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1867-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. wilson@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*chemistry/immunology/metabolism ; Binding Sites ; CD4-Positive T-Lymphocytes/immunology/metabolism ; CD8-Positive T-Lymphocytes/immunology/metabolism ; Crystallography, X-Ray ; Histocompatibility Antigens Class I/chemistry/immunology/metabolism ; Histocompatibility Antigens Class II/*chemistry/immunology/metabolism ; Mice ; Models, Molecular ; Peptides/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism
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  • 12
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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
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  • 13
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    Role of nonexercise activity thermogenesis in resistance to fat gain in humans (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability 〈 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, J A -- Eberhardt, N L -- Jensen, M D -- DK45343/DK/NIDDK NIH HHS/ -- DK50456/DK/NIDDK NIH HHS/ -- M01 RR00535/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):212-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Endocrine Research Unit, Mayo Clinic and Mayo Foundation, 200 First Street Southwest, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880251" target="_blank"〉PubMed〈/a〉
    Keywords: Activities of Daily Living ; *Adipose Tissue ; Adult ; Basal Metabolism ; Body Composition ; Calorimetry, Indirect ; *Energy Intake ; *Energy Metabolism ; Exercise ; Female ; Humans ; Hyperphagia/*physiopathology ; Male ; *Movement ; Posture ; *Weight Gain
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  • 14
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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
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  • 15
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    Stability, precision, and near-24-hour period of the human circadian pacemaker (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Regulation of circadian period in humans was thought to differ from that of other species, with the period of the activity rhythm reported to range from 13 to 65 hours (median 25.2 hours) and the period of the body temperature rhythm reported to average 25 hours in adulthood, and to shorten with age. However, those observations were based on studies of humans exposed to light levels sufficient to confound circadian period estimation. Precise estimation of the periods of the endogenous circadian rhythms of melatonin, core body temperature, and cortisol in healthy young and older individuals living in carefully controlled lighting conditions has now revealed that the intrinsic period of the human circadian pacemaker averages 24.18 hours in both age groups, with a tight distribution consistent with other species. These findings have important implications for understanding the pathophysiology of disrupted sleep in older people.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Duffy, J F -- Shanahan, T L -- Brown, E N -- Mitchell, J F -- Rimmer, D W -- Ronda, J M -- Silva, E J -- Allan, J S -- Emens, J S -- Dijk, D J -- Kronauer, R E -- MO1-RR02635/RR/NCRR NIH HHS/ -- P01-AG09975/AG/NIA NIH HHS/ -- R01-GM53559/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2177-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Circadian, Neuroendocrine, and Sleep Disorders Section, Division of Endocrinology, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381883" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aging/*physiology ; Biological Clocks/genetics/*physiology ; Body Temperature ; Circadian Rhythm/genetics/*physiology ; Darkness ; Female ; Humans ; Hydrocortisone/blood ; Light ; Male ; Melatonin/blood ; Middle Aged ; Sleep
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    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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  • 17
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    Regulation of maternal behavior and offspring growth by paternally expressed Peg3 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Imprinted genes display parent-of-origin-dependent monoallelic expression that apparently regulates complex mammalian traits, including growth and behavior. The Peg3 gene is expressed in embryos and the adult brain from the paternal allele only. A mutation in the Peg3 gene resulted in growth retardation, as well as a striking impairment of maternal behavior that frequently resulted in death of the offspring. This result may be partly due to defective neuronal connectivity, as well as reduced oxytocin neurons in the hypothalamus, because mutant mothers were deficient in milk ejection. This study provides further insights on the evolution of epigenetic regulation of imprinted gene dosage in modulating mammalian growth and behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Keverne, E B -- Aparicio, S A -- Ishino, F -- Barton, S C -- Surani, M A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):330-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome CRC Institute of Cancer and Developmental Biology, and Physiological Laboratory, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/metabolism ; Crosses, Genetic ; Female ; Gene Expression ; Gene Targeting ; *Genomic Imprinting ; *Growth ; Hypothalamus/cytology/metabolism ; Kruppel-Like Transcription Factors ; Lactation ; Male ; *Maternal Behavior ; Mice ; Mutation ; Neural Pathways ; Neurons/metabolism ; Oxytocin/metabolism ; Phenotype ; *Protein Kinases ; Proteins/genetics/*physiology ; *Transcription Factors ; *Weight Gain
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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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    Chaperonin function: folding by forced unfolding (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: The ability of the GroEL chaperonin to unfold a protein trapped in a misfolded condition was detected and studied by hydrogen exchange. The GroEL-induced unfolding of its substrate protein is only partial, requires the complete chaperonin system, and is accomplished within the 13 seconds required for a single system turnover. The binding of nucleoside triphosphate provides the energy for a single unfolding event; multiple turnovers require adenosine triphosphate hydrolysis. The substrate protein is released on each turnover even if it has not yet refolded to the native state. These results suggest that GroEL helps partly folded but blocked proteins to fold by causing them first to partially unfold. The structure of GroEL seems well suited to generate the nonspecific mechanical stretching force required for forceful protein unfolding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427652/" 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/PMC3427652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shtilerman, M -- Lorimer, G H -- Englander, S W -- GM31847/GM/NIGMS NIH HHS/ -- R01 GM031847/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Johnson Research Foundation, Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221918" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adenylyl Imidodiphosphate/metabolism ; Binding Sites ; Chaperonin 10/chemistry/metabolism/physiology ; Chaperonin 60/chemistry/metabolism/*physiology ; Hydrogen/chemistry/metabolism ; Models, Molecular ; Protein Binding ; Protein Conformation ; *Protein Folding ; Protein Structure, Secondary ; Ribulose-Bisphosphate Carboxylase/*chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Stevenson's fingers (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, T M -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577189" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchiectasis/history ; Depressive Disorder/*history/pathology ; *Famous Persons ; Fingers/*pathology ; History, 19th Century ; Humans ; Literature, Modern/*history ; Male ; Medicine in Art ; Paintings ; Tuberculosis/*history/pathology
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  • 20
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    Self-organization of microtubule asters induced in Xenopus egg extracts by GTP-bound Ran (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: The nucleotide exchange activity of RCC1, the only known nucleotide exchange factor for Ran, a Ras-like small guanosine triphosphatase, was required for microtubule aster formation with or without demembranated sperm in Xenopus egg extracts arrested in meiosis II. Consistently, in the RCC1-depleted egg extracts, Ran guanosine triphosphate (RanGTP), but not Ran guanosine diphosphate (RanGDP), induced self-organization of microtubule asters, and the process required the activity of dynein. Thus, Ran was shown to regulate formation of the microtubule network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohba, T -- Nakamura, M -- Nishitani, H -- Nishimoto, T -- New York, N.Y. -- Science. 1999 May 21;284(5418):1356-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Graduate School of Medical Science, Kyushu University, Maidashi Higashi-ku, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle Proteins ; Cell Extracts ; Cell Nucleus/metabolism ; DNA-Binding Proteins/metabolism ; Dyneins/metabolism ; Female ; GTP Phosphohydrolases/*metabolism ; *Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/*metabolism ; Male ; Microtubules/chemistry/*metabolism/ultrastructure ; Nuclear Proteins/analysis/*metabolism ; Ovum ; Recombinant Proteins/metabolism ; Sperm Head/physiology ; Spindle Apparatus/chemistry/*metabolism/ultrastructure ; Xenopus ; *Xenopus Proteins ; ran GTP-Binding Protein
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  • 21
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    Intracytoplasmic sperm injection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawkins, M M -- Barratt, C L -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):51-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10532889" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Congenital Abnormalities/etiology ; Developmental Disabilities/etiology ; Female ; Fertilization in Vitro/*adverse effects ; Great Britain ; Humans ; Male ; Neoplasms/etiology ; Pregnancy ; Pregnancy Outcome ; Registries ; Risk Factors
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  • 22
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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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  • 23
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    Behaviorists listen in as animals call and croak (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bagla, P -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1480-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498530" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; Anura/*physiology ; Female ; Grasshoppers/*physiology ; Male
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  • 24
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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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  • 25
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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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  • 26
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    Cell surgery (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1498.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology ; Cell Differentiation ; Cell Separation ; Dystrophin/biosynthesis ; Female ; *Hematopoietic Stem Cell Transplantation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscle, Skeletal/*cytology/metabolism ; *Stem Cell Transplantation ; Stem Cells/*cytology
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  • 27
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    Dosage compensation proteins targeted to X chromosomes by a determinant of hermaphrodite fate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: In many organisms, master control genes coordinately regulate sex-specific aspects of development. SDC-2 was shown to induce hermaphrodite sexual differentiation and activate X chromosome dosage compensation in Caenorhabditis elegans. To control these distinct processes, SDC-2 acts as a strong gene-specific repressor and a weaker chromosome-wide repressor. To initiate hermaphrodite development, SDC-2 associates with the promoter of the male sex-determining gene her-1 to repress its transcription. To activate dosage compensation, SDC-2 triggers assembly of a specialized protein complex exclusively on hermaphrodite X chromosomes to reduce gene expression by half. SDC-2 can localize to X chromosomes without other components of the dosage compensation complex, suggesting that SDC-2 targets dosage compensation machinery to X chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawes, H E -- Berlin, D S -- Lapidus, D M -- Nusbaum, C -- Davis, T L -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/physiology ; *Caenorhabditis elegans Proteins ; *DNA-Binding Proteins ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*physiology ; *Sex Determination Processes ; Transgenes ; X Chromosome/genetics/*metabolism
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  • 28
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    Genomic views of human history (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: New tools of genomic analysis shed light on historical puzzles. Migrations of ancient peoples, differences in migration patterns of males and females, historical demography of cultures with ancient roots, and patterns of human genetic diversity are increasingly the focus of integrated analysis by historians, anthropologists, and geneticists.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owens, K -- King, M C -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):451-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medicine, Box 357720, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521333" target="_blank"〉PubMed〈/a〉
    Keywords: *Anthropology ; Biological Evolution ; Continental Population Groups/genetics ; Culture ; Emigration and Immigration ; Ethnic Groups/genetics ; Female ; Genetic Variation ; *Genetics, Population ; *Genome, Human ; History, Ancient ; Humans ; Jews/genetics ; Male
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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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    Beating the odds with Big K (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silberberg, S D -- Magleby, K L -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1859-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Life Sciences, Ben-Gurion University of the Negev, Beer Sheva 84105, Israel. silber@bgumail.bgu.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515790" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/drug effects/*physiology ; Estradiol/*metabolism/pharmacology ; Female ; Humans ; Large-Conductance Calcium-Activated Potassium Channels ; Longevity/physiology ; Male ; Muscle Contraction ; Muscle, Smooth, Vascular/drug effects/metabolism ; Potassium Channels/*metabolism ; *Potassium Channels, Calcium-Activated ; Recombinant Proteins/metabolism ; Sex Characteristics ; Xenopus
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    Evolution of shape complementarity and catalytic efficiency from a primordial antibody template (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: The crystal structure of an efficient Diels-Alder antibody catalyst at 1.9 angstrom resolution reveals almost perfect shape complementarity with its transition state analog. Comparison with highly related progesterone and Diels-Alderase antibodies that arose from the same primordial germ line template shows the relatively subtle mutational steps that were able to evolve both structural complementarity and catalytic efficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, J -- Deng, Q -- Chen, J -- Houk, K N -- Bartek, J -- Hilvert, D -- Wilson, I A -- CA27489/CA/NCI NIH HHS/ -- GM38273/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2345-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, 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/10600746" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Catalytic/*chemistry/genetics/*metabolism ; Binding Sites, Antibody ; Catalysis ; Chemistry, Physical ; Crystallography, X-Ray ; *Evolution, Molecular ; Haptens/chemistry/metabolism ; Hydrogen Bonding ; Immunoglobulin Fab Fragments/chemistry/metabolism ; Ligands ; Models, Molecular ; Mutation ; Physicochemical Phenomena ; Progesterone/immunology ; Protein Conformation ; Solubility ; Temperature ; Templates, Genetic
    Print ISSN: 0036-8075
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    Insights into editing from an ile-tRNA synthetase structure with tRNAile and mupirocin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: Isoleucyl-transfer RNA (tRNA) synthetase (IleRS) joins Ile to tRNA(Ile) at its synthetic active site and hydrolyzes incorrectly acylated amino acids at its editing active site. The 2.2 angstrom resolution crystal structure of Staphylococcus aureus IleRS complexed with tRNA(Ile) and Mupirocin shows the acceptor strand of the tRNA(Ile) in the continuously stacked, A-form conformation with the 3' terminal nucleotide in the editing active site. To position the 3' terminus in the synthetic active site, the acceptor strand must adopt the hairpinned conformation seen in tRNA(Gln) complexed with its synthetase. The amino acid editing activity of the IleRS may result from the incorrect products shuttling between the synthetic and editing active sites, which is reminiscent of the editing mechanism of DNA polymerases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silvian, L F -- Wang, J -- Steitz, T A -- GM22778/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1074-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics, Yale University, and Howard Hughes Medical Institute, New Haven, CT 06520-8114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10446055" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Adenosine Monophosphate/analogs & derivatives/metabolism ; Amino Acids/metabolism ; Binding Sites ; Crystallography, X-Ray ; DNA-Directed DNA Polymerase/metabolism ; Glutamate-tRNA Ligase/chemistry/metabolism ; Isoleucine/metabolism ; Isoleucine-tRNA Ligase/*chemistry/*metabolism ; Models, Molecular ; Mupirocin/chemistry/*metabolism ; Nucleic Acid Conformation ; Oligopeptides/metabolism ; Protein Conformation ; Protein Structure, Secondary ; RNA, Transfer, Gln/chemistry/metabolism ; RNA, Transfer, Ile/*chemistry/*metabolism ; Staphylococcus aureus/enzymology ; Substrate Specificity
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    Unlimited mileage from telomerase? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- DePinho, R A -- CA76027/CA/NCI NIH HHS/ -- HD 348880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Aging ; *Cell Division ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Neoplasms/enzymology/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; ras Proteins/metabolism
    Print ISSN: 0036-8075
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    A long season puts Catalhoyuk in context (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):890-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577237" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Female ; *Fossils ; History, Ancient ; Humans ; Male ; Paleopathology ; Skull/*pathology ; Turkey
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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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    Animal testing. One mouse's meat is another one's poison (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmuth, L -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1190-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/*pharmacology/toxicity ; *Genetic Variation ; Humans ; Litter Size ; Male ; Maximum Allowable Concentration ; Mice ; Mice, Inbred Strains ; Species Specificity ; Spermatogenesis/*drug effects ; Testis/*drug effects ; *Toxicity Tests
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    Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Epithelia permit selective and regulated flux from apical to basolateral surfaces by transcellular passage through cells or paracellular flux between cells. Tight junctions constitute the barrier to paracellular conductance; however, little is known about the specific molecules that mediate paracellular permeabilities. Renal magnesium ion (Mg2+) resorption occurs predominantly through a paracellular conductance in the thick ascending limb of Henle (TAL). Here, positional cloning has identified a human gene, paracellin-1 (PCLN-1), mutations in which cause renal Mg2+ wasting. PCLN-1 is located in tight junctions of the TAL and is related to the claudin family of tight junction proteins. These findings provide insight into Mg2+ homeostasis, demonstrate the role of a tight junction protein in human disease, and identify an essential component of a selective paracellular conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simon, D B -- Lu, Y -- Choate, K A -- Velazquez, H -- Al-Sabban, E -- Praga, M -- Casari, G -- Bettinelli, A -- Colussi, G -- Rodriguez-Soriano, J -- McCredie, D -- Milford, D -- Sanjad, S -- Lifton, R P -- F.1/Telethon/Italy -- R01DK51696/DK/NIDDK NIH HHS/ -- TGM06S01/Telethon/Italy -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Genetics, 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/10390358" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/urine ; Chromosomes, Human, Pair 3/genetics ; Claudins ; Cloning, Molecular ; Female ; Genes, Recessive ; Homeostasis ; Humans ; Kidney Diseases/*genetics/metabolism ; Kidney Tubules/chemistry ; Loop of Henle/chemistry/*metabolism ; Magnesium/blood/*metabolism ; Magnesium Deficiency/*genetics/metabolism ; Male ; Membrane Proteins/analysis/chemistry/genetics/*physiology ; Molecular Sequence Data ; Mutation ; Pedigree ; Physical Chromosome Mapping ; Tight Junctions/*metabolism
    Print ISSN: 0036-8075
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    Crystallographic evidence for preformed dimers of erythropoietin receptor before ligand activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: Erythropoietin receptor (EPOR) is thought to be activated by ligand-induced homodimerization. However, structures of agonist and antagonist peptide complexes of EPOR, as well as an EPO-EPOR complex, have shown that the actual dimer configuration is critical for the biological response and signal efficiency. The crystal structure of the extracellular domain of EPOR in its unliganded form at 2.4 angstrom resolution has revealed a dimer in which the individual membrane-spanning and intracellular domains would be too far apart to permit phosphorylation by JAK2. This unliganded EPOR dimer is formed from self-association of the same key binding site residues that interact with EPO-mimetic peptide and EPO ligands. This model for a preformed dimer on the cell surface provides insights into the organization, activation, and plasticity of recognition of hematopoietic cell surface receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Livnah, O -- Stura, E A -- Middleton, S A -- Johnson, D L -- Jolliffe, L K -- Wilson, I A -- GM49497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):987-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute of Chemical Biology, The Scripps Research Institute, 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/9974392" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane/chemistry ; Crystallography, X-Ray ; Dimerization ; Erythropoietin/metabolism ; Humans ; Hydrogen Bonding ; Janus Kinase 2 ; Ligands ; Models, Molecular ; Peptide Fragments/*chemistry/metabolism ; Peptides, Cyclic/metabolism ; Protein Conformation ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Erythropoietin/*chemistry/metabolism
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    Regulated delivery of therapeutic proteins after in vivo somatic cell gene transfer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999
    Description: Stable delivery of a therapeutic protein under pharmacologic control was achieved through in vivo somatic gene transfer. This system was based on the expression of two chimeric, human-derived proteins that were reconstituted by rapamycin into a transcription factor complex. A mixture of two adeno-associated virus vectors, one expressing the transcription factor chimeras and one containing erythropoietin (Epo) under the control of a promoter responsive to the transcription factor, was injected into skeletal muscle of immune-competent mice. Administration of rapamycin resulted in 200-fold induction of plasma Epo. Stable engraftment of this humanized system in immune-competent mice was achieved for 6 months with similar results for at least 3 months in a rhesus monkey.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, X -- Rivera, V M -- Zoltick, P -- Cerasoli, F Jr -- Schnell, M A -- Gao, G -- Hughes, J V -- Gilman, M -- Wilson, J M -- P01 AR/NS43648-03/AR/NIAMS NIH HHS/ -- P30 DK47757-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Human Gene Therapy, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics ; Dependovirus/genetics ; Erythropoietin/administration & dosage/blood/*genetics ; Female ; Gene Expression Regulation ; *Gene Transfer Techniques ; Genetic Therapy/*methods ; Genetic Vectors ; Hematocrit ; Injections, Intramuscular ; Macaca mulatta ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Muscle, Skeletal ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Recombinant Proteins ; Sirolimus/*pharmacology ; Transcription Factors/*genetics
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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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    Search for cross-species transmission of porcine endogenous retrovirus in patients treated with living pig tissue. The XEN 111 Study Group (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Pig organs may offer a solution to the shortage of human donor organs for transplantation, but concerns remain about possible cross-species transmission of porcine endogenous retrovirus (PERV). Samples were collected from 160 patients who had been treated with various living pig tissues up to 12 years earlier. Reverse transcription-polymerase chain reaction (RT-PCR) and protein immunoblot analyses were performed on serum from all 160 patients. No viremia was detected in any patient. Peripheral blood mononuclear cells from 159 of the patients were analyzed by PCR using PERV-specific primers. No PERV infection was detected in any of the patients from whom sufficient DNA was extracted to allow complete PCR analysis (97 percent of the patients). Persistent microchimerism (presence of donor cells in the recipient) was observed in 23 patients for up to 8.5 years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paradis, K -- Langford, G -- Long, Z -- Heneine, W -- Sandstrom, P -- Switzer, W M -- Chapman, L E -- Lockey, C -- Onions, D -- Otto, E -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1236-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imutran Ltd. (a Novartis Pharma AG company), Post Office Box 399, Cambridge CB2 2YP, UK. khazal.paradis@pharma.novartis.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455044" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Antibodies, Viral/blood ; Child ; Child, Preschool ; Chimera ; DNA, Viral/analysis ; Extracorporeal Circulation ; Female ; *Gammaretrovirus/genetics/immunology/isolation & purification ; Humans ; Immunoblotting ; Islets of Langerhans Transplantation ; Male ; Middle Aged ; RNA, Viral/analysis ; Retrospective Studies ; Retroviridae Infections/diagnosis/*transmission ; Reverse Transcriptase Polymerase Chain Reaction ; Skin Transplantation ; Swine ; *Transplantation, Heterologous/adverse effects ; Tumor Virus Infections/diagnosis/*transmission ; Viremia/diagnosis ; *Zoonoses
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    Sources of mathematical thinking: behavioral and brain-imaging evidence (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Does the human capacity for mathematical intuition depend on linguistic competence or on visuo-spatial representations? A series of behavioral and brain-imaging experiments provides evidence for both sources. Exact arithmetic is acquired in a language-specific format, transfers poorly to a different language or to novel facts, and recruits networks involved in word-association processes. In contrast, approximate arithmetic shows language independence, relies on a sense of numerical magnitudes, and recruits bilateral areas of the parietal lobes involved in visuo-spatial processing. Mathematical intuition may emerge from the interplay of these brain systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dehaene, S -- Spelke, E -- Pinel, P -- Stanescu, R -- Tsivkin, S -- HD23103/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 May 7;284(5416):970-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 334, Service Hospitalier Frederic Joliot, CEA/DSV, 91401 Orsay Cedex, France. dehaene@shfj.cea.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320379" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Mapping ; Evoked Potentials ; Female ; Frontal Lobe/*physiology ; Humans ; Intuition ; *Language ; Magnetic Resonance Imaging ; Male ; *Mathematics ; Parietal Lobe/*physiology ; *Thinking
    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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    Structure of the VHL-ElonginC-ElonginB complex: implications for VHL tumor suppressor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-16
    Description: Mutation of the VHL tumor suppressor is associated with the inherited von Hippel-Lindau (VHL) cancer syndrome and the majority of kidney cancers. VHL binds the ElonginC-ElonginB complex and regulates levels of hypoxia-inducible proteins. The structure of the ternary complex at 2.7 angstrom resolution shows two interfaces, one between VHL and ElonginC and another between ElonginC and ElonginB. Tumorigenic mutations frequently occur in a 35-residue domain of VHL responsible for ElonginC binding. A mutational patch on a separate domain of VHL indicates a second macromolecular binding site. The structure extends the similarities to the SCF (Skp1-Cul1-F-box protein) complex that targets proteins for degradation, supporting the hypothesis that VHL may function in an analogous pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stebbins, C E -- Kaelin, W G Jr -- Pavletich, N P -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):455-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Structural Biology, Joan and Sanford I. Weill Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10205047" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cell Cycle Proteins/chemistry/metabolism ; Cloning, Molecular ; Crystallography, X-Ray ; *Genes, Tumor Suppressor ; Humans ; Hydrogen Bonding ; *Ligases ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Mutation, Missense ; Neoplasms/genetics ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Proteins/*chemistry/genetics/metabolism ; S-Phase Kinase-Associated Proteins ; Surface Properties ; Transcription Factors/*chemistry/metabolism ; *Tumor Suppressor Proteins ; *Ubiquitin-Protein Ligases ; Von Hippel-Lindau Tumor Suppressor Protein ; von Hippel-Lindau Disease/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
    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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, J W -- Yoon, C S -- Lim, H W -- Huang, Q Q -- Kang, Y -- Pyun, K H -- Hirasawa, K -- Sherwin, R S -- Jun, H S -- DK 45735/DK/NIDDK NIH HHS/ -- DK 53015-01/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral and Immunopathogenesis of Diabetes, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada. yoon@ucalgary.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325232" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/genetics/*immunology/physiology ; Autoimmunity ; DNA, Antisense ; Diabetes Mellitus, Type 1/*enzymology/*immunology/pathology ; Female ; Gene Expression ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Insulin/blood/metabolism ; Islets of Langerhans/*enzymology/immunology/metabolism/pathology ; Islets of Langerhans Transplantation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; T-Lymphocytes/immunology ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Abnormal morphogenesis but intact IKK activation in mice lacking the IKKalpha subunit of IkappaB kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The oligomeric IkappaB kinase (IKK) is composed of three polypeptides: IKKalpha and IKKbeta, the catalytic subunits, and IKKgamma, a regulatory subunit. IKKalpha and IKKbeta are similar in structure and thought to have similar function-phosphorylation of the IkappaB inhibitors in response to proinflammatory stimuli. Such phosphorylation leads to degradation of IkappaB and activation of nuclear factor kappaB transcription factors. The physiological function of these protein kinases was explored by analysis of IKKalpha-deficient mice. IKKalpha was not required for activation of IKK and degradation of IkappaB by proinflammatory stimuli. Instead, loss of IKKalpha interfered with multiple morphogenetic events, including limb and skeletal patterning and proliferation and differentiation of epidermal keratinocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Y -- Baud, V -- Delhase, M -- Zhang, P -- Deerinck, T -- Ellisman, M -- Johnson, R -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- RR04050/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):316-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Cancer Center, University of California San Diego, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195896" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/enzymology/genetics ; Animals ; Apoptosis ; Body Patterning ; Bone and Bones/abnormalities/embryology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Dimerization ; *Embryonic and Fetal Development ; Enzyme Activation ; Epidermis/cytology/embryology ; Female ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Keratinocytes ; Limb Deformities, Congenital/enzymology ; Male ; Mice ; *Morphogenesis ; Mutation ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Skin/embryology ; Skin Abnormalities/enzymology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecular architecture of the rotary motor in ATP synthase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Adenosine triphosphate (ATP) synthase contains a rotary motor involved in biological energy conversion. Its membrane-embedded F0 sector has a rotation generator fueled by the proton-motive force, which provides the energy required for the synthesis of ATP by the F1 domain. An electron density map obtained from crystals of a subcomplex of yeast mitochondrial ATP synthase shows a ring of 10 c subunits. Each c subunit forms an alpha-helical hairpin. The interhelical loops of six to seven of the c subunits are in close contact with the gamma and delta subunits of the central stalk. The extensive contact between the c ring and the stalk suggests that they may rotate as an ensemble during catalysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stock, D -- Leslie, A G -- Walker, J E -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1700-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576729" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Catalysis ; Crystallization ; Crystallography, X-Ray ; Hydrogen Bonding ; Mitochondria/enzymology ; Models, Molecular ; Molecular Motor Proteins/*chemistry/metabolism ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Proton-Motive Force ; Proton-Translocating ATPases/*chemistry/metabolism ; Protons ; Saccharomyces cerevisiae/enzymology
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    Communication goes multimodal (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Partan, S -- Marler, P -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1272-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Animal Behavior, University of California, Davis, CA 95616, USA. srpartan@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10084931" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; *Communication ; Cues ; Facial Expression ; Female ; Humans ; Male ; Pheromones/physiology ; Speech Perception ; Vocalization, Animal
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    X-ray crystallographic structure of the Norwalk virus capsid (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Norwalk virus, a noncultivatable human calicivirus, is the major cause of epidemic gastroenteritis in humans. The first x-ray structure of a calicivirus capsid, which consists of 180 copies of a single protein, has been determined by phase extension from a low-resolution electron microscopy structure. The capsid protein has a protruding (P) domain connected by a flexible hinge to a shell (S) domain that has a classical eight-stranded beta-sandwich motif. The structure of the P domain is unlike that of any other viral protein with a subdomain exhibiting a fold similar to that of the second domain in the eukaryotic translation elongation factor-Tu. This subdomain, located at the exterior of the capsid, has the largest sequence variation among Norwalk-like human caliciviruses and is likely to contain the determinants of strain specificity and cell binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prasad, B V -- Hardy, M E -- Dokland, T -- Bella, J -- Rossmann, M G -- Estes, M K -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):287-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs Mclean Department of Biochemistry, Division of Molecular Virology, Baylor College of Medicine, Houston, TX 77030, USA. bprasad@bcm.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514371" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Capsid/*chemistry/metabolism ; *Capsid Proteins ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Dimerization ; Genome, Viral ; Humans ; Hydrogen Bonding ; Image Processing, Computer-Assisted ; Models, Molecular ; Molecular Sequence Data ; Norwalk virus/*chemistry/genetics/physiology ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Recombinant Proteins/chemistry ; Virus Assembly
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    Chemical etiology of nucleic acid structure (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-06-26
    Description: Systematic chemical studies indicate that the capability of Watson-Crick base-pairing is widespread among potentially natural nucleic acid alternatives taken from RNA's close structural neighborhood. A comparison of RNA and such alternatives with regard to chemical properties that are fundamental to the biological function of RNA provides chemical facts that may contain clues to RNA's origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eschenmoser, A -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2118-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology at The Scripps Research Institute (TSRI), 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/10381870" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Pairing ; DNA/chemistry ; *Evolution, Chemical ; Isomerism ; Models, Molecular ; Nucleic Acid Conformation ; Oligonucleotides/*chemistry ; RNA/*chemistry ; Structure-Activity Relationship ; Templates, Genetic
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    Structural maturation of neural pathways in children and adolescents: in vivo study (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-03-19
    Description: Structural maturation of fiber tracts in the human brain, including an increase in the diameter and myelination of axons, may play a role in cognitive development during childhood and adolescence. A computational analysis of structural magnetic resonance images obtained in 111 children and adolescents revealed age-related increases in white matter density in fiber tracts constituting putative corticospinal and frontotemporal pathways. The maturation of the corticospinal tract was bilateral, whereas that of the frontotemporal pathway was found predominantly in the left (speech-dominant) hemisphere. These findings provide evidence for a gradual maturation, during late childhood and adolescence, of fiber pathways presumably supporting motor and speech functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paus, T -- Zijdenbos, A -- Worsley, K -- Collins, D L -- Blumenthal, J -- Giedd, J N -- Rapoport, J L -- Evans, A C -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1908-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, Quebec H3A 2B4, Canada. tomas@bic.mni.mcgill.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082463" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; *Aging ; Axons/physiology/ultrastructure ; Brain/anatomy & histology/*growth & development ; Brain Mapping ; Child ; Child, Preschool ; Female ; Frontal Lobe/anatomy & histology/growth & development ; Humans ; Magnetic Resonance Imaging ; Male ; Motor Skills ; Myelin Sheath/ultrastructure ; Nerve Fibers/ultrastructure ; Neural Conduction ; Neural Pathways/anatomy & histology/*growth & development ; Regression Analysis ; Speech ; Spinal Cord/anatomy & histology ; Synaptic Transmission ; Temporal Lobe/anatomy & histology/growth & development
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    Real-time tracking of memory formation in the human rhinal cortex and hippocampus (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-09-08
    Description: A fundamental question about human memory is which brain structures are involved, and when, in transforming experiences into memories. This experiment sought to identify neural correlates of memory formation with the use of intracerebral electrodes implanted in the brains of patients with temporal lobe epilepsy. Event-related potentials (ERPs) were recorded directly from the medial temporal lobe (MTL) as the patients studied single words. ERPs elicited by words subsequently recalled in a memory test were contrasted with ERPs elicited by unrecalled words. Memory formation was associated with distinct but interrelated ERP differences within the rhinal cortex and the hippocampus, which arose after about 300 and 500 milliseconds, respectively. These findings suggest that declarative memory formation is dissociable into subprocesses and sequentially organized within the MTL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, G -- Effern, A -- Grunwald, T -- Pezer, N -- Lehnertz, K -- Dumpelmann, M -- Van Roost, D -- Elger, C E -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Epileptology, University of Bonn, 53105 Bonn, Germany. gf@mailer.meb.uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477525" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Analysis of Variance ; Brain Mapping ; Electrodes, Implanted ; Epilepsy, Temporal Lobe/physiopathology ; Evoked Potentials ; Female ; Hippocampus/*physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Middle Aged ; Neurons/physiology ; Temporal Lobe/*physiology ; Time Factors
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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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    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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    Sex in an age of mechanical reproduction (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djerassi, C -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):53-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, Stanford, CA 94305-5080, USA. djerassi@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428703" target="_blank"〉PubMed〈/a〉
    Keywords: *Bioethics ; Female ; *Fertilization in Vitro ; Humans ; Male ; Posthumous Conception ; *Reproductive Techniques
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    RNA, whither goest thou? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tiedge, H -- Bloom, F E -- Richter, D -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):186-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, State Univeristy of New York Health Science Center at Brooklyn, Brooklyn, NY 11203, USA. tiedge@hscbklyn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Biological Transport ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dendrites/*metabolism ; Gene Expression Regulation ; *Neuronal Plasticity ; Protein Biosynthesis ; RNA, Messenger/chemistry/genetics/*metabolism ; Ribonucleoproteins/metabolism ; Signal Transduction ; Synapses/metabolism/*physiology
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    Key molecular signals identified in plants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206881" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/*genetics/growth & development/metabolism ; *Arabidopsis Proteins ; *Genes, Plant ; Ligands ; Meristem/growth & development ; Phosphotransferases/genetics/metabolism ; Plant Proteins/chemistry/*genetics/metabolism/physiology ; Signal Transduction
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    Rapid infection of oral mucosal-associated lymphoid tissue with simian immunodeficiency virus (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-08-24
    Description: The early events during infection with an immunodeficiency virus were followed by application of pathogenic simian immunodeficiency virus atraumatically to the tonsils of macaques. Analyses by virologic assays and in situ hybridization revealed that the infection started locally in the tonsils, a mucosal-associated lymphoid organ, and quickly spread to other lymphoid tissues. At day 3, there were few infected cells, but then the number increased rapidly, reaching a high plateau between days 4 and 7. The infection was not detected in the dendritic cell-rich squamous epithelium to which the virus was applied; instead, it was primarily in CD4+ tonsillar T cells, close to the specialized antigen-transporting epithelium of the tonsillar crypts. Transport of the virus and immune-activating stimuli across this epithelium would allow mucosal lymphoid tissue to function in the atraumatic transmission of immunodeficiency viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stahl-Hennig, C -- Steinman, R M -- Tenner-Racz, K -- Pope, M -- Stolte, N -- Matz-Rensing, K -- Grobschupff, G -- Raschdorff, B -- Hunsmann, G -- Racz, P -- AI 40874/AI/NIAID NIH HHS/ -- AI 40877/AI/NIAID NIH HHS/ -- AI 42129/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1261-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉German Primate Center, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/virology ; Epithelium/virology ; Female ; In Situ Hybridization ; Leukocytes, Mononuclear/virology ; Lymph Nodes/virology ; Lymphoid Tissue/*virology ; Macaca mulatta ; Male ; Mouth Mucosa/*virology ; Palatine Tonsil/*virology ; Simian Acquired Immunodeficiency Syndrome/transmission/*virology ; Simian Immunodeficiency Virus/*physiology ; Viral Load ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    The rotary enzyme of the cell: the rotation of F1-ATPase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noji, H -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1844-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉"Genetic Programming" Team 13, Teikyo Unmiversity Biotechnology Center, Nogawa, Kawasaki, Japan. noji@phys.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874637" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/metabolism ; Adenosine Triphosphate/metabolism ; *Awards and Prizes ; *Biochemistry/history ; Catalytic Domain ; History, 20th Century ; Japan ; Microscopy, Fluorescence ; Models, Molecular ; Protein Conformation ; Protein Structure, Secondary ; Proton-Translocating ATPases/*chemistry/*metabolism ; Protons ; Thermodynamics
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    Requirement of circadian genes for cocaine sensitization in Drosophila (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: The circadian clock consists of a feedback loop in which clock genes are rhythmically expressed, giving rise to cycling levels of RNA and proteins. Four of the five circadian genes identified to date influence responsiveness to freebase cocaine in the fruit fly, Drosophila melanogaster. Sensitization to repeated cocaine exposures, a phenomenon also seen in humans and animal models and associated with enhanced drug craving, is eliminated in flies mutant for period, clock, cycle, and doubletime, but not in flies lacking the gene timeless. Flies that do not sensitize owing to lack of these genes do not show the induction of tyrosine decarboxylase normally seen after cocaine exposure. These findings indicate unexpected roles for these genes in regulating cocaine sensitization and indicate that they function as regulators of tyrosine decarboxylase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andretic, R -- Chaney, S -- Hirsh, J -- DA05942/DA/NIDA NIH HHS/ -- GM/DA 27318/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1066-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Gilmer Hall, University of Virginia, Charlottesville, VA 22903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10446052" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Behavior, Animal/drug effects ; Biological Clocks/genetics ; CLOCK Proteins ; *Casein Kinase Iepsilon ; Circadian Rhythm/*genetics ; Cocaine/*pharmacology ; Dopamine Agonists/pharmacology ; *Drosophila Proteins ; Drosophila melanogaster/*drug effects/genetics/physiology ; *Genes, Insect ; Insect Proteins/genetics/physiology ; Male ; Motor Activity/drug effects ; Mutation ; Nuclear Proteins/*genetics/physiology ; Period Circadian Proteins ; Protein Kinases/genetics/physiology ; Quinpirole/pharmacology ; Receptors, Dopamine D2/agonists/physiology ; Trans-Activators/genetics/physiology ; Transcription Factors/genetics ; Tyramine/metabolism/pharmacology ; Tyrosine Decarboxylase/metabolism
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    Genetics of mouse behavior: interactions with laboratory environment (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-06-05
    Description: Strains of mice that show characteristic patterns of behavior are critical for research in neurobehavioral genetics. Possible confounding influences of the laboratory environment were studied in several inbred strains and one null mutant by simultaneous testing in three laboratories on a battery of six behaviors. Apparatus, test protocols, and many environmental variables were rigorously equated. Strains differed markedly in all behaviors, and despite standardization, there were systematic differences in behavior across labs. For some tests, the magnitude of genetic differences depended upon the specific testing lab. Thus, experiments characterizing mutants may yield results that are idiosyncratic to a particular laboratory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, J C -- Wahlsten, D -- Dudek, B C -- AA00170/AA/NIAAA NIH HHS/ -- AA10760/AA/NIAAA NIH HHS/ -- DA10731/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1670-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Portland Alcohol Research Center, Department of Veterans Affairs Medical Center, Portland, OR 97201, USA. crabbe@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10356397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory/genetics ; Anxiety ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Drinking Behavior ; *Environment ; Female ; Genetics, Behavioral/*methods ; Genotype ; Male ; Mice ; Mice, Inbred Strains/genetics ; Mice, Mutant Strains/genetics ; Motor Activity ; Psychological Tests ; Reproducibility of Results
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    Gene expression profile of aging and its retardation by caloric restriction (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-08-28
    Description: The gene expression profile of the aging process was analyzed in skeletal muscle of mice. Use of high-density oligonucleotide arrays representing 6347 genes revealed that aging resulted in a differential gene expression pattern indicative of a marked stress response and lower expression of metabolic and biosynthetic genes. Most alterations were either completely or partially prevented by caloric restriction, the only intervention known to retard aging in mammals. Transcriptional patterns of calorie-restricted animals suggest that caloric restriction retards the aging process by causing a metabolic shift toward increased protein turnover and decreased macromolecular damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, C K -- Klopp, R G -- Weindruch, R -- Prolla, T A -- P01 AG11915/AG/NIA NIH HHS/ -- R01 CA78723/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1390-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Environmental Toxicology Center, Institute on Aging, Department of Genetics, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464095" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; DNA Damage/genetics ; DNA Repair/genetics ; *Diet ; *Energy Intake ; Energy Metabolism/genetics ; *Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Muscle/metabolism ; Muscle, Skeletal/innervation/*metabolism ; Oligonucleotide Array Sequence Analysis ; Oxidative Stress/genetics ; Proteins/metabolism ; RNA, Messenger/genetics/metabolism
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    An allele of COL9A2 associated with intervertebral disc disease (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-20
    Description: Intervertebral disc disease is one of the most common musculoskeletal disorders. A number of environmental and anthropometric risk factors may contribute to it, and recent reports have suggested the importance of genetic factors as well. The COL9A2 gene, which codes for one of the polypeptide chains of collagen IX that is expressed in the intervertebral disc, was screened for sequence variations in individuals with intervertebral disc disease. The analysis identified a putative disease-causing sequence variation that converted a codon for glutamine to one for tryptophan in six out of the 157 individuals but in none of 174 controls. The tryptophan allele cosegregated with the disease phenotype in the four families studied, giving a lod score (logarithm of odds ratio) for linkage of 4.5, and subsequent linkage disequilibrium analysis conditional on linkage gave an additional lod score of 7.1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Annunen, S -- Paassilta, P -- Lohiniva, J -- Perala, M -- Pihlajamaa, T -- Karppinen, J -- Tervonen, O -- Kroger, H -- Lahde, S -- Vanharanta, H -- Ryhanen, L -- Goring, H H -- Ott, J -- Prockop, D J -- Ala-Kokko, L -- AR39740/AR/NIAMS NIH HHS/ -- HG00008/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):409-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Collagen Research Unit, Biocenter and Department of Medical Biochemistry, University of Oulu, 90220 Oulu, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10411504" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Alleles ; Amino Acid Substitution ; Case-Control Studies ; Codon ; Collagen/chemistry/*genetics ; *Collagen Type IX ; Female ; Genetic Linkage ; *Genetic Predisposition to Disease ; Humans ; Intervertebral Disc Displacement/*genetics ; Linkage Disequilibrium ; Male ; Middle Aged ; Mutation ; Penetrance ; Polymorphism, Genetic ; Sciatica/*genetics ; Tryptophan/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Crystal structure of the ectodomain of human transferrin receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: The transferrin receptor (TfR) undergoes multiple rounds of clathrin-mediated endocytosis and reemergence at the cell surface, importing iron-loaded transferrin (Tf) and recycling apotransferrin after discharge of iron in the endosome. The crystal structure of the dimeric ectodomain of the human TfR, determined here to 3.2 angstroms resolution, reveals a three-domain subunit. One domain closely resembles carboxy- and aminopeptidases, and features of membrane glutamate carboxypeptidase can be deduced from the TfR structure. A model is proposed for Tf binding to the receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrence, C M -- Ray, S -- Babyonyshev, M -- Galluser, R -- Borhani, D W -- Harrison, S C -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Children's Hospital Laboratory of Molecular Medicine, 320 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531064" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CHO Cells ; Carboxypeptidases/chemistry ; Cell Membrane/chemistry ; Conserved Sequence ; Cricetinae ; Crystallography, X-Ray ; Dimerization ; Ferric Compounds/metabolism ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Transferrin/*chemistry/metabolism ; Transferrin/metabolism
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    Discovery of 'gay gene' questioned (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):571.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328731" target="_blank"〉PubMed〈/a〉
    Keywords: *Genetic Linkage ; Homosexuality, Male/*genetics ; Humans ; Male ; *Microsatellite Repeats ; Nuclear Family ; Research Design ; X Chromosome/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Evolutionarily conserved pathways of energetic connectivity in protein families (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: For mapping energetic interactions in proteins, a technique was developed that uses evolutionary data for a protein family to measure statistical interactions between amino acid positions. For the PDZ domain family, this analysis predicted a set of energetically coupled positions for a binding site residue that includes unexpected long-range interactions. Mutational studies confirm these predictions, demonstrating that the statistical energy function is a good indicator of thermodynamic coupling in proteins. Sets of interacting residues form connected pathways through the protein fold that may be the basis for efficient energy conduction within proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lockless, S W -- Ranganathan, R -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):295-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514373" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/chemistry/metabolism ; Binding Sites ; Conserved Sequence ; *Evolution, Molecular ; Models, Molecular ; Mutation ; Probability ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Tertiary ; Proteins/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment ; Statistics as Topic ; Thermodynamics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    PEG antibodies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorsky, R -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites, Antibody ; Biological Availability ; Half-Life ; Immunoglobulin Fab Fragments/*immunology/*metabolism ; Male ; Polyethylene Glycols/*metabolism ; Rats ; Rats, Wistar
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    Structure of an E6AP-UbcH7 complex: insights into ubiquitination by the E2-E3 enzyme cascade (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: The E6AP ubiquitin-protein ligase (E3) mediates the human papillomavirus-induced degradation of the p53 tumor suppressor in cervical cancer and is mutated in Angelman syndrome, a neurological disorder. The crystal structure of the catalytic hect domain of E6AP reveals a bilobal structure with a broad catalytic cleft at the junction of the two lobes. The cleft consists of conserved residues whose mutation interferes with ubiquitin-thioester bond formation and is the site of Angelman syndrome mutations. The crystal structure of the E6AP hect domain bound to the UbcH7 ubiquitin-conjugating enzyme (E2) reveals the determinants of E2-E3 specificity and provides insights into the transfer of ubiquitin from the E2 to the E3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, L -- Kinnucan, E -- Wang, G -- Beaudenon, S -- Howley, P M -- Huibregtse, J M -- Pavletich, N P -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1321-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cellular Biochemistry and Biophysics Program, Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558980" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angelman Syndrome/genetics ; Binding Sites ; Catalytic Domain ; Conserved Sequence ; Crystallography, X-Ray ; Cysteine/chemistry ; Humans ; Ligases/*chemistry/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Structure, Secondary ; Substrate Specificity ; Ubiquitin-Conjugating Enzymes ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The structural era of endocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: Endocytosis is crucial for an array of cellular functions and can occur through several distinct mechanisms with the capacity to internalize anything from small molecules to entire cells. The clathrin-mediated endocytic pathway has recently received considerable attention because of (i) the identification of an array of molecules that orchestrate the assembly of clathrin-coated vesicles and the selection of the vesicle cargo and (ii) the resolution of structures for a number of these proteins. Together, these data provide an initial three-dimensional framework for understanding the clathrin endocytic machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, M -- McMahon, H T -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):215-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK. m.marsh@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Calcium-Binding Proteins/chemistry/physiology ; Cell Membrane/ultrastructure ; Clathrin/chemistry/*physiology ; Coated Pits, Cell-Membrane/physiology/ultrastructure ; Coated Vesicles/physiology/ultrastructure ; Dynamins ; *Endocytosis ; GTP Phosphohydrolases/chemistry/physiology ; Membrane Proteins/chemistry/physiology ; Nerve Tissue Proteins/chemistry/physiology ; Phosphoproteins/chemistry/physiology ; Signal Transduction
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    Regulation of neurotrophin-3 expression by epithelial-mesenchymal interactions: the role of Wnt factors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: Neurotrophins regulate survival, axonal growth, and target innervation of sensory and other neurons. Neurotrophin-3 (NT-3) is expressed specifically in cells adjacent to extending axons of dorsal root ganglia neurons, and its absence results in loss of most of these neurons before their axons reach their targets. However, axons are not required for NT-3 expression in limbs; instead, local signals from ectoderm induce NT-3 expression in adjacent mesenchyme. Wnt factors expressed in limb ectoderm induce NT-3 in the underlying mesenchyme. Thus, epithelial-mesenchymal interactions mediated by Wnt factors control NT-3 expression and may regulate axonal growth and guidance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710127/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710127/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patapoutian, A -- Backus, C -- Kispert, A -- Reichardt, L F -- MH48200/MH/NIMH NIH HHS/ -- P01 NS016033/NS/NINDS NIH HHS/ -- P01 NS016033-190014/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1180-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143-0723, USA. ardem@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024246" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Coculture Techniques ; Ectoderm/metabolism/*physiology ; Embryo, Mammalian/metabolism ; Epithelium/metabolism ; Extremities/embryology/innervation ; Ganglia, Spinal/physiology ; *Gene Expression Regulation, Developmental ; *Glycoproteins ; Mesoderm/*metabolism ; Mice ; Motor Neurons/physiology ; Nerve Growth Factors/biosynthesis/*genetics ; Neurons, Afferent/physiology ; Neurotrophin 3 ; Organ Culture Techniques ; Proto-Oncogene Proteins/*physiology ; Signal Transduction ; Wnt Proteins ; Wnt4 Protein
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    Structural analysis of the mechanism of adenovirus binding to its human cellular receptor, CAR (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Binding of virus particles to specific host cell surface receptors is known to be an obligatory step in infection even though the molecular basis for these interactions is not well characterized. The crystal structure of the adenovirus fiber knob domain in complex with domain I of its human cellular receptor, coxsackie and adenovirus receptor (CAR), is presented here. Surface-exposed loops on knob contact one face of CAR, forming a high-affinity complex. Topology mismatches between interacting surfaces create interfacial solvent-filled cavities and channels that may be targets for antiviral drug therapy. The structure identifies key determinants of binding specificity, which may suggest ways to modify the tropism of adenovirus-based gene therapy vectors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bewley, M C -- Springer, K -- Zhang, Y B -- Freimuth, P -- Flanagan, J M -- 1P41 RR12408-01A1/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1579-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, Brookhaven National Laboratory, Upton, NY 11973, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567268" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/chemistry/*metabolism ; Amino Acid Substitution ; Binding Sites ; Capsid/*chemistry/*metabolism ; *Capsid Proteins ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Crystallization ; Crystallography, X-Ray ; Hydrogen Bonding ; Models, Molecular ; Mutagenesis ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Virus/*chemistry/*metabolism ; Recombinant Proteins/chemistry/metabolism ; Thermodynamics
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    BRCA1 inhibition of estrogen receptor signaling in transfected cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, S -- Wang, J -- Yuan, R -- Ma, Y -- Meng, Q -- Erdos, M R -- Pestell, R G -- Yuan, F -- Auborn, K J -- Goldberg, I D -- Rosen, E M -- R01-CA75503/CA/NCI NIH HHS/ -- R01-ES09169/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, 270-05 76th Avenue, New Hyde Park, NY 11040, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334989" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*physiology ; Breast/cytology ; Breast Neoplasms/etiology ; Cell Division ; Enhancer Elements, Genetic ; Epithelial Cells/cytology ; Estradiol/metabolism ; Estrogen Receptor alpha ; Female ; Genes, BRCA1 ; Genes, Reporter ; Humans ; Ligands ; Male ; Receptors, Estrogen/*metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    Effects of angiogenesis inhibitors on multistage carcinogenesis in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: Solid tumors depend on angiogenesis for their growth. In a transgenic mouse model of pancreatic islet cell carcinogenesis (RIP1-Tag2), an angiogenic switch occurs in premalignant lesions, and angiogenesis persists during progression to expansive solid tumors and invasive carcinomas. RIP1-Tag2 mice were treated so as to compare the effects of four angiogenesis inhibitors at three distinct stages of disease progression. AGM-1470, angiostatin, BB-94, and endostatin each produced distinct efficacy profiles in trials aimed at preventing the angiogenic switch in premalignant lesions, intervening in the rapid expansion of small tumors, or inducing the regression of large end-stage cancers. Thus, anti-angiogenic drugs may prove most efficacious when they are targeted to specific stages of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bergers, G -- Javaherian, K -- Lo, K M -- Folkman, J -- Hanahan, D -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics and Hormone Research Institute, University of California, San Francisco, 513 Parnassus Ave, San Francisco, CA 94143-0534, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221914" target="_blank"〉PubMed〈/a〉
    Keywords: Angiostatins ; Animals ; Anticarcinogenic Agents/pharmacology ; Antineoplastic Agents/*pharmacology ; Apoptosis ; Carcinoma, Islet Cell/blood supply/*drug therapy/pathology/prevention & control ; Collagen/pharmacology ; Cyclohexanes ; Disease Progression ; Drug Evaluation, Preclinical ; Endostatins ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasm Staging ; Neovascularization, Pathologic/*prevention & control ; Pancreatic Neoplasms/blood supply/*drug therapy/pathology/prevention & control ; Peptide Fragments/pharmacology ; Phenylalanine/analogs & derivatives/pharmacology ; Plasminogen/pharmacology ; Sesquiterpenes/pharmacology ; Thiophenes/pharmacology
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    Impaired immunoproteasome assembly and immune responses in PA28-/- mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: In vitro PA28 binds and activates proteasomes. It is shown here that mice with a disrupted PA28b gene lack PA28a and PA28b polypeptides, demonstrating that PA28 functions as a hetero-oligomer in vivo. Processing of antigenic epitopes derived from exogenous or endogenous antigens is altered in PA28-/- mice. Cytotoxic T lymphocyte responses are impaired, and assembly of immunoproteasomes is greatly inhibited in mice lacking PA28. These results show that PA28 is necessary for immunoproteasome assembly and is required for efficient antigen processing, thus demonstrating the importance of PA28-mediated proteasome function in immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preckel, T -- Fung-Leung, W P -- Cai, Z -- Vitiello, A -- Salter-Cid, L -- Winqvist, O -- Wolfe, T G -- Von Herrath, M -- Angulo, A -- Ghazal, P -- Lee, J D -- Fourie, A M -- Wu, Y -- Pang, J -- Ngo, K -- Peterson, P A -- Fruh, K -- Yang, Y -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2162-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The R. W. Johnson Pharmaceutical Research Institute, 3210 Merryfield Row, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Autoantigens ; Cysteine Endopeptidases/chemistry/*metabolism ; Enzyme Activators/*metabolism ; Epitopes, T-Lymphocyte/immunology ; Female ; H-Y Antigen/immunology ; Herpesviridae Infections/immunology ; Histocompatibility Antigens Class I/immunology/metabolism ; Interferons/pharmacology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/immunology ; Male ; Mice ; Multienzyme Complexes/chemistry/*metabolism ; Muromegalovirus/immunology ; Ovalbumin/immunology ; Peptide Fragments/immunology ; Proteasome Endopeptidase Complex ; Proteins/genetics/*metabolism ; T-Lymphocytes, Cytotoxic/*immunology
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    Can mitochondrial clocks keep time? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1435, 1437-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/*genetics ; *Evolution, Molecular ; Female ; Fossils ; Humans ; Male ; Mutation ; Ovum ; *Paleontology ; Recombination, Genetic ; Spermatozoa ; Statistics as Topic
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  • 83
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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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  • 84
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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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  • 85
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    Uses and abuses of Tuskegee (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fairchild, A L -- Bayer, R -- New York, N.Y. -- Science. 1999 May 7;284(5416):919-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in the History of Public Health and Medicine, Division of Sociomedical Sciences, The Joseph L. Mailman School of Public Health, Columbia University, New York, NY 10032-2625, USA. alf4@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10357678" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/history ; Alabama ; Anonymous Testing ; Anti-HIV Agents/*therapeutic use ; Clinical Trials as Topic ; Developing Countries ; Disclosure ; Ethics, Medical ; Female ; HIV Infections/prevention & control/*transmission ; *HIV Seroprevalence ; History, 20th Century ; *Human Experimentation/history ; Humans ; Infectious Disease Transmission, Vertical/*prevention & control ; Informed Consent/history ; Male ; *Needle-Exchange Programs ; *Persons ; Pregnant Women ; Syphilis/history ; *Trust ; United States ; *Vulnerable Populations ; Withholding Treatment
    Print ISSN: 0036-8075
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  • 86
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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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  • 87
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    Structural changes in bacteriorhodopsin during ion transport at 2 angstrom resolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Crystal structures of the Asp96 to Asn mutant of the light-driven proton pump bacteriorhodopsin and its M photointermediate produced by illumination at ambient temperature have been determined to 1.8 and 2.0 angstroms resolution, respectively. The trapped photoproduct corresponds to the late M state in the transport cycle-that is, after proton transfer to Asp85 and release of a proton to the extracellular membrane surface, but before reprotonation of the deprotonated retinal Schiff base. Its density map describes displacements of side chains near the retinal induced by its photoisomerization to 13-cis,15-anti and an extensive rearrangement of the three-dimensional network of hydrogen-bonded residues and bound water that accounts for the changed pKa values (where Ka is the acid constant) of the Schiff base and Asp85. The structural changes detected suggest the means for conserving energy at the active site and for ensuring the directionality of proton translocation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luecke, H -- Schobert, B -- Richter, H T -- Cartailler, J P -- Lanyi, J K -- R01-GM29498/GM/NIGMS NIH HHS/ -- R01-GM56445/GM/NIGMS NIH HHS/ -- R01-GM59970/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):255-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA. hudel@uci.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514362" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriorhodopsins/*chemistry/*metabolism ; Binding Sites ; Crystallography, X-Ray ; Cytoplasm/chemistry ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Ion Transport ; Isomerism ; Light ; Models, Molecular ; Photolysis ; Photons ; Point Mutation ; Protein Conformation ; Protein Structure, Secondary ; Proton Pumps/*chemistry/*metabolism ; Protons ; Retinaldehyde/chemistry/metabolism ; Schiff Bases ; Thermodynamics ; Water
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  • 88
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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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  • 89
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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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  • 90
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    Two-metal-Ion catalysis in adenylyl cyclase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Adenylyl cyclase (AC) converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate, a ubiquitous second messenger that regulates many cellular functions. Recent structural studies have revealed much about the structure and function of mammalian AC but have not fully defined its active site or catalytic mechanism. Four crystal structures were determined of the catalytic domains of AC in complex with two different ATP analogs and various divalent metal ions. These structures provide a model for the enzyme-substrate complex and conclusively demonstrate that two metal ions bind in the active site. The similarity of the active site of AC to those of DNA polymerases suggests that the enzymes catalyze phosphoryl transfer by the same two-metal-ion mechanism and likely have evolved from a common ancestor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tesmer, J J -- Sunahara, R K -- Johnson, R A -- Gosselin, G -- Gilman, A G -- Sprang, S R -- DK38828/DK/NIDDK NIH HHS/ -- DK46371/DK/NIDDK NIH HHS/ -- GM34497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):756-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427002" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/chemistry/genetics/*metabolism ; Animals ; Aspartic Acid/metabolism ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Deoxyadenine Nucleotides/metabolism/pharmacology ; Dideoxynucleotides ; Dimerization ; Enzyme Inhibitors/metabolism ; Hydrogen Bonding ; Ligands ; Magnesium/*metabolism ; Manganese/*metabolism ; Models, Molecular ; Mutation ; Protein Conformation ; Protein Folding ; Rats ; Thionucleotides/metabolism/pharmacology ; Zinc/*metabolism
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  • 91
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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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    Research risks. California probes prison teens study (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1337-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490403" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; California ; Clinical Trials as Topic/legislation & jurisprudence/*standards ; Conduct Disorder/*drug therapy ; Ethics Committees, Research ; Government Regulation ; Human Experimentation/legislation & jurisprudence ; Humans ; Male ; Nontherapeutic Human Experimentation ; Placebos ; *Prisoners/legislation & jurisprudence ; Therapeutic Human Experimentation ; Valproic Acid/*administration & dosage/therapeutic use ; Violence
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  • 93
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    Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holash, J -- Maisonpierre, P C -- Compton, D -- Boland, P -- Alexander, C R -- Zagzag, D -- Yancopoulos, G D -- Wiegand, S J -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1994-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/blood supply/pathology ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/pathology ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/pathology/physiology ; Glioblastoma/blood supply/pathology ; Glioma/blood supply/pathology ; In Situ Hybridization ; Lymphokines/genetics/*physiology ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/pathology/physiology ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*pathology ; *Neovascularization, Pathologic ; Proteins/genetics/*physiology ; Rats ; Rats, Sprague-Dawley ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    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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    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
    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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  • 95
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    Tired old cliches? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soule, H R -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):261.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232971" target="_blank"〉PubMed〈/a〉
    Keywords: Commerce ; *Foundations ; Humans ; Male ; Prostatic Neoplasms/*therapy ; *Research
    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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    The race to the ribosome structure (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2048-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523195" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/chemistry ; Cryoelectron Microscopy ; Crystallization ; Crystallography, X-Ray ; Image Processing, Computer-Assisted ; Models, Molecular ; Nucleic Acid Conformation ; Protein Conformation ; RNA, Bacterial/chemistry/metabolism ; RNA, Messenger/chemistry/metabolism ; RNA, Ribosomal/chemistry ; RNA, Transfer/chemistry/metabolism ; Ribosomal Proteins/chemistry ; Ribosomes/*chemistry/*ultrastructure
    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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  • 97
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    Genetic variation in susceptibility to endocrine disruption by estrogen in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Large (more than 16-fold) differences in susceptibility to disruption of juvenile male reproductive development by 17beta-estradiol (E2) were detected between strains of mice. Effects of strain, E2 dose, and the interaction of strain and E2 dose on testes weight and spermatogenesis were all highly significant (P 〈 0.0001). Spermatid maturation was eliminated by low doses of E2 in strains such as C57BL/6J and C17/Jls. In contrast, mice of the widely used CD-1 line, which has been selected for large litter size, showed little or no inhibition of spermatid maturation even in response to 16 times as much E2. Product safety bioassays conducted with animals selected for fecundity may greatly underestimate disruption of male reproductive development by estradiol and environmental estrogenic compounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spearow, J L -- Doemeny, P -- Sera, R -- Leffler, R -- Barkley, M -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1259-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Physiology and Behavior, University of California at Davis, Davis, CA 95616, USA. jlspearow@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/drug effects ; Dose-Response Relationship, Drug ; Estradiol/*pharmacology/toxicity ; *Genetic Variation ; Litter Size ; Male ; Mice ; Mice, Inbred Strains ; Organ Size/drug effects ; Species Specificity ; Spermatids/drug effects ; Spermatogenesis/*drug effects ; Testis/anatomy & histology/*drug effects ; Toxicity Tests
    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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    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
    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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    Ribosome finally begins to yield its complete structure (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1343.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490407" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallography, X-Ray ; Haloarcula marismortui/ultrastructure ; Models, Molecular ; Neutrons ; Nucleic Acid Conformation ; Protein Conformation ; RNA, Ribosomal/*chemistry ; Ribosomal Proteins/*chemistry ; Ribosomes/*chemistry/*ultrastructure ; Scattering, Radiation ; Thermus thermophilus/ultrastructure
    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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    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
    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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