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  • Base Sequence  (382)
  • Rats  (326)
  • American Association for the Advancement of Science (AAAS)  (688)
  • American Institute of Physics (AIP)
  • 1995-1999  (688)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (688)
  • American Institute of Physics (AIP)
  • Springer  (12)
  • Wiley-Blackwell  (1)
Years
Year
  • 1
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    Neurons and silicon get intimate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):578-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Electrodes ; Electrodes, Implanted ; *Electronics ; Electrophysiology ; Humans ; Nerve Net/*physiology ; Nervous System Diseases/*therapy ; Neurons/*physiology ; Rats ; Silicon ; *Transistors, Electronic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Stem cells. Rat spinal cord function partially restored (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1826-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Cell Differentiation ; Cell Survival ; Embryo, Mammalian ; Mice ; Neurons/cytology ; Oligodendroglia/cytology ; Rats ; Spinal Cord/cytology/*physiology ; Spinal Cord Injuries/*therapy ; *Stem Cell Transplantation ; Stem Cells/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Key brain receptor gets an unusual regulator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1265-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*enzymology ; Brain/*enzymology ; Cloning, Molecular ; Glutamic Acid/metabolism ; Neurons/metabolism ; Racemases and Epimerases/*genetics/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Serine/*biosynthesis/metabolism ; Stereoisomerism ; Synapses/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Filling in the blanks of the GABAB receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    The promise of comparative genomics in mammals (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Dense genetic maps of human, mouse, and rat genomes that are based on coding genes and on microsatellite and single-nucleotide polymorphism markers have been complemented by precise gene homolog alignment with moderate-resolution maps of livestock, companion animals, and additional mammal species. Comparative genetic assessment expands the utility of these maps in gene discovery, in functional genomics, and in tracking the evolutionary forces that sculpted the genome organization of modern mammalian species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, S J -- Menotti-Raymond, M -- Murphy, W J -- Nash, W G -- Wienberg, J -- Stanyon, R -- Copeland, N G -- Jenkins, N A -- Womack, J E -- Marshall Graves, J A -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):458-62, 479-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521336" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Domestic/genetics ; Base Sequence ; *Chromosome Mapping ; *Evolution, Molecular ; Genetic Markers ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Mutation ; *Phylogeny ; Rodentia/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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  • 6
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    Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: To monitor changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor distribution in living neurons, the AMPA receptor subunit GluR1 was tagged with green fluorescent protein (GFP). This protein (GluR1-GFP) was functional and was transiently expressed in hippocampal CA1 neurons. In dendrites visualized with two-photon laser scanning microscopy or electron microscopy, most of the GluR1-GFP was intracellular, mimicking endogenous GluR1 distribution. Tetanic synaptic stimulation induced a rapid delivery of tagged receptors into dendritic spines as well as clusters in dendrites. These postsynaptic trafficking events required synaptic N-methyl-D-aspartate (NMDA) receptor activation and may contribute to the enhanced AMPA receptor-mediatedtransmission observed during long-term potentiation and activity-dependent synaptic maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, S H -- Hayashi, Y -- Petralia, R S -- Zaman, S H -- Wenthold, R J -- Svoboda, K -- Malinow, R -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1811-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/*metabolism/ultrastructure ; Electric Stimulation ; Hippocampus/cytology/physiology ; Humans ; Long-Term Potentiation ; *Neuronal Plasticity ; Neurons/*physiology ; Organ Culture Techniques ; Rats ; Receptor Aggregation ; Receptors, AMPA/*metabolism ; Receptors, N-Methyl-D-Aspartate/*physiology ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Tetany
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Calmodulin dependence of presynaptic metabotropic glutamate receptor signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Glutamatergic neurotransmission is controlled by presynaptic metabotropic glutamate receptors (mGluRs). A subdomain in the intracellular carboxyl-terminal tail of group III mGluRs binds calmodulin and heterotrimeric guanosine triphosphate-binding protein (G protein) betagamma subunits in a mutually exclusive manner. Mutations interfering with calmodulin binding and calmodulin antagonists inhibit G protein-mediated modulation of ionic currents by mGluR 7. Calmodulin antagonists also prevent inhibition of excitatory neurotransmission via presynaptic mGluRs. These results reveal a novel mechanism of presynaptic modulation in which Ca(2+)-calmodulin is required to release G protein betagamma subunits from the C-tail of group III mGluRs in order to mediate glutamatergic autoinhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, V -- El Far, O -- Bofill-Cardona, E -- Nanoff, C -- Freissmuth, M -- Karschin, A -- Airas, J M -- Betz, H -- Boehm, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1180-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calmodulin/antagonists & inhibitors/*metabolism ; Cells, Cultured ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*metabolism ; Glutamic Acid/*metabolism ; Hippocampus/cytology/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Presynaptic Terminals/metabolism ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sesterterpenes ; Signal Transduction ; Swine ; *Synaptic Transmission ; Terpenes/pharmacology
    Print ISSN: 0036-8075
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  • 8
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    A cytotoxic ribonuclease targeting specific transfer RNA anticodons (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: The carboxyl-terminal domain of colicin E5 was shown to inhibit protein synthesis of Escherichia coli. Its target, as revealed through in vivo and in vitro experiments, was not ribosomes as in the case of E3, but the transfer RNAs (tRNAs) for Tyr, His, Asn, and Asp, which contain a modified base, queuine, at the wobble position of each anticodon. The E5 carboxyl-terminal domain hydrolyzed these tRNAs just on the 3' side of this nucleotide. Tight correlation was observed between the toxicity of E5 and the cleavage of intracellular tRNAs of this group, implying that these tRNAs are the primary targets of colicin E5.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, T -- Tomita, K -- Ueda, T -- Watanabe, K -- Uozumi, T -- Masaki, H -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2097-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biotechnology, Graduate School of Agricultural and Life Sciences, University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092236" target="_blank"〉PubMed〈/a〉
    Keywords: Anticodon/*metabolism ; Bacterial Proteins/biosynthesis/genetics/pharmacology ; Base Sequence ; Cloning, Molecular ; Colicins/genetics/*metabolism/pharmacology ; Escherichia coli/drug effects/metabolism ; *Escherichia coli Proteins ; Guanine/analogs & derivatives/analysis ; Molecular Sequence Data ; RNA, Bacterial/chemistry/*metabolism ; RNA, Ribosomal, 16S/metabolism ; RNA, Transfer, Amino Acid-Specific/chemistry/*metabolism ; RNA, Transfer, Asn/chemistry/metabolism ; RNA, Transfer, Asp/chemistry/metabolism ; RNA, Transfer, His/chemistry/metabolism ; RNA, Transfer, Tyr/chemistry/metabolism ; Ribonucleases/genetics/*metabolism/pharmacology ; Ribosomes/metabolism
    Print ISSN: 0036-8075
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  • 9
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    AP-2 recruitment to synaptotagmin stimulated by tyrosine-based endocytic motifs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Clathrin-mediated endocytosis is initiated by the recruitment of the clathrin adaptor protein AP-2 to the plasma membrane where the membrane protein synaptotagmin is thought to act as a docking site. AP-2 also interacts with endocytic motifs present in other cargo proteins. Peptides with a tyrosine-based endocytic motif stimulated binding of AP-2 to synaptotagmin and enhanced AP-2 recruitment to the plasma membrane of neuronal and non-neuronal cells. This suggests a mechanism by which nucleation of clathrin-coated pits is stimulated by the loading of cargo proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haucke, V -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36252/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455054" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Proteins, Vesicular Transport ; Animals ; Binding Sites ; CHO Cells ; *Calcium-Binding Proteins ; Cattle ; Cell Membrane/metabolism ; Clathrin/*metabolism ; Coated Pits, Cell-Membrane/*metabolism ; Cricetinae ; *Endocytosis ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/metabolism ; Oligopeptides/chemistry/metabolism/*pharmacology ; Phospholipase D/metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; Synaptic Membranes/*metabolism ; Synaptotagmins ; Tyrosine/chemistry
    Print ISSN: 0036-8075
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  • 10
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    Techsigting. Neural regeneration. Some nerve! (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Separation ; Chick Embryo ; Neural Crest/*cytology/embryology ; Neuroglia/*cytology ; Neurons/*cytology ; Rats ; Regeneration ; Sciatic Nerve/*cytology/embryology ; Stem Cells/*cytology
    Print ISSN: 0036-8075
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  • 11
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    Role of DNA 5-methylcytosine transferase in cell transformation by fos (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The Fos and Jun oncoproteins form dimeric complexes that stimulate transcription of genes containing activator protein-1 regulatory elements. We found, by representational difference analysis, that expression of DNA 5-methylcytosine transferase (dnmt1) in fos-transformed cells is three times the expression in normal fibroblasts and that fos-transformed cells contain about 20 percent more 5-methylcytosine than normal fibroblasts. Transfection of the gene encoding Dnmt1 induced morphological transformation, whereas inhibition of dnmt1 expression or activity resulted in reversion of fos transformation. Inhibition of histone deacetylase, which associates with methylated DNA, also caused reversion. These results suggest that fos may transform cells through alterations in DNA methylation and in histone deacetylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakin, A V -- Curran, T -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888853" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Acetylation ; Animals ; Cell Size ; *Cell Transformation, Neoplastic ; Cytosine/analogs & derivatives/metabolism ; DNA (Cytosine-5-)-Methyltransferase/genetics/*metabolism ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Neoplastic ; *Genes, fos ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; Proto-Oncogene Proteins c-fos/*metabolism ; Rats ; Transcription, Genetic ; Transfection
    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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  • 12
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    Pigment epithelium-derived factor: a potent inhibitor of angiogenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: In the absence of disease, the vasculature of the mammalian eye is quiescent, in part because of the action of angiogenic inhibitors that prevent vessels from invading the cornea and vitreous. Here, an inhibitor responsible for the avascularity of these ocular compartments is identified as pigment epithelium-derived factor (PEDF), a protein previously shown to have neurotrophic activity. The amount of inhibitory PEDF produced by retinal cells was positively correlated with oxygen concentrations, suggesting that its loss plays a permissive role in ischemia-driven retinal neovascularization. These results suggest that PEDF may be of therapeutic use, especially in retinopathies where pathological neovascularization compromises vision and leads to blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, D W -- Volpert, O V -- Gillis, P -- Crawford, S E -- Xu, H -- Benedict, W -- Bouck, N P -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Department of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies/immunology ; Cattle ; Cells, Cultured ; Chemotaxis/drug effects ; Culture Media, Conditioned ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/cytology/drug effects/physiology ; Eye/blood supply ; *Eye Proteins ; Humans ; Lymphokines/metabolism ; Mice ; Neovascularization, Pathologic/*drug therapy/metabolism/pathology ; Neovascularization, Physiologic/*drug effects ; *Nerve Growth Factors ; Oxygen/physiology ; Proteins/genetics/immunology/*pharmacology/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/*metabolism/pathology ; Retinal Neovascularization/*drug therapy ; Retinal Vessels/growth & development ; Serpins/genetics/immunology/*pharmacology/*physiology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 13
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    Mechanism of intrinsic transcription termination and antitermination (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Gene expression is modulated by regulatory elements that influence transcription elongation by RNA polymerase: terminators that disrupt the elongation complex and release RNA, and regulators that overcome termination signals. RNA release from Escherichia coli RNA polymerase can be induced by a complementary oligonucleotide that replaces the upstream half of the RNA hairpin stem of intrinsic terminator transcripts, implying that RNA hairpins act by extracting RNA from the transcription complex. A transcription antiterminator inhibits this activity of oligonucleotides and therefore protects the elongation complex from destabilizing attacks on the emerging transcript. These effects illuminate the structure of the complex and the mechanism of transcription termination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yarnell, W S -- Roberts, J W -- GM 21941/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):611-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Biotechnology Building, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213678" target="_blank"〉PubMed〈/a〉
    Keywords: Base Pairing ; Base Sequence ; DNA, Bacterial/chemistry/genetics/metabolism ; DNA-Directed RNA Polymerases/genetics/*metabolism ; Escherichia coli/*genetics/metabolism ; Models, Genetic ; Molecular Sequence Data ; Nucleic Acid Conformation ; Oligodeoxyribonucleotides/chemistry/metabolism ; RNA, Bacterial/chemistry/genetics/metabolism ; RNA, Messenger/chemistry/genetics/*metabolism ; Templates, Genetic ; *Terminator Regions, Genetic ; *Transcription, Genetic ; Viral Proteins/*metabolism
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  • 14
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    Focal adhesion motility revealed in stationary fibroblasts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Focal adhesions (FAs) are clustered integrins and associated proteins that mediate cell adhesion and signaling. A green fluorescent protein-beta1 integrin chimera was used to label FAs in living cells. In stationary cells, FAs were highly motile, moving linearly for several plaque lengths toward the cell center. FA motility was independent of cell density and resulted from contraction of associated actin fibers. In migrating cells, FAs were stationary and only moved in the tail. FA motility in stationary cells suggests that cell movement may be regulated by a clutch-like mechanism by which the affinity of integrins to substrate may be altered in response to migratory cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smilenov, L B -- Mikhailov, A -- Pelham, R J -- Marcantonio, E E -- Gundersen, G G -- GM42026/GM/NIGMS NIH HHS/ -- GM44585/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1172-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/physiology ; Animals ; Antigens, CD29/*metabolism ; *Cell Adhesion ; Cell Count ; Cell Line ; *Cell Movement ; Fibroblasts/*cytology/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins ; Mice ; Microscopy, Interference ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 15
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    Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bosch, F -- Miksa, M -- Bittigau, P -- Vockler, J -- Dikranian, K -- Tenkova, T I -- Stefovska, V -- Turski, L -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):70-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/*cytology/drug effects/embryology/growth & development ; Calcium Channel Blockers/pharmacology ; Dizocilpine Maleate/pharmacology ; Dopamine Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Fetus ; Haloperidol/pharmacology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Electron ; Muscarinic Antagonists/pharmacology ; *Nerve Degeneration ; Neurons/*cytology/drug effects/metabolism ; Quinoxalines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/metabolism ; Scopolamine Hydrobromide/pharmacology
    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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  • 16
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    The mammalian gene collection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: The Mammalian Gene Collection (MGC) project is a new effort by the NIH to generate full-length complementary DNA (cDNA) resources. This project will provide publicly accessible resources to the full research community. The MGC project entails the production of libraries, sequencing, and database and repository development, as well as the support of library construction, sequencing, and analytic technologies dedicated to the goal of obtaining a full set of human and other mammalian full-length (open reading frame) sequences and clones of expressed genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strausberg, R L -- Feingold, E A -- Klausner, R D -- Collins, F S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):455-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Computational Biology ; DNA, Complementary ; Databases, Factual ; Expressed Sequence Tags ; *Gene Library ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Mice ; National Institutes of Health (U.S.) ; Private Sector ; Public Sector ; *Sequence Analysis, DNA ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Building neural representations of habits (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Memories for habits and skills ("implicit or procedural memory") and memories for facts ("explicit or episodic memory") are built up in different brain systems and are vulnerable to different neurodegenerative disorders in humans. So that the striatum-based mechanisms underlying habit formation could be studied, chronic recordings from ensembles of striatal neurons were made with multiple tetrodes as rats learned a T-maze procedural task. Large and widely distributed changes in the neuronal activity patterns occurred in the sensorimotor striatum during behavioral acquisition, culminating in task-related activity emphasizing the beginning and end of the automatized procedure. The new ensemble patterns remained stable during weeks of subsequent performance of the same task. These results suggest that the encoding of action in the sensorimotor striatum undergoes dynamic reorganization as habit learning proceeds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jog, M S -- Kubota, Y -- Connolly, C I -- Hillegaart, V -- Graybiel, A M -- R03 MH57878/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1745-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London Health Sciences Center, London, Ontario N6A 5A5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576743" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal ; Brain Mapping ; Corpus Striatum/*physiology ; Electrodes, Implanted ; Evoked Potentials ; *Habits ; Locomotion ; *Maze Learning ; Memory/physiology ; Motor Activity ; Neurons/physiology ; Rats ; Reaction Time
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: A mechanism by which the Ras-mitogen-activated protein kinase (MAPK) signaling pathway mediates growth factor-dependent cell survival was characterized. The MAPK-activated kinases, the Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro and in vivo. The Rsk-induced phosphorylation of BAD at serine 112 suppressed BAD-mediated apoptosis in neurons. Rsks also are known to phosphorylate the transcription factor CREB (cAMP response element-binding protein) at serine 133. Activated CREB promoted cell survival, and inhibition of CREB phosphorylation at serine 133 triggered apoptosis. These findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Brunet, A -- West, A E -- Datta, S R -- Takasu, M A -- Greenberg, M E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 HD 24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1358-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain-Derived Neurotrophic Factor/pharmacology ; Carrier Proteins/genetics/metabolism ; *Cell Survival ; Cells, Cultured ; Cerebellum/cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Kinase 1 ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Mutation ; Neurons/*cytology/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; *Protein-Serine-Threonine Kinases ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; bcl-Associated Death Protein ; ras Proteins/metabolism
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  • 19
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    Dissecting dendrite dynamics (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, S J -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1860-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. sjsmith@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206891" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Action Potentials ; Animals ; Dendrites/*physiology/ultrastructure ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Microscopy, Fluorescence ; Neurons/physiology/ultrastructure ; Pseudopodia/*physiology/ultrastructure ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology/ultrastructure ; Synaptic Membranes/physiology
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  • 20
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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  • 21
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    Precisely localized LTD in the neocortex revealed by infrared-guided laser stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: In a direct approach to elucidate the origin of long-term depression (LTD), glutamate was applied onto dendrites of neurons in rat neocortical slices. An infrared-guided laser stimulation was used to release glutamate from caged glutamate in the focal spot of an ultraviolet laser. A burst of light flashes caused an LTD-like depression of glutamate receptor responses, which was highly confined to the region of "tetanic" stimulation (〈10 micrometers). A similar depression of glutamate receptor responses was observed during LTD of synaptic transmission. A spatially highly specific postsynaptic mechanism can account for the LTD induced by glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodt, H -- Eder, M -- Frick, A -- Zieglgansberger, W -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, 80804 Munich, Germany. dodt@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamates/pharmacology ; Glutamic Acid/metabolism ; In Vitro Techniques ; Infrared Rays ; Lasers ; Microscopy, Video ; Neocortex/cytology/*physiology ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Photolysis ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/*metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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  • 22
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    Transmission of chronic nociception by spinal neurons expressing the substance P receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Substance P receptor (SPR)-expressing spinal neurons were ablated with the selective cytotoxin substance P-saporin. Loss of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated with persistent neuropathic and inflammatory pain states. This loss appeared to be permanent. Responses to mildly painful stimuli and morphine analgesia were unaffected by this treatment. These results identify a target for treating persistent pain and suggest that the small population of SPR-expressing neurons in the dorsal horn of the spinal cord plays a pivotal role in the generation and maintenance of chronic neuropathic and inflammatory pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nichols, M L -- Allen, B J -- Rogers, S D -- Ghilardi, J R -- Honore, P -- Luger, N M -- Finke, M P -- Li, J -- Lappi, D A -- Simone, D A -- Mantyh, P W -- 23970/PHS HHS/ -- 31223/PHS HHS/ -- DEO 7288/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preventive Sciences, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Ganglia, Spinal/drug effects/physiology ; *Immunotoxins ; Inflammation/physiopathology ; Ligation ; *N-Glycosyl Hydrolases ; Neuralgia/drug therapy/physiopathology ; Pain/*drug therapy/*physiopathology ; Plant Proteins/administration & dosage/*pharmacology ; Posterior Horn Cells/drug effects/*physiology ; Rats ; Receptors, Neurokinin-1/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Spinal Nerves ; Substance P/administration & dosage/*pharmacology ; Time Factors
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  • 23
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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
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  • 24
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    Genome maps 10. Comparative genomics. Mammalian radiations. Wall chart (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, S J -- Eisenberg, J F -- Miyamoto, M -- Hedges, S B -- Kumar, S -- Wilson, D E -- Menotti-Raymond, M -- Murphy, W J -- Nash, W G -- Lyons, L A -- Menninger, J C -- Stanyon, R -- Wienberg, J -- Copeland, N G -- Jenkins, N A -- Gellin, J -- Yerle, M -- Andersson, L -- Womack, J -- Broad, T -- Postlethwait, J -- Serov, O -- Bailey, E -- James, M R -- Marshall Graves, J A -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):463-78.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Frederick, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577209" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Chromosome Mapping ; Chromosome Painting ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Nucleic Acid Hybridization ; Phylogeny
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  • 25
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    Stem cells as potential nerve therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):650-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Diffuse Cerebral Sclerosis of Schilder/*therapy ; Embryo, Mammalian/cytology ; Financing, Government ; Germany ; Humans ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/physiology/transplantation ; Rats ; Research Support as Topic ; Spinal Cord ; Stem Cells/*cytology/physiology
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  • 26
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    PEG antibodies (1999)
    American Association for the Advancement of Science (AAAS)
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    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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  • 27
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    Regulation of myosin phosphatase by a specific interaction with cGMP- dependent protein kinase Ialpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Contraction and relaxation of smooth muscle are regulated by myosin light-chain kinase and myosin phosphatase through phosphorylation and dephosphorylation of myosin light chains. Cyclic guanosine monophosphate (cGMP)-dependent protein kinase Ialpha (cGKIalpha) mediates physiologic relaxation of vascular smooth muscle in response to nitric oxide and cGMP. It is shown here that cGKIalpha is targeted to the smooth muscle cell contractile apparatus by a leucine zipper interaction with the myosin-binding subunit (MBS) of myosin phosphatase. Uncoupling of the cGKIalpha-MBS interaction prevents cGMP-dependent dephosphorylation of myosin light chain, demonstrating that this interaction is essential to the regulation of vascular smooth muscle cell tone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surks, H K -- Mochizuki, N -- Kasai, Y -- Georgescu, S P -- Tang, K M -- Ito, M -- Lincoln, T M -- Mendelsohn, M E -- HL09330/HL/NHLBI NIH HHS/ -- HL55309/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1583-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Research Institute and Cardiology Division, Department of Medicine, Tufts University School of Medicine and New England Medical Center, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567269" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/genetics/*metabolism ; Histones/metabolism ; Humans ; Isoenzymes/chemistry/metabolism ; Leucine Zippers ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular/*enzymology/physiology ; Mutagenesis, Site-Directed ; Myosin Light Chains/*metabolism ; Myosin-Light-Chain Phosphatase ; Phosphoprotein Phosphatases/chemistry/*metabolism ; Phosphorylation ; Precipitin Tests ; Rats ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Transfection ; Two-Hybrid System Techniques
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  • 28
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    Biosequence exegesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Annotation of large-scale gene sequence data will benefit from comprehensive and consistent application of well-documented, standard analysis methods and from progressive and vigilant efforts to ensure quality and utility and to keep the annotation up to date. However, it is imperative to learn how to apply information derived from functional genomics and proteomics technologies to conceptualize and explain the behaviors of biological systems. Quantitative and dynamical models of systems behaviors will supersede the limited and static forms of single-gene annotation that are now the norm. Molecular biological epistemology will increasingly encompass both teleological and causal explanations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boguski, M S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):453-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD 20894, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; *Computational Biology ; Databases, Factual ; *Genetic Techniques ; *Genome ; Genome, Human ; Human Genome Project ; Humans ; Molecular Biology ; *Proteome ; *Sequence Analysis, DNA
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Potential target found for antimetastasis drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Cloning, Molecular ; *Glucuronidase ; Glycoside Hydrolases/*antagonists & inhibitors/*genetics/isolation & ; purification/metabolism ; Humans ; Mice ; Neoplasm Metastasis/*prevention & control ; Rats ; Tumor Cells, Cultured
    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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    Mapping smells in the brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):508.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Diagnostic Imaging ; Light ; Mice ; *Odors ; Olfactory Bulb/*physiology ; Olfactory Receptor Neurons/physiology ; Rats ; Receptors, Odorant/*physiology ; Smell/*physiology
    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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    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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    Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holash, J -- Maisonpierre, P C -- Compton, D -- Boland, P -- Alexander, C R -- Zagzag, D -- Yancopoulos, G D -- Wiegand, S J -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1994-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/blood supply/pathology ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/pathology ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/pathology/physiology ; Glioblastoma/blood supply/pathology ; Glioma/blood supply/pathology ; In Situ Hybridization ; Lymphokines/genetics/*physiology ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/pathology/physiology ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*pathology ; *Neovascularization, Pathologic ; Proteins/genetics/*physiology ; Rats ; Rats, Sprague-Dawley ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Arabidopsis galactolipid biosynthesis and lipid trafficking mediated by DGD1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: The photosynthetic apparatus in plant cells is associated with membranes of the thylakoids within the chloroplast and is embedded into a highly specialized lipid matrix. Diacylglycerol galactolipids are common in thylakoid membranes but are excluded from all others. Isolation of the gene DGD1, encoding a galactosyltransferase-like protein, now provides insights into assembly of the thylakoid lipid matrix and subcellular lipid trafficking in Arabidopsis thaliana.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dormann, P -- Balbo, I -- Benning, C -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2181-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Michigan State University, East Lansing, MI 48824, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381884" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/growth & development/*metabolism ; *Arabidopsis Proteins ; Base Sequence ; Chloroplasts/metabolism ; Chromosome Mapping ; DNA, Complementary/genetics ; Endoplasmic Reticulum/metabolism ; Exons ; Galactolipids ; Galactosyltransferases/chemistry/*genetics/*metabolism ; Genes, Plant ; Glycolipids/*biosynthesis ; Intracellular Membranes/metabolism ; *Lipid Metabolism ; Molecular Sequence Data ; Mutation ; Plants, Genetically Modified ; Recombinant Proteins/metabolism
    Print ISSN: 0036-8075
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    New clues to how neurons strengthen their connections (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1755-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10391789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/physiology ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Glutamic Acid/*physiology ; Long-Term Potentiation/*physiology ; Mice ; Neurons/physiology ; Rats ; Receptors, AMPA/*physiology ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Odor response properties of rat olfactory receptor neurons (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Molecular biology studies of olfaction have identified a multigene family of molecular receptors that are likely to be involved in odor transduction mechanisms. However, because previous functional data on peripheral coding were mainly collected from inferior vertebrates, it has been difficult to document the degree of specificity of odor interaction mechanisms. As a matter of fact, studies of the functional expression of olfactory receptors have not demonstrated the low or high specificity of olfactory receptors. In this study, the selectivity of olfactory receptor neurons was investigated in the rat at the cellular level under physiological conditions by unitary extracellular recordings. Individual olfactory receptor neurons were broadly responsive to qualitatively distinct odor compounds. We conclude that peripheral coding is based on activated arrays of olfactory receptor cells with overlapping tuning profiles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duchamp-Viret, P -- Chaput, M A -- Duchamp, A -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Neurosciences et Systemes Sensoriels, CNRS, UMR, Universite Claude Bernard, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne cedex, France. pduchamp@olfac.univ-lyon1.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381881" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones ; Action Potentials ; Animals ; Anisoles ; Benzaldehydes ; Camphor ; Cyclohexenes ; *Odors ; Olfactory Receptor Neurons/*physiology ; Pentanols ; Rats ; Rats, Wistar ; Receptors, Odorant/genetics/*physiology ; Terpenes
    Print ISSN: 0036-8075
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    Dual function of the selenoprotein PHGPx during sperm maturation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: The selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) changes its physical characteristics and biological functions during sperm maturation. PHGPx exists as a soluble peroxidase in spermatids but persists in mature spermatozoa as an enzymatically inactive, oxidatively cross-linked, insoluble protein. In the midpiece of mature spermatozoa, PHGPx protein represents at least 50 percent of the capsule material that embeds the helix of mitochondria. The role of PHGPx as a structural protein may explain the mechanical instability of the mitochondrial midpiece that is observed in selenium deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ursini, F -- Heim, S -- Kiess, M -- Maiorino, M -- Roveri, A -- Wissing, J -- Flohe, L -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1393-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartmento di Chimica Biologica, Universita di Padova, Viale G. Colombo 3, I-35121 Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophoresis, Gel, Two-Dimensional ; Electrophoresis, Polyacrylamide Gel ; Glutathione Peroxidase/chemistry/isolation & purification/*physiology ; Infertility, Male/metabolism ; Male ; Mitochondria/chemistry/enzymology ; Oxidation-Reduction ; Proteins/chemistry/isolation & purification/*physiology ; Rats ; Rats, Wistar ; Selenium/deficiency/*physiology ; Selenoproteins ; Solubility ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Spermatids/chemistry/enzymology ; *Spermatogenesis ; Spermatozoa/chemistry/enzymology/*physiology
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    UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Modification of cell surface molecules with sialic acid is crucial for their function in many biological processes, including cell adhesion and signal transduction. Uridine diphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase) is an enzyme that catalyzes an early, rate-limiting step in the sialic acid biosynthetic pathway. UDP-GlcNAc 2-epimerase was found to be a major determinant of cell surface sialylation in human hematopoietic cell lines and a critical regulator of the function of specific cell surface adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keppler, O T -- Hinderlich, S -- Langner, J -- Schwartz-Albiez, R -- Reutter, W -- Pawlita, M -- New York, N.Y. -- Science. 1999 May 21;284(5418):1372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Tumor Virology Program, Tumor Immunology Program, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, CD14/biosynthesis ; Antigens, CD15/biosynthesis ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Carbohydrate Epimerases/genetics/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Culture Media ; *Escherichia coli Proteins ; Glycoconjugates/*metabolism ; HL-60 Cells ; Histocompatibility Antigens Class I/biosynthesis ; Humans ; Lectins/metabolism ; Oligosaccharides/biosynthesis ; Rats ; Sialic Acid Binding Ig-like Lectin 2 ; Sialic Acids/*biosynthesis ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    A nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Many human diseases are associated with the overproduction of oxygen free radicals that inflict cell damage. A manganese(II) complex with a bis(cyclohexylpyridine)-substituted macrocyclic ligand (M40403) was designed to be a functional mimic of the superoxide dismutase (SOD) enzymes that normally remove these radicals. M40403 had high catalytic SOD activity and was chemically and biologically stable in vivo. Injection of M40403 into rat models of inflammation and ischemia-reperfusion injury protected the animals against tissue damage. Such mimics may result in better clinical therapies for diseases mediated by superoxide radicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salvemini, D -- Wang, Z Q -- Zweier, J L -- Samouilov, A -- Macarthur, H -- Misko, T P -- Currie, M G -- Cuzzocrea, S -- Sikorski, J A -- Riley, D P -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MetaPhore Pharmaceuticals, 1910 Innerbelt Business Center Drive, St. Louis, MO 63114, USA. dsalvemini@metaphore.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/metabolism/*therapeutic use ; Cytoprotection ; Dinoprostone/metabolism ; Dose-Response Relationship, Drug ; Drug Design ; Drug Stability ; Inflammation/*drug therapy ; Interleukin-1/metabolism ; L-Lactate Dehydrogenase/metabolism ; Male ; Manganese ; Molecular Mimicry ; Neutrophils/drug effects ; Organometallic Compounds/chemical synthesis/chemistry/metabolism/*toxicity ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/*drug therapy ; Splanchnic Circulation ; *Superoxide Dismutase/metabolism ; Superoxides/*metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/metabolism
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    Cholesterol-lowering drugs may boost bones (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticholesteremic Agents/*pharmacology ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis ; Clinical Trials as Topic ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology ; Lovastatin/*pharmacology ; Mice ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Rats ; Simvastatin/pharmacology ; *Transforming Growth Factor beta
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    Drosophila S6 kinase: a regulator of cell size (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-09-25
    Description: Cell proliferation requires cell growth; that is, cells only divide after they reach a critical size. However, the mechanisms by which cells grow and maintain their appropriate size have remained elusive. Drosophila deficient in the S6 kinase gene (dS6K) exhibited an extreme delay in development and a severe reduction in body size. These flies had smaller cells rather than fewer cells. The effect was cell-autonomous, displayed throughout larval development, and distinct from that of ribosomal protein mutants (Minutes). Thus, the dS6K gene product regulates cell size in a cell-autonomous manner without impinging on cell number.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montagne, J -- Stewart, M J -- Stocker, H -- Hafen, E -- Kozma, S C -- Thomas, G -- F32 GM15926/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute, Maulbeerstrasse 66, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10497130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Body Constitution ; Cell Count ; Cell Division ; Cell Size ; Drosophila melanogaster/cytology/*enzymology/genetics/*growth & development ; Epithelial Cells/cytology ; Female ; Genes, Insect ; Larva/cytology/growth & development ; Male ; Metamorphosis, Biological ; Molecular Sequence Data ; Mutation ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; Wings, Animal/*cytology/growth & development
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    Modulation of respiratory frequency by peptidergic input to rhythmogenic neurons in the preBotzinger complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Neurokinin-1 receptor (NK1R) and mu-opioid receptor (muOR) agonists affected respiratory rhythm when injected directly into the preBotzinger Complex (preBotC), the hypothesized site for respiratory rhythmogenesis in mammals. These effects were mediated by actions on preBotC rhythmogenic neurons. The distribution of NK1R+ neurons anatomically defined the preBotC. Type 1 neurons in the preBotC, which have rhythmogenic properties, expressed both NK1Rs and muORs, whereas type 2 neurons expressed only NK1Rs. These findings suggest that the preBotC is a definable anatomic structure with unique physiological function and that a subpopulation of neurons expressing both NK1Rs and muORs generate respiratory rhythm and modulate respiratory frequency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, P A -- Rekling, J C -- Bocchiaro, C M -- Feldman, J L -- HL37941/HL/NHLBI NIH HHS/ -- HL40959/HL/NHLBI NIH HHS/ -- R01 HL040959/HL/NHLBI NIH HHS/ -- R01 HL040959-12/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of California Los Angeles, Box 951763, Los Angeles, CA 90095-1763, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Female ; In Vitro Techniques ; Medulla Oblongata/cytology/drug effects/*physiology ; Mice ; Mice, Inbred BALB C ; Neurons/chemistry/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/analysis/physiology ; Receptors, Neurokinin-1/agonists/analysis/*physiology ; Receptors, Opioid, mu/agonists/analysis/*physiology ; Respiratory Mechanics/drug effects/*physiology ; Substance P/pharmacology ; Synaptic Transmission/drug effects
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    Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H G -- Pathan, N -- Ethell, I M -- Krajewski, S -- Yamaguchi, Y -- Shibasaki, F -- McKeon, F -- Bobo, T -- Franke, T F -- Reed, J C -- AG-1593/AG/NIA NIH HHS/ -- CA-69381/CA/NCI NIH HHS/ -- HD25938/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195903" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; *Apoptosis ; Calcineurin/genetics/*metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism/pharmacology ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Dimerization ; Enzyme Inhibitors/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology ; Humans ; Mitochondria/metabolism ; Neurons/cytology/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Transfection ; *Tyrosine 3-Monooxygenase ; bcl-Associated Death Protein ; bcl-X Protein
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    Techview: DNA sequencing. Sequencing the genome, fast (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mullikin, J C -- McMurragy, A A -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1867-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanger Centre, Wellcome Trust Genome Campus, Hinxton, Cambs, UK. jcm@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206892" target="_blank"〉PubMed〈/a〉
    Keywords: Automation ; Base Sequence ; Fluorescence ; *Genome, Human ; Human Genome Project ; Humans ; Sequence Analysis, DNA/*instrumentation/methods ; Software
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    Stimulation of bone formation in vitro and in rodents by statins (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Osteoporosis and other diseases of bone loss are a major public health problem. Here it is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents. This effect was associated with increased expression of the bone morphogenetic protein-2 (BMP-2) gene in bone cells. Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats. Thus, in appropriate doses, statins may have therapeutic applications for the treatment of osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mundy, G -- Garrett, R -- Harris, S -- Chan, J -- Chen, D -- Rossini, G -- Boyce, B -- Zhao, M -- Gutierrez, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉OsteoScreen, 2040 Babcock Road, San Antonio, TX 78229, USA. mundy@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis/genetics/pharmacology ; Cell Line ; Female ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/*pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Organ Culture Techniques ; Osteoblasts/*drug effects/metabolism ; Osteoclasts/drug effects ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Promoter Regions, Genetic/drug effects ; Rats ; Recombinant Proteins/pharmacology ; Simvastatin/*pharmacology ; Skull ; Transfection ; *Transforming Growth Factor beta
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    Role of heteromer formation in GABAB receptor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
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    Probing alcoholism's 'dark side' (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1473.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498528" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/cerebrospinal fluid/*metabolism ; Animals ; Brain/*metabolism ; Corticotropin-Releasing Hormone/cerebrospinal fluid/*metabolism ; Dopamine/metabolism ; Humans ; Rats ; Substance Withdrawal Syndrome/metabolism/prevention & control
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    Meeting. American Chemical Society. Raising a glass to health and nanotubes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2053, 2055.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523196" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/*metabolism ; Animals ; Carbon ; Electronics ; Ethanol/metabolism ; Glucose/chemistry/metabolism ; Glycosylation End Products, Advanced/*metabolism ; Hemoglobin A, Glycosylated/chemistry ; Humans ; Rats
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  • 48
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    Long-term depression in hippocampal interneurons: joint requirement for pre- and postsynaptic events (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: Long-term depression (LTD) is a well-known form of synaptic plasticity of principal neurons in the mammalian brain. Whether such changes occur in interneurons is still controversial. CA3 hippocampal interneurons expressing Ca2+-permeable AMPA receptors exhibited LTD after tetanic stimulation of CA3 excitatory inputs. LTD was independent of NMDA receptors and required both Ca2+ influx through postsynaptic AMPA receptors and activation of presynaptic mGluR7-like receptors. These results point to the capability of interneurons to undergo plastic changes of synaptic strength through joint activation of pre- and postsynaptic glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laezza, F -- Doherty, J J -- Dingledine, R -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1411-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/*physiology ; Male ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/drug effects/*metabolism ; Receptors, Metabotropic Glutamate/drug effects/*metabolism ; Synapses/*physiology ; Synaptic Transmission ; Tetany
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    Modulation of brain reward circuitry by leptin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Leptin, a hormone secreted by fat cells, suppresses food intake and promotes weight loss. To assess the action of this hormone on brain reward circuitry, changes in the rewarding effect of lateral hypothalamic stimulation were measured after leptin administration. At five stimulation sites near the fornix, the effectiveness of the rewarding electrical stimulation was enhanced by chronic food restriction and attenuated by intracerebroventricular infusion of leptin. In contrast, the rewarding effect of stimulating neighboring sites was insensitive to chronic food restriction and was enhanced by leptin in three of four cases. These opposing effects of leptin may mirror complementary changes in the rewarding effects of feeding and of competing behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fulton, S -- Woodside, B -- Shizgal, P -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Studies in Behavioural Neurobiology, Concordia University, Montreal, QC, H3G 1M8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Energy Metabolism ; Feeding Behavior ; Food Deprivation/*physiology ; Hypothalamic Area, Lateral/drug effects/*physiology ; Injections, Intraventricular ; Leptin/administration & dosage/*pharmacology ; Male ; Neurons/physiology ; Neuropeptides/physiology ; Rats ; Rats, Long-Evans ; Recombinant Proteins/administration & dosage/pharmacology ; *Reward ; Self Stimulation/physiology ; Time Factors
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  • 50
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    Regulation of NMDA receptors by an associated phosphatase-kinase signaling complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Regulation of N-methyl-D-aspartate (NMDA) receptor activity by kinases and phosphatases contributes to the modulation of synaptic transmission. Targeting of these enzymes near the substrate is proposed to enhance phosphorylation-dependent modulation. Yotiao, an NMDA receptor-associated protein, bound the type I protein phosphatase (PP1) and the adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (PKA) holoenzyme. Anchored PP1 was active, limiting channel activity, whereas PKA activation overcame constitutive PP1 activity and conferred rapid enhancement of NMDA receptor currents. Hence, yotiao is a scaffold protein that physically attaches PP1 and PKA to NMDA receptors to regulate channel activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westphal, R S -- Tavalin, S J -- Lin, J W -- Alto, N M -- Fraser, I D -- Langeberg, L K -- Sheng, M -- Scott, J D -- F32 NS010202/NS/NINDS NIH HHS/ -- GM 48231/GM/NIGMS NIH HHS/ -- NS10202/NS/NINDS NIH HHS/ -- NS10543/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):93-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Vollum Institute, Oregon Health Sciences University, 3181 S.W. Sam Jackson Road, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390370" target="_blank"〉PubMed〈/a〉
    Keywords: A Kinase Anchor Proteins ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; Cyclic AMP/analogs & derivatives/pharmacology ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Cytoskeletal Proteins/*metabolism ; Enzyme Inhibitors/pharmacology ; Holoenzymes/metabolism ; Humans ; Molecular Sequence Data ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thionucleotides/pharmacology ; Transfection
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    American Chemical Society. Chemists mix it up in California (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):243-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biocompatible Materials ; *Biomedical Engineering ; Brain/*drug effects/metabolism ; Caffeine/administration & dosage/adverse effects/*pharmacology ; Catalysis ; Genetic Engineering ; Genetic Therapy/*methods ; Humans ; Polycarboxylate Cement/chemical synthesis ; Polymers/chemical synthesis ; Rats ; Substance-Related Disorders/*etiology
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    Isolation of West Nile virus from mosquitoes, crows, and a Cooper's hawk in Connecticut (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: West Nile (WN) virus, a mosquito-transmitted virus native to Africa, Asia, and Europe, was isolated from two species of mosquitoes, Culex pipiens and Aedes vexans, and from brain tissues of 28 American crows, Corvus brachyrhynchos, and one Cooper's hawk, Accipiter cooperii, in Connecticut. A portion of the genome of virus isolates from four different hosts was sequenced and analyzed by comparative phylogenetic analysis. Our isolates from Connecticut were similar to one another and most closely related to two WN isolates from Romania (2.8 and 3.6 percent difference). If established in North America, WN virus will likely have severe effects on human health and on the health of populations of birds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, J F -- Andreadis, T G -- Vossbrinck, C R -- Tirrell, S -- Wakem, E M -- French, R A -- Garmendia, A E -- Van Kruiningen, H J -- P01-AI-30548/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2331-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Entomology, Department of Soil and Water, the Connecticut Agricultural Experiment Station, Post Office Box 1106, New Haven, CT 06504, USA. john.f.anderson@po.state.ct.us〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600741" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Animals ; Base Sequence ; Bird Diseases/epidemiology/*virology ; Brain/*virology ; Connecticut/epidemiology ; Culex/virology ; Culicidae/*virology ; Genome, Viral ; Humans ; Insect Vectors/*virology ; Phylogeny ; Raptors/virology ; Romania ; Songbirds/virology ; West Nile Fever/epidemiology/*veterinary/virology ; West Nile virus/classification/genetics/*isolation & purification
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    Enhanced cortical dopamine output and antipsychotic-like effects of raclopride by alpha2 adrenoceptor blockade (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Clozapine exerts superior clinical efficacy and markedly enhances cortical dopamine output compared with classical antipsychotic drugs. Here the alpha2 adrenoceptor antagonist idazoxan was administered to rats alone or in combination with the D2/3 dopamine receptor antagonist raclopride. Dopamine efflux in the medial prefrontal cortex and conditioned avoidance responding were analyzed. Idazoxan selectively potentiated the cortical output of dopamine and augmented the suppression of conditioned avoidance responding induced by raclopride. These results challenge basic assumptions underlying the dopamine hypothesis of schizophrenia and provide insight into clozapine's mode of action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hertel, P -- Fagerquist, M V -- Svensson, T H -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):105-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, Section of Neuropsychopharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506554" target="_blank"〉PubMed〈/a〉
    Keywords: *Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Antipsychotic Agents/*pharmacology ; Avoidance Learning/drug effects ; Catalepsy/chemically induced ; Conditioning (Psychology) ; Corpus Striatum/drug effects/metabolism ; Dopamine/*metabolism ; Dopamine Antagonists/*pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Idazoxan/*pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Prefrontal Cortex/*drug effects/metabolism ; Raclopride ; Rats ; Receptors, Adrenergic, alpha-2/metabolism ; Salicylamides/*pharmacology ; Schizophrenia/drug therapy/metabolism
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    Neuronal activity-dependent cell survival mediated by transcription factor MEF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: During mammalian development, electrical activity promotes the calcium-dependent survival of neurons that have made appropriate synaptic connections. However, the mechanisms by which calcium mediates neuronal survival during development are not well characterized. A transcription-dependent mechanism was identified by which calcium influx into neurons promoted cell survival. The transcription factor MEF2 was selectively expressed in newly generated postmitotic neurons and was required for the survival of these neurons. Calcium influx into cerebellar granule neurons led to activation of p38 mitogen-activated protein kinase-dependent phosphorylation and activation of MEF2. Once activated, MEF2 regulated neuronal survival by stimulating MEF2-dependent gene transcription. These findings demonstrate that MEF2 is a calcium-regulated transcription factor and define a function for MEF2 during nervous system development that is distinct from previously well-characterized functions of MEF2 during muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Z -- Bonni, A -- Xia, F -- Nadal-Vicens, M -- Greenberg, M E -- 5T32NS07112/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):785-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Department of Neurology, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/embryology/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dimerization ; Immunohistochemistry ; MEF2 Transcription Factors ; Mitogen-Activated Protein Kinases/metabolism ; Mitosis ; Mutation ; Myogenic Regulatory Factors ; Neurons/*cytology/*metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; p38 Mitogen-Activated Protein Kinases
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    Preliminary data touch off genetic food fight (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1094-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Crops, Agricultural/*adverse effects ; Digestive System/pathology ; Food Technology ; Great Britain ; *Growth ; *Immunity ; Infection/pathology ; Lectins/genetics ; Plant Lectins ; Plants, Genetically Modified/*adverse effects ; Rats ; Solanum tuberosum/adverse effects/*genetics
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    Dracula's wish (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1999 May 21;284(5418):1294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticoagulants/*chemical synthesis/chemistry/pharmacology ; Antithrombins/metabolism ; Bleeding Time ; Heparin/chemistry/metabolism/*pharmacology ; Humans ; Molecular Mimicry ; Platelet Activation/drug effects ; Polysaccharides/*chemical synthesis/chemistry/pharmacology ; Rats ; Thrombin/*antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Bone marrow as a potential source of hepatic oval cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Bone marrow stem cells develop into hematopoietic and mesenchymal lineages but have not been known to participate in production of hepatocytes, biliary cells, or oval cells during liver regeneration. Cross-sex or cross-strain bone marrow and whole liver transplantation were used to trace the origin of the repopulating liver cells. Transplanted rats were treated with 2-acetylaminofluorene, to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation. Markers for Y chromosome, dipeptidyl peptidase IV enzyme, and L21-6 antigen were used to identify liver cells of bone marrow origin. From these cells, a proportion of the regenerated hepatic cells were shown to be donor-derived. Thus, a stem cell associated with the bone marrow has epithelial cell lineage capability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, B E -- Bowen, W C -- Patrene, K D -- Mars, W M -- Sullivan, A K -- Murase, N -- Boggs, S S -- Greenberger, J S -- Goff, J P -- New York, N.Y. -- Science. 1999 May 14;284(5417):1168-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA. bryon+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325227" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/pharmacology ; Animals ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carbon Tetrachloride/pharmacology ; Cell Differentiation ; Cell Division ; DNA-Binding Proteins/genetics ; Dipeptidyl Peptidase 4/metabolism ; Epithelial Cells/cytology ; Female ; Hematopoietic Stem Cells/cytology ; In Situ Hybridization ; Liver/*cytology/drug effects/physiology ; *Liver Regeneration ; Liver Transplantation ; Male ; *Nuclear Proteins ; Polymerase Chain Reaction ; Rats ; Rats, Inbred F344 ; Rats, Inbred Lew ; Sex-Determining Region Y Protein ; Stem Cells/*cytology ; *Transcription Factors ; Y Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Redefining rats, mice, and birds. AAA (American Association of Anatomists) Public Affairs Committee (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besharse, J C -- Carlson, B M -- Jenkins, D P -- Lester, D S -- Olds, J L -- Satir, P -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10215528" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Rights/*legislation & jurisprudence ; Animal Welfare/*legislation & jurisprudence ; Animals ; *Animals, Laboratory ; Birds ; Mice ; Rats ; Research ; Societies, Scientific ; United States ; United States Department of Agriculture/legislation & jurisprudence
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Turning thoughts into actions (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):888-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Computer Systems ; Cybernetics ; Electrodes, Implanted ; Electroencephalography ; Female ; Humans ; Male ; Models, Neurological ; Motivation ; Motor Cortex/physiology ; Paralysis/*rehabilitation ; Prostheses and Implants ; Psychomotor Performance/*physiology ; Rats ; *Robotics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Learning visualised, on the double (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1661.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology/*ultrastructure ; Calcium/metabolism ; Image Processing, Computer-Assisted ; In Vitro Techniques ; Learning/*physiology ; *Long-Term Potentiation ; Microscopy, Electron ; Rats ; Synapses/*ultrastructure ; Synaptic Transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Novel endotheliotropic herpesviruses fatal for Asian and African elephants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: A highly fatal hemorrhagic disease has been identified in 10 young Asian and African elephants at North American zoos. In the affected animals there was ultrastructural evidence for herpesvirus-like particles in endothelial cells of the heart, liver, and tongue. Consensus primer polymerase chain reaction combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and another in African elephants. Otherwise healthy African elephants with external herpetic lesions yielded herpesvirus sequences identical to that found in Asian elephants with endothelial disease. This finding suggests that the Asian elephant deaths were caused by cross-species infection with a herpesvirus that is naturally latent in, but normally not lethal to, African elephants. A reciprocal relationship may exist for the African elephant disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richman, L K -- Montali, R J -- Garber, R L -- Kennedy, M A -- Lehnhardt, J -- Hildebrandt, T -- Schmitt, D -- Hardy, D -- Alcendor, D J -- Hayward, G S -- 1 K08 AI01526-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1171-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Smithsonian, National Zoological Park, Washington, DC 20008, USA. lkrichma@welchlink.welch.jhu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024244" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Amino Acid Sequence ; Animals ; Animals, Zoo/*virology ; Asia ; Base Sequence ; DNA, Viral/genetics ; DNA-Directed DNA Polymerase/chemistry/genetics ; Elephants/*virology ; Endodeoxyribonucleases/chemistry/genetics ; Endothelium, Vascular/pathology/*virology ; Female ; Genes, Viral ; Hemorrhage/pathology/veterinary/virology ; Herpesviridae/classification/genetics/*isolation & purification ; Herpesviridae Infections/pathology/transmission/*veterinary/virology ; Inclusion Bodies, Viral/ultrastructure ; Male ; Molecular Sequence Data ; Phylogeny ; Polymerase Chain Reaction ; United States ; Viral Proteins/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immortal time: circadian clock properties of rat suprachiasmatic cell lines (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: Cell lines derived from the rat suprachiasmatic nucleus (SCN) were screened for circadian clock properties distinctive of the SCN in situ. Immortalized SCN cells generated robust rhythms in uptake of the metabolic marker 2-deoxyglucose and in their content of neurotrophins. The phase relationship between these rhythms in vitro was identical to that exhibited by the SCN in vivo. Transplantation of SCN cell lines, but not mesencephalic or fibroblast lines, restored the circadian activity rhythm in arrhythmic, SCN-lesioned rats. Thus, distinctive oscillator, pacemaker, and clock properties of the SCN are not only retained but also maintained in an appropriate circadian phase relationship by immortalized SCN progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Earnest, D J -- Liang, F Q -- Ratcliff, M -- Cassone, V M -- NS35822/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):693-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Anatomy and Medical Neurobiology, College of Medicine, Texas A&M University Health Science Center, College Station, TX 77843-1114, USA. dearnest@tamu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Clocks ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Line ; Cell Transplantation ; *Circadian Rhythm ; Deoxyglucose/metabolism ; Glucose-6-Phosphate/analogs & derivatives/metabolism ; Glycogen/metabolism ; Graft Survival ; Male ; Motor Activity ; Nerve Growth Factors/metabolism ; Neurons/metabolism/*physiology/transplantation ; Neurotrophin 3 ; Rats ; Rats, Sprague-Dawley ; Stem Cells/cytology/metabolism/*physiology ; Suprachiasmatic Nucleus/*cytology/metabolism/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Embryonic stem cell-derived glial precursors: a source of myelinating transplants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Self-renewing, totipotent embryonic stem (ES) cells may provide a virtually unlimited donor source for transplantation. A protocol that permits the in vitro generation of precursors for oligodendrocytes and astrocytes from ES cells was devised. Transplantation in a rat model of a human myelin disease shows that these ES cell-derived precursors interact with host neurons and efficiently myelinate axons in brain and spinal cord. Thus, ES cells can serve as a valuable source of cell type-specific somatic precursors for neural transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brustle, O -- Jones, K N -- Learish, R D -- Karram, K -- Choudhary, K -- Wiestler, O D -- Duncan, I D -- McKay, R D -- NS33710/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):754-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropathology, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. brustle@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Brain/embryology/metabolism ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebral Ventricles/embryology/surgery ; Diffuse Cerebral Sclerosis of Schilder/genetics/*therapy ; Embryo, Mammalian/cytology ; Growth Substances/pharmacology ; Humans ; Male ; Mice ; Myelin Basic Protein/biosynthesis ; Myelin Proteolipid Protein/biosynthesis/genetics ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/metabolism/*transplantation/ultrastructure ; Rats ; Spinal Cord ; Stem Cell Transplantation ; Stem Cells/*cytology
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    A nonhyperthermophilic common ancestor to extant life forms (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: The G+C nucleotide content of ribosomal RNA (rRNA) sequences is strongly correlated with the optimal growth temperature of prokaryotes. This property allows inference of the environmental temperature of the common ancestor to all life forms from knowledge of the G+C content of its rRNA sequences. A model of sequence evolution, assuming varying G+C content among lineages and unequal substitution rates among sites, was devised to estimate ancestral base compositions. This method was applied to rRNA sequences of various species representing the major lineages of life. The inferred G+C content of the common ancestor to extant life forms appears incompatible with survival at high temperature. This finding challenges a widely accepted hypothesis about the origin of life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galtier, N -- Tourasse, N -- Gouy, M -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):220-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biometrie, Genetique et Biologie des Populations, Universite C. Bernard Lyon 1, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Base Sequence ; Computer Simulation ; Confidence Intervals ; Cytosine/*analysis ; *Evolution, Molecular ; Guanine/*analysis ; Hot Temperature ; Likelihood Functions ; Markov Chains ; Models, Chemical ; *Origin of Life ; Phylogeny ; RNA, Archaeal/chemistry ; RNA, Bacterial/chemistry ; RNA, Ribosomal/*chemistry ; Temperature
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    Rbx1, a component of the VHL tumor suppressor complex and SCF ubiquitin ligase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: The von Hippel-Lindau (VHL) tumor suppressor gene is mutated in most human kidney cancers. The VHL protein is part of a complex that includes Elongin B, Elongin C, and Cullin-2, proteins associated with transcriptional elongation and ubiquitination. Here it is shown that the endogenous VHL complex in rat liver also includes Rbx1, an evolutionarily conserved protein that contains a RING-H2 fingerlike motif and that interacts with Cullins. The yeast homolog of Rbx1 is a subunit and potent activator of the Cdc53-containing SCFCdc4 ubiquitin ligase required for ubiquitination of the cyclin-dependent kinase inhibitor Sic1 and for the G1 to S cell cycle transition. These findings provide a further link between VHL and the cellular ubiquitination machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamura, T -- Koepp, D M -- Conrad, M N -- Skowyra, D -- Moreland, R J -- Iliopoulos, O -- Lane, W S -- Kaelin, W G Jr -- Elledge, S J -- Conaway, R C -- Harper, J W -- Conaway, J W -- AG-11085/AG/NIA NIH HHS/ -- GM41628/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):657-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213691" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Line ; *Cullin Proteins ; Cyclin-Dependent Kinase Inhibitor Proteins ; *F-Box Proteins ; Fungal Proteins/metabolism ; *Ligases ; Liver ; Male ; Molecular Sequence Data ; Peptide Synthases/*metabolism ; Proteins/*metabolism ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/metabolism ; S-Phase Kinase-Associated Proteins ; SKP Cullin F-Box Protein Ligases ; Saccharomyces cerevisiae/metabolism ; *Saccharomyces cerevisiae Proteins ; Sequence Alignment ; Transcription Factors/metabolism ; *Tumor Suppressor Proteins ; *Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism ; Von Hippel-Lindau Tumor Suppressor Protein
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    Nonproteolytic neuroprotection by human recombinant tissue plasminogen activator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Human recombinant tissue plasminogen activator (tPA) may benefit ischemic stroke patients by dissolving clots. However, independent of thrombolysis, tPA may also have deleterious effects on neurons by promoting excitotoxicity. Zinc neurotoxicity has been shown to be an additional key mechanism in brain injuries. Hence, if tPA affects zinc neurotoxicity, this may provide additional insights into its effect on neuronal death. Independent of its proteolytic action, tPA markedly attenuated zinc-induced cell death in cortical culture, and, when injected into cerebrospinal fluid, also reduced kainate seizure-induced hippocampal neuronal death in adult rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Y H -- Park, J H -- Hong, S H -- Koh, J Y -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):647-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, 388-1 Poongnap-Dong Songpa-Gu, Seoul 138-736, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; *Cytoprotection ; Fibrinolysin/pharmacology ; Hippocampus/pathology ; Humans ; Kainic Acid/pharmacology ; Male ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/drug effects ; Neuroprotective Agents/*pharmacology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/cerebrospinal fluid/pharmacology ; Seizures/chemically induced/pathology ; Tissue Plasminogen Activator/cerebrospinal fluid/*pharmacology ; Zinc/metabolism/*toxicity
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    Differential stimulation of PKC phosphorylation of potassium channels by ZIP1 and ZIP2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Targeting of protein modification enzymes is a key biochemical step to achieve specific and effective posttranslational modifications. Two alternatively spliced ZIP1 and ZIP2 proteins are described, which bind to both Kvbeta2 subunits of potassium channel and protein kinase C (PKC) zeta, thereby acting as a physical link in the assembly of PKCzeta-ZIP-potassium channel complexes. ZIP1 and ZIP2 differentially stimulate phosphorylation of Kvbeta2 by PKCzeta. They also interact to form heteromultimers, which allows for a hybrid stimulatory activity to PKCzeta. Finally, ZIP1 and ZIP2 coexist in the same cell type and are elevated differentially by neurotrophic factors. These results provide a mechanism for specificity and regulation of PKCzeta-targeted phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, J -- Xu, J -- Bezanilla, M -- van Huizen, R -- Derin, R -- Li, M -- NS33324/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1565-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477520" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Binding Sites ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cerebellum/metabolism ; DNA, Complementary ; Isoenzymes/metabolism ; Molecular Sequence Data ; Myelin Basic Protein/metabolism ; Nerve Growth Factors/pharmacology ; Neurons/*metabolism ; Phosphorylation ; Potassium Channels/*metabolism ; Protein Kinase C/*metabolism ; Pyramidal Cells/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/chemistry/metabolism ; Substrate Specificity ; Transfection
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    Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: In late summer 1999, an outbreak of human encephalitis occurred in the northeastern United States that was concurrent with extensive mortality in crows (Corvus species) as well as the deaths of several exotic birds at a zoological park in the same area. Complete genome sequencing of a flavivirus isolated from the brain of a dead Chilean flamingo (Phoenicopterus chilensis), together with partial sequence analysis of envelope glycoprotein (E-glycoprotein) genes amplified from several other species including mosquitoes and two fatal human cases, revealed that West Nile (WN) virus circulated in natural transmission cycles and was responsible for the human disease. Antigenic mapping with E-glycoprotein-specific monoclonal antibodies and E-glycoprotein phylogenetic analysis confirmed these viruses as WN. This North American WN virus was most closely related to a WN virus isolated from a dead goose in Israel in 1998.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanciotti, R S -- Roehrig, J T -- Deubel, V -- Smith, J -- Parker, M -- Steele, K -- Crise, B -- Volpe, K E -- Crabtree, M B -- Scherret, J H -- Hall, R A -- MacKenzie, J S -- Cropp, C B -- Panigrahy, B -- Ostlund, E -- Schmitt, B -- Malkinson, M -- Banet, C -- Weissman, J -- Komar, N -- Savage, H M -- Stone, W -- McNamara, T -- Gubler, D J -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2333-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, CO 80522, USA. rsl2@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600742" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Base Sequence ; Bird Diseases/epidemiology/virology ; Birds/virology ; *Disease Outbreaks ; Encephalitis Viruses, Japanese/classification/genetics ; Fluorescent Antibody Technique, Indirect ; Genome, Viral ; Humans ; Molecular Sequence Data ; New England/epidemiology ; New York City/epidemiology ; Phylogeny ; Songbirds/virology ; Viral Envelope Proteins/chemistry/genetics/immunology ; West Nile Fever/*epidemiology/veterinary/*virology ; West Nile virus/*classification/*genetics/immunology/isolation & purification
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    Crystal structure of a conserved ribosomal protein-RNA complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: The structure of a highly conserved complex between a 58-nucleotide domain of large subunit ribosomal RNA and the RNA-binding domain of ribosomal protein L11 has been solved at 2.8 angstrom resolution. It reveals a precisely folded RNA structure that is stabilized by extensive tertiary contacts and contains an unusually large core of stacked bases. A bulge loop base from one hairpin of the RNA is intercalated into the distorted major groove of another helix; the protein locks this tertiary interaction into place by binding to the intercalated base from the minor groove side. This direct interaction with a key ribosomal RNA tertiary interaction suggests that part of the role of L11 is to stabilize an unusual RNA fold within the ribosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conn, G L -- Draper, D E -- Lattman, E E -- Gittis, A G -- R37 GM29048/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Johns Hopkins University, Baltimore, MD 21218, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325228" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/metabolism ; Base Pairing ; Base Sequence ; Binding Sites ; Crystallography, X-Ray ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Peptide Elongation Factor G ; Peptide Elongation Factors/metabolism ; Phylogeny ; Protein Conformation ; RNA, Bacterial/*chemistry/metabolism ; RNA, Ribosomal/*chemistry/metabolism ; Ribosomal Proteins/*chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-19
    Description: Activity shapes the structure of neurons and their circuits. Two-photon imaging of CA1 neurons expressing enhanced green fluorescent protein in developing hippocampal slices from rat brains was used to characterize dendritic morphogenesis in response to synaptic activity. High-frequency focal synaptic stimulation induced a period (longer than 30 minutes) of enhanced growth of small filopodia-like protrusions (typically less than 5 micrometers long). Synaptically evoked growth was long-lasting and localized to dendritic regions close (less than 50 micrometers) to the stimulating electrode and was prevented by blockade of N-methyl-D-aspartate receptors. Thus, synaptic activation can produce rapid input-specific changes in dendritic structure. Such persistent structural changes could contribute to the development of neural circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maletic-Savatic, M -- Malinow, R -- Svoboda, K -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1923-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082466" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Culture Techniques ; Dendrites/drug effects/physiology/*ultrastructure ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology ; Luminescent Proteins/genetics ; Microscopy/methods ; Morphogenesis/drug effects ; Pseudopodia/drug effects/physiology/*ultrastructure ; Pyramidal Cells/physiology/*ultrastructure/virology ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; Sindbis Virus/genetics/physiology ; Synapses/*physiology/ultrastructure ; Synaptic Membranes/physiology ; Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Transgenic food debate. The Lancet scolded over Pusztai paper (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):656.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Crops, Agricultural/*adverse effects/genetics ; Diet ; Genetic Engineering ; Intestinal Mucosa/pathology ; Lectins/genetics ; *Mannose-Binding Lectins ; *Peer Review, Research ; *Periodicals as Topic ; Plant Lectins ; Plants, Genetically Modified/*adverse effects ; Publishing ; Rats ; Solanum tuberosum/adverse effects/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Testing the genetics of behavior in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pohorecky, L A -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2067-8; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Genetics, Behavioral/*methods ; Handling (Psychology) ; *Housing, Animal ; Mice ; Rats
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    Possible new anti-inflammatory agent (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):209-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577184" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/*pharmacology ; Computer Simulation ; *Drug Design ; Inflammation/drug therapy ; Intestines/blood supply ; Manganese ; Molecular Mimicry ; Organometallic Compounds/chemical synthesis/chemistry/*pharmacology ; Rats ; Reperfusion Injury/drug therapy ; *Superoxide Dismutase/metabolism ; Superoxides/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Receptor for motilin identified in the human gastrointestinal system (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Motilin is a 22-amino acid peptide hormone expressed throughout the gastrointestinal (GI) tract of humans and other species. It affects gastric motility by stimulating interdigestive antrum and duodenal contractions. A heterotrimeric guanosine triphosphate-binding protein (G protein)-coupled receptor for motilin was isolated from human stomach, and its amino acid sequence was found to be 52 percent identical to the human receptor for growth hormone secretagogues. The macrolide antibiotic erythromycin also interacted with the cloned motilin receptor, providing a molecular basis for its effects on the human GI tract. The motilin receptor is expressed in enteric neurons of the human duodenum and colon. Development of motilin receptor agonists and antagonists may be useful in the treatment of multiple disorders of GI motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feighner, S D -- Tan, C P -- McKee, K K -- Palyha, O C -- Hreniuk, D L -- Pong, S S -- Austin, C P -- Figueroa, D -- MacNeil, D -- Cascieri, M A -- Nargund, R -- Bakshi, R -- Abramovitz, M -- Stocco, R -- Kargman, S -- O'Neill, G -- Van Der Ploeg, L H -- Evans, J -- Patchett, A A -- Smith, R G -- Howard, A D -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2184-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Disorders, Department of Medicinal Chemistry, Merck Research Laboratories, Building RY-80Y-265, 126 East Lincoln Avenue, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381885" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Base Sequence ; Binding Sites ; Calcium/metabolism ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 13 ; Cloning, Molecular ; Colon/*metabolism ; Erythromycin/metabolism ; GTP-Binding Proteins/metabolism ; Humans ; In Situ Hybridization ; Intestine, Small/*metabolism ; Ligands ; Molecular Sequence Data ; Motilin/analogs & derivatives/*metabolism ; Receptors, Gastrointestinal Hormone/*chemistry/*genetics/metabolism ; Receptors, Neuropeptide/*chemistry/*genetics/metabolism ; Stomach/*metabolism ; Thyroid Gland/metabolism ; Transfection
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    Extensive nuclear DNA sequence diversity among chimpanzees (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Although data on nucleotide sequence variation in the human nuclear genome have begun to accumulate, little is known about genomic diversity in chimpanzees (Pan troglodytes) and bonobos (Pan paniscus). A 10,154-base pair sequence on the chimpanzee X chromosome is reported, representing all major subspecies and bonobos. Comparison to humans shows the diversity of the chimpanzee sequences to be almost four times as high and the age of the most recent common ancestor three times as great as the corresponding values of humans. Phylogenetic analyses show the sequences from the different chimpanzee subspecies to be intermixed and the distance between some chimpanzee sequences to be greater than the distance between them and the bonobo sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaessmann, H -- Wiebe, V -- Paabo, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1159-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Evolutionary Anthropology, Inselstrasse 22, D-04103 Leipzig, Germany. kaessmann@eva.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/*genetics ; *Genetic Variation ; *Genome ; Gorilla gorilla/genetics ; Humans ; Molecular Sequence Data ; Mutation ; Pan paniscus/classification/*genetics ; Pan troglodytes/classification/*genetics ; Phylogeny ; Recombination, Genetic ; Species Specificity ; X Chromosome/*genetics
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    Mediation by a CREB family transcription factor of NGF-dependent survival of sympathetic neurons (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Nerve growth factor (NGF) and other neurotrophins support survival of neurons through processes that are incompletely understood. The transcription factor CREB is a critical mediator of NGF-dependent gene expression, but whether CREB family transcription factors regulate expression of genes that contribute to NGF-dependent survival of sympathetic neurons is unknown. CREB-mediated gene expression was both necessary for NGF-dependent survival and sufficient on its own to promote survival of sympathetic neurons. Moreover, expression of Bcl-2 was activated by NGF and other neurotrophins by a CREB-dependent transcriptional mechanism. Overexpression of Bcl-2 reduced the death-promoting effects of CREB inhibition. Together, these data support a model in which neurotrophins promote survival of neurons, in part through a mechanism involving CREB family transcription factor-dependent expression of genes encoding prosurvival factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riccio, A -- Ahn, S -- Davenport, C M -- Blendy, J A -- Ginty, D D -- NS34814-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205-2185, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Axons/drug effects/metabolism ; Brain-Derived Neurotrophic Factor/pharmacology ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/antagonists & inhibitors/*metabolism ; *Gene Expression Regulation ; Genes, bcl-2 ; Genetic Vectors ; Nerve Growth Factor/*pharmacology ; Neurons/*cytology/drug effects/metabolism ; PC12 Cells ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Sympathetic Nervous System/*cytology/drug effects/metabolism ; Transfection
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    Nongenomic transmission across generations of maternal behavior and stress responses in the rat (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: In the rat, variations in maternal care appear to influence the development of behavioral and endocrine responses to stress in the offspring. The results of cross-fostering studies reported here provide evidence for (i) a causal relationship between maternal behavior and stress reactivity in the offspring and (ii) the transmission of such individual differences in maternal behavior from one generation of females to the next. Moreover, an environmental manipulation imposed during early development that alters maternal behavior can then affect the pattern of transmission in subsequent generations. Taken together, these findings indicate that variations in maternal care can serve as the basis for a nongenomic behavioral transmission of individual differences in stress reactivity across generations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Francis, D -- Diorio, J -- Liu, D -- Meaney, M J -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1155-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neuroendocrinology Laboratory, Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, H4H 1R3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550053" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Brain/*metabolism ; Corticotropin-Releasing Hormone/*genetics/metabolism ; Female ; Gene Expression ; Handling (Psychology) ; Hippocampus/metabolism ; Male ; *Maternal Behavior ; Paraventricular Hypothalamic Nucleus/metabolism ; Rats ; Receptors, GABA-A/*genetics/metabolism ; Receptors, Glucocorticoid/*genetics/metabolism ; Stress, Physiological/genetics/*metabolism
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    Dirty transcripts from clean DNA (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridges, B A -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):62-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Cell Mutation Unit, University of Sussex, Falmer, Brighton BN1 9RR, UK. b.a.bridges@sussex.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10215532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Pair Mismatch ; *DNA Damage ; DNA Repair ; DNA, Bacterial/genetics ; Escherichia coli/*genetics ; Humans ; *Mutagenesis ; Neurons/metabolism ; Phenotype ; RNA, Bacterial/genetics ; RNA, Messenger/*genetics ; Rats ; Rats, Brattleboro ; Sequence Deletion ; Templates, Genetic ; *Transcription, Genetic ; Uracil/*metabolism ; Vasopressins/genetics
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    Acute activation of Maxi-K channels (hSlo) by estradiol binding to the beta subunit (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Maxi-K channels consist of a pore-forming alpha subunit and a regulatory beta subunit, which confers the channel with a higher Ca(2+) sensitivity. Estradiol bound to the beta subunit and activated the Maxi-K channel (hSlo) only when both alpha and beta subunits were present. This activation was independent of the generation of intracellular signals and could be triggered by estradiol conjugated to a membrane-impenetrable carrier protein. This study documents the direct interaction of a hormone with a voltage-gated channel subunit and provides the molecular mechanism for the modulation of vascular smooth muscle Maxi-K channels by estrogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valverde, M A -- Rojas, P -- Amigo, J -- Cosmelli, D -- Orio, P -- Bahamonde, M I -- Mann, G E -- Vergara, C -- Latorre, R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1929-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Ciencies Experimentals i de la Salut, Universidad Pompeu Fabra, C/Doctor Aiguader 80, 08003 Barcelona, Spain. miguel.valverde@cexs.upf.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Electrophysiology ; Estradiol/genetics/*metabolism ; Humans ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Patch-Clamp Techniques ; Potassium Channels/*metabolism ; *Potassium Channels, Calcium-Activated ; Protein Binding ; RNA, Messenger ; Rats ; Xenopus laevis
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    Cutting back the calories (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerhard, G S -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1679-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610562" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Cerebral Cortex/metabolism ; *Energy Intake ; Gene Expression ; *Gene Expression Profiling ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*metabolism ; Oligonucleotide Array Sequence Analysis ; Rats ; Research Design
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    Interaction of RAFT1 with gephyrin required for rapamycin-sensitive signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: RAFT1 (rapamycin and FKBP12 target 1; also called FRAP or mTOR) is a member of the ATM (ataxia telangiectasia mutated)-related family of proteins and functions as the in vivo mediator of the effects of the immunosuppressant rapamycin and as an important regulator of messenger RNA translation. In mammalian cells RAFT1 interacted with gephyrin, a widely expressed protein necessary for the clustering of glycine receptors at the cell membrane of neurons. RAFT1 mutants that could not associate with gephyrin failed to signal to downstream molecules, including the p70 ribosomal S6 kinase and the eIF-4E binding protein, 4E-BP1. The interaction with gephyrin ascribes a function to the large amino-terminal region of an ATM-related protein and reveals a role in signal transduction for the clustering protein gephyrin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabatini, D M -- Barrow, R K -- Blackshaw, S -- Burnett, P E -- Lai, M M -- Field, M E -- Bahr, B A -- Kirsch, J -- Betz, H -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- GM-07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1161-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Johns Hopkins University School of Medicine, Department of Neuroscience, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325225" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Gene Expression ; HeLa Cells ; Humans ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Phosphoproteins/*metabolism ; Phosphorylation ; *Phosphotransferases (Alcohol Group Acceptor) ; Rats ; Receptors, Glycine/metabolism ; Repressor Proteins/metabolism ; Ribosomal Protein S6 Kinases/*metabolism ; *Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases
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    Structural basis for a Ca2+-sensing function of the metabotropic glutamate receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: The metabotropic glutamate receptors (mGluRs) are widely distributed in the brain and play important roles in synaptic plasticity. Here it is shown that some types of mGluRs are activated not only by glutamate but also by extracellular Ca2+ (Ca2+o). A single amino acid residue was found to determine the sensitivity of mGluRs to Ca2+o. One of the receptors, mGluR1alpha, but not its point mutant with reduced sensitivity to Ca2+o, caused morphological changes when transfected into mammalian cells. Thus, the sensing of Ca2+o by mGluRs may be important in cells under physiological condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kubo, Y -- Miyashita, T -- Murata, Y -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Musashidai 2-6, Fuchu, Tokyo 183-8526, Japan. ykubo@tmin.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497291" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/ultrastructure ; Amino Acid Sequence ; Animals ; Binding Sites ; Brain/metabolism ; CHO Cells ; Calcium/*metabolism/pharmacology ; Cell Size ; Cricetinae ; Cyclic AMP/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; Glutamic Acid/metabolism/pharmacology ; Molecular Sequence Data ; Oocytes ; Point Mutation ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Metabotropic Glutamate/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Transfection ; Xenopus laevis
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    Role of phosphorylation in regulation of the assembly of endocytic coat complexes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
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  • 84
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    Cholinergic switching within neocortical inhibitory networks (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: Differential actions of acetylcholine on the excitability of two subtypes of interneurons in layer V of the rat visual cortex were examined. Acetylcholine excited low-threshold spike (LTS) cells through nicotinic receptors, whereas it elicited hyperpolarization in fast spiking (FS) cells through muscarinic receptors. Axons of LTS cells were mainly distributed vertically to upper layers, and those of FS cells were primarily confined to layer V. Thus, cortical cholinergic activation may reduce some forms of intralaminar inhibition, promote intracolumnar inhibition, and change the direction of information flow within cortical circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, Z -- Huguenard, J R -- Prince, D A -- NS 06477/NS/NINDS NIH HHS/ -- NS 07280/NS/NINDS NIH HHS/ -- NS 12151/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):985-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703513" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*physiology ; Animals ; Hexamethonium/pharmacology ; In Vitro Techniques ; Interneurons/physiology ; Membrane Potentials ; Muscarinic Antagonists/pharmacology ; Nerve Net/*physiology ; *Neural Inhibition ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Nicotinic/physiology ; Scopolamine Hydrobromide/pharmacology ; Visual Cortex/cytology/*physiology
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  • 85
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    Mismatch repair co-opted by hypermutation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Mice homozygous for a disrupted allele of the mismatch repair gene Pms2 have a mutator phenotype. When this allele is crossed into quasi-monoclonal (QM) mice, which have a very limited B cell repertoire, homozygotes have fewer somatic mutations at the immunoglobulin heavy chain and lambda chain loci than do heterozygotes or wild-type QM mice. That is, mismatch repair seems to contribute to somatic hypermutation rather than stifling it. It is suggested that at immunoglobulin loci in hypermutable B cells, mismatched base pairs are "corrected" according to the newly synthesized DNA strand, thereby fixing incipient mutations instead of eliminating them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cascalho, M -- Wong, J -- Steinberg, C -- Wabl, M -- 1R01 GM37699/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1207-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469811" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenosine Triphosphatases ; Alleles ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Composition ; Base Sequence ; Cloning, Molecular ; Crosses, Genetic ; *DNA Repair ; *DNA Repair Enzymes ; *DNA-Binding Proteins ; Female ; Gene Rearrangement ; *Genes, Immunoglobulin ; Heterozygote ; Immunoglobulin Heavy Chains/chemistry/genetics ; Immunoglobulin Variable Region/chemistry/*genetics ; Immunoglobulin lambda-Chains/chemistry/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Mutation ; Proteins/*genetics/physiology
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  • 86
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    A preorganized active site in the crystal structure of the Tetrahymena ribozyme (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: Group I introns possess a single active site that catalyzes the two sequential reactions of self-splicing. An RNA comprising the two domains of the Tetrahymena thermophila group I intron catalytic core retains activity, and the 5.0 angstrom crystal structure of this 247-nucleotide ribozyme is now described. Close packing of the two domains forms a shallow cleft capable of binding the short helix that contains the 5' splice site. The helix that provides the binding site for the guanosine substrate deviates significantly from A-form geometry, providing a tight binding pocket. The binding pockets for both the 5' splice site helix and guanosine are formed and oriented in the absence of these substrates. Thus, this large ribozyme is largely preorganized for catalysis, much like a globular protein enzyme.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golden, B L -- Gooding, A R -- Podell, E R -- Cech, T R -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):259-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309-0215, USA. bgolden@petunia.colorado.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Pairing ; Base Sequence ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Guanosine/metabolism ; Introns ; Magnesium/metabolism ; Manganese/metabolism ; *Models, Molecular ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Phosphates/metabolism ; RNA Splicing ; RNA, Catalytic/*chemistry/metabolism ; Tetrahymena thermophila/*genetics
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  • 87
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    Errors in genome reviews (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kyrpides, N C -- Ouzounis, C A -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750114" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Genes, Archaeal ; Open Reading Frames ; Publishing/*standards ; *Review Literature as Topic ; Sequence Analysis, DNA/*standards
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  • 88
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    RNA-mediated trans-activation of transcription from a viral RNA (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The red clover necrotic mosaic virus genome is composed of two single-stranded RNA components, RNA-1 and RNA-2. The viral capsid protein is translated from a subgenomic RNA (sgRNA) that is transcribed from genomic RNA-1. Here, a 34-nucleotide sequence in RNA-2 is shown to be required for transcription of sgRNA. Mutations that prevent base-pairing between the RNA-1 subgenomic promoter and the 34-nucleotide trans-activator prevent expression of a reporter gene. A model is proposed in which direct binding of RNA-2 to RNA-1 trans-activates sgRNA synthesis. This RNA-mediated regulation of transcription is unusual among RNA viruses, which typically rely on protein regulators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sit, T L -- Vaewhongs, A A -- Lommel, S A -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):829-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, North Carolina State University, Raleigh, NC 27695-7616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694655" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; Base Sequence ; DNA, Complementary ; Gene Expression ; Genes, Reporter ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Models, Genetic ; Molecular Sequence Data ; Mosaic Viruses/*genetics ; Mutation ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; RNA, Double-Stranded/genetics/metabolism ; RNA, Messenger/biosynthesis/genetics ; RNA, Viral/biosynthesis/chemistry/*genetics ; Sequence Alignment ; *Transcriptional Activation
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  • 89
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    A closer look at SNPs suggests difficulties (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1787-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9776677" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Ethnic Groups/genetics ; *Genetic Markers ; Genetic Predisposition to Disease ; *Genetic Techniques ; Genetic Variation ; *Genetics, Medical ; *Genome, Human ; Humans ; Point Mutation ; *Polymorphism, Genetic ; Recombination, Genetic
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  • 90
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    Inner workings of a transcription factor partnership (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, B J -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1000-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah, Salt Lake City, UT 84132, USA. graves@bioscience.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9490475" target="_blank"〉PubMed〈/a〉
    Keywords: Ankyrins/chemistry ; Base Sequence ; Binding Sites ; DNA/chemistry/*metabolism ; DNA-Binding Proteins/*chemistry/*metabolism ; Dimerization ; GA-Binding Protein Transcription Factor ; Hydrogen Bonding ; Leucine Zippers ; Models, Molecular ; Protein Conformation ; Protein Structure, Secondary ; Transcription Factors/*chemistry/*metabolism ; Transcriptional Activation
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  • 91
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    Protein kinase B kinases that mediate phosphatidylinositol 3,4,5-trisphosphate-dependent activation of protein kinase B (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: Protein kinase B (PKB) is activated in response to phosphoinositide 3-kinases and their lipid products phosphatidylinositol 3,4, 5-trisphosphate [PtdIns(3,4,5)P3] and PtdIns(3,4)P2 in the signaling pathways used by a wide variety of growth factors, antigens, and inflammatory stimuli. PKB is a direct target of these lipids, but this regulation is complex. The lipids can bind to the pleckstrin homologous domain of PKB, causing its translocation to the membrane, and also enable upstream, Thr308-directed kinases to phosphorylate and activate PKB. Four isoforms of these PKB kinases were purified from sheep brain. They bound PtdIns(3,4,5)P3 and associated with lipid vesicles containing it. These kinases contain an NH2-terminal catalytic domain and a COOH-terminal pleckstrin homologous domain, and their heterologous expression augments receptor activation of PKB, which suggests they are the primary signal transducers that enable PtdIns(3,4,5)P3 or PtdIns- (3,4)P2 to activate PKB and hence to control signaling pathways regulating cell survival, glucose uptake, and glycogen metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, L -- Anderson, K -- Stokoe, D -- Erdjument-Bromage, H -- Painter, G F -- Holmes, A B -- Gaffney, P R -- Reese, C B -- McCormick, F -- Tempst, P -- Coadwell, J -- Hawkins, P T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):710-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inositide Laboratory, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445477" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Alternative Splicing ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cloning, Molecular ; DNA, Complementary ; Drosophila ; Drosophila Proteins ; Enzyme Activation ; Humans ; Liposomes/metabolism ; Molecular Sequence Data ; Open Reading Frames ; Phosphatidylinositol Phosphates/*metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/chemistry/genetics/isolation & ; purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Recombinant Proteins/metabolism ; Sheep ; *Signal Transduction
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  • 92
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    Activation of the OxyR transcription factor by reversible disulfide bond formation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: The OxyR transcription factor is sensitive to oxidation and activates the expression of antioxidant genes in response to hydrogen peroxide in Escherichia coli. Genetic and biochemical studies revealed that OxyR is activated through the formation of a disulfide bond and is deactivated by enzymatic reduction with glutaredoxin 1 (Grx1). The gene encoding Grx1 is regulated by OxyR, thus providing a mechanism for autoregulation. The redox potential of OxyR was determined to be -185 millivolts, ensuring that OxyR is reduced in the absence of stress. These results represent an example of redox signaling through disulfide bond formation and reduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, M -- Aslund, F -- Storz, G -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497290" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Bacterial Proteins/genetics/metabolism ; Base Sequence ; Cysteine/metabolism ; *DNA-Binding Proteins ; Disulfides/*metabolism ; Escherichia coli/genetics/*metabolism ; Escherichia coli Proteins ; Gene Expression Regulation, Bacterial ; Glutaredoxins ; Glutathione/metabolism ; Glutathione Disulfide/metabolism ; Glutathione Reductase/metabolism ; Hydrogen Peroxide/*metabolism/pharmacology ; Molecular Sequence Data ; Oxidation-Reduction ; Oxidative Stress ; *Oxidoreductases ; Proteins/genetics/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Thioredoxins/metabolism ; Transcription Factors/genetics/*metabolism
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  • 93
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    Transition from moderate to excessive drug intake: change in hedonic set point (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-09
    Description: Differential access to cocaine self-administration produced two patterns of drug intake in rats. With 1 hour of access per session, drug intake remained low and stable. In contrast, with 6 hours of access, drug intake gradually escalated over days. After escalation, drug consumption was characterized by an increased early drug loading and an upward shift in the cocaine dose-response function, suggesting an increase in hedonic set point. After 1 month of abstinence, escalation of cocaine intake was reinstated to a higher level than before. These findings may provide an animal model for studying the development of excessive drug intake and the basis of addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmed, S H -- Koob, G F -- DA04398/DA/NIDA NIH HHS/ -- DA08467/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Psychopharmacology, Department of Neuropharmacology, CVN-7, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. aserge@sage.scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*etiology ; Dose-Response Relationship, Drug ; Drug Tolerance ; Male ; Rats ; Rats, Wistar ; Reinforcement (Psychology) ; Time Factors
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  • 94
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    Target-specific expression of presynaptic mossy fiber plasticity (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Mossy fiber synaptic transmission at hippocampal CA3 pyramidal cells and interneurons was compared in rat brain slices to determine whether mossy terminals are functionally equivalent. Tetanic stimulation of mossy fibers induced long-term potentiation in pyramidal neurons but was either without effect or it induced depression at synapses onto interneurons. Unlike transmission onto pyramidal neurons, transmission onto interneurons was not potentiated after adenosine 3',5'-monophosphate (cAMP) activation. Furthermore, metabotropic glutamate receptor depression of transmission onto interneurons did not involve cAMP-dependent pathways. Thus, synaptic terminals arising from a common afferent pathway do not function as a single compartment but are specialized, depending on their postsynaptic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maccaferri, G -- Toth, K -- McBain, C J -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Neurophysiology, Room 5A72, Building 49, National Institute of Child Health and Human Development, 9000 Rockville Pike, Bethesda MD 20892-4495, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478900" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Cycloleucine/analogs & derivatives/pharmacology ; Cyclopropanes/pharmacology ; Electric Stimulation ; Excitatory Postsynaptic Potentials/drug effects ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; *Long-Term Potentiation ; Mossy Fibers, Hippocampal/*physiology ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/agonists/physiology ; Synaptic Transmission/drug effects
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  • 95
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    Src activation in the induction of long-term potentiation in CA1 hippocampal neurons (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Long-term potentiation (LTP) is an activity-dependent strengthening of synaptic efficacy that is considered to be a model of learning and memory. Protein tyrosine phosphorylation is necessary to induce LTP. Here, induction of LTP in CA1 pyramidal cells of rats was prevented by blocking the tyrosine kinase Src, and Src activity was increased by stimulation producing LTP. Directly activating Src in the postsynaptic neuron enhanced excitatory synaptic responses, occluding LTP. Src-induced enhancement of alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) receptor-mediated synaptic responses required raised intracellular Ca2+ and N-methyl-D-aspartate (NMDA) receptors. Thus, Src activation is necessary and sufficient for inducing LTP and may function by up-regulating NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Y M -- Roder, J C -- Davidow, J -- Salter, M W -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1363-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Molecular and Medical Genetics, University of Toronto, M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478899" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Electric Stimulation ; Enzyme Activation ; Excitatory Postsynaptic Potentials/drug effects ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation ; Molecular Sequence Data ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Proto-Oncogene Proteins pp60(c-src)/pharmacology ; Pyramidal Cells/enzymology/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Recombinant Proteins/pharmacology ; Up-Regulation ; src-Family Kinases/*metabolism
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  • 96
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    Biological action of leptin as an angiogenic factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 97
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    Gene therapy. Treating with HIV (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1438.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/virology ; Genetic Therapy/*methods ; *Genetic Vectors ; HIV/*genetics/physiology ; Neurons/virology ; Rats ; Retina/virology
    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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  • 98
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    Regulation of cocaine reward by CREB (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: Cocaine regulates the transcription factor CREB (adenosine 3', 5'-monophosphate response element binding protein) in rat nucleus accumbens, a brain region that is important for addiction. Overexpression of CREB in this region decreases the rewarding effects of cocaine and makes low doses of the drug aversive. Conversely, overexpression of a dominant-negative mutant CREB increases the rewarding effects of cocaine. Altered transcription of dynorphin likely contributes to these effects: Its expression is increased by overexpression of CREB and decreased by overexpression of mutant CREB. Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of CREB on cocaine reward. These results identify an intracellular cascade-culminating in gene expression-through which exposure to cocaine modifies subsequent responsiveness to the drug.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlezon, W A Jr -- Thome, J -- Olson, V G -- Lane-Ladd, S B -- Brodkin, E S -- Hiroi, N -- Duman, R S -- Neve, R L -- Nestler, E J -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2272-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine and Connecticut Mental Health Center, New Haven, CT 06508, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/administration & dosage/*pharmacology ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/*metabolism ; Dose-Response Relationship, Drug ; Dynorphins/genetics/metabolism ; Gene Expression ; Gene Expression Regulation ; Gene Transfer Techniques ; Genetic Vectors ; Naltrexone/analogs & derivatives/pharmacology ; Narcotic Antagonists/pharmacology ; Neurons/metabolism ; Nucleus Accumbens/*metabolism ; Point Mutation ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Opioid, kappa/antagonists & inhibitors/metabolism ; *Reward ; Simplexvirus/genetics
    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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  • 99
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    More SNPs on the way (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garber, K -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1788.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9776678" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromatography, High Pressure Liquid ; Databases, Factual ; *Genetic Markers ; Genetic Predisposition to Disease ; *Genetic Techniques ; *Genome, Human ; Humans ; National Institutes of Health (U.S.) ; Neoplasms/*genetics ; Point Mutation ; *Polymorphism, Genetic ; United States
    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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  • 100
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    New views of the origin of mammals (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normilw, D -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):774-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9714680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Artiodactyla/anatomy & histology/classification ; Base Sequence ; *Biological Evolution ; DNA/genetics ; Evolution, Molecular ; *Fossils ; *Mammals/anatomy & histology/classification/genetics ; Paleodontology ; Phylogeny ; Whales/anatomy & histology/classification
    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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