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  • Rats  (326)
  • Transfection  (270)
  • American Association for the Advancement of Science (AAAS)  (563)
  • American Institute of Physics (AIP)
  • 1995-1999  (563)
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  • American Association for the Advancement of Science (AAAS)  (563)
  • American Institute of Physics (AIP)
  • Springer  (18)
  • Wiley-Blackwell  (3)
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Year
  • 1
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    Neurons and silicon get intimate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):578-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Electrodes ; Electrodes, Implanted ; *Electronics ; Electrophysiology ; Humans ; Nerve Net/*physiology ; Nervous System Diseases/*therapy ; Neurons/*physiology ; Rats ; Silicon ; *Transistors, Electronic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Affinity-driven peptide selection of an NFAT inhibitor more selective than cyclosporin A (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: The flow of information from calcium-mobilizing receptors to nuclear factor of activated T cells (NFAT)-dependent genes is critically dependent on interaction between the phosphatase calcineurin and the transcription factor NFAT. A high-affinity calcineurin-binding peptide was selected from combinatorial peptide libraries based on the calcineurin docking motif of NFAT. This peptide potently inhibited NFAT activation and NFAT-dependent expression of endogenous cytokine genes in T cells, without affecting the expression of other cytokines that require calcineurin but not NFAT. Substitution of the optimized peptide sequence into the natural calcineurin docking site increased the calcineurin responsiveness of NFAT. Compounds that interfere selectively with the calcineurin-NFAT interaction without affecting calcineurin phosphatase activity may be useful as therapeutic agents that are less toxic than current drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aramburu, J -- Yaffe, M B -- Lopez-Rodriguez, C -- Cantley, L C -- Hogan, P G -- Rao, A -- R01 AI 40127/AI/NIAID NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01 HL 03601/HL/NHLBI NIH HHS/ -- R43 AI 43726/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10497131" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Calcineurin/*metabolism ; Calcineurin Inhibitors ; Cell Nucleus/metabolism ; Cyclosporine/pharmacology ; Cytokines/biosynthesis/genetics ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/metabolism ; Gene Expression Regulation ; Genes, Reporter ; HeLa Cells ; Humans ; Immunosuppressive Agents/chemistry/metabolism/*pharmacology ; Jurkat Cells ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Oligopeptides/chemistry/metabolism/*pharmacology ; Peptide Library ; Peptides/chemistry/metabolism/*pharmacology ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/*drug effects/immunology ; Transcription Factors/*antagonists & inhibitors/chemistry/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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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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  • 4
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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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  • 5
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    Filling in the blanks of the GABAB receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Coordinated regulation of iron-controlling genes, H-ferritin and IRP2, by c-MYC (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: The protein encoded by the c-MYC proto-oncogene is a transcription factor that can both activate and repress the expression of target genes, but few of its transcriptional targets have been identified. Here, c-MYC is shown to repress the expression of the heavy subunit of the protein ferritin (H-ferritin), which sequesters intracellular iron, and to stimulate the expression of the iron regulatory protein-2 (IRP2), which increases the intracellular iron pool. Down-regulation of the expression of H-ferritin gene was required for cell transformation by c-MYC. These results indicate that c-MYC coordinately regulates genes controlling intracellular iron concentrations and that this function is essential for the control of cell proliferation and transformation by c-MYC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, K J -- Polack, A -- Dalla-Favera, R -- CA-37165/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):676-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Department of Pathology, Columbia University, New York, NY 10032, USA. an.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; DNA/biosynthesis ; Down-Regulation ; Ferritins/*genetics/metabolism ; *Gene Expression Regulation ; Genes, myc ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 2 ; Iron-Regulatory Proteins ; Iron-Sulfur Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-myc/*physiology ; RNA/metabolism ; RNA-Binding Proteins/*genetics/metabolism ; Receptors, Transferrin/genetics ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: The bacterial pathogen Yersinia uses a type III secretion system to inject several virulence factors into target cells. One of the Yersinia virulence factors, YopJ, was shown to bind directly to the superfamily of MAPK (mitogen-activated protein kinase) kinases (MKKs) blocking both phosphorylation and subsequent activation of the MKKs. These results explain the diverse activities of YopJ in inhibiting the extracellular signal-regulated kinase, c-Jun amino-terminal kinase, p38, and nuclear factor kappa B signaling pathways, preventing cytokine synthesis and promoting apoptosis. YopJ-related proteins that are found in a number of bacterial pathogens of animals and plants may function to block MKKs so that host signaling responses can be modulated upon infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orth, K -- Palmer, L E -- Bao, Z Q -- Stewart, S -- Rudolph, A E -- Bliska, J B -- Dixon, J E -- 18024/PHS HHS/ -- AI35175/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1920-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-0606, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489373" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*physiology ; Calcium-Calmodulin-Dependent Protein Kinases/*antagonists & inhibitors ; Cell Line ; Enzyme Activation ; Enzyme Inhibitors/*pharmacology ; HeLa Cells ; Humans ; *MAP Kinase Kinase Kinase 1 ; NF-kappa B/metabolism ; Phosphorylation ; Protein Binding ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Transfection ; Virulence ; Yersinia pseudotuberculosis/genetics/metabolism/pathogenicity/*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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  • 11
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Role of DNA 5-methylcytosine transferase in cell transformation by fos (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The Fos and Jun oncoproteins form dimeric complexes that stimulate transcription of genes containing activator protein-1 regulatory elements. We found, by representational difference analysis, that expression of DNA 5-methylcytosine transferase (dnmt1) in fos-transformed cells is three times the expression in normal fibroblasts and that fos-transformed cells contain about 20 percent more 5-methylcytosine than normal fibroblasts. Transfection of the gene encoding Dnmt1 induced morphological transformation, whereas inhibition of dnmt1 expression or activity resulted in reversion of fos transformation. Inhibition of histone deacetylase, which associates with methylated DNA, also caused reversion. These results suggest that fos may transform cells through alterations in DNA methylation and in histone deacetylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakin, A V -- Curran, T -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888853" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Acetylation ; Animals ; Cell Size ; *Cell Transformation, Neoplastic ; Cytosine/analogs & derivatives/metabolism ; DNA (Cytosine-5-)-Methyltransferase/genetics/*metabolism ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Neoplastic ; *Genes, fos ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; Proto-Oncogene Proteins c-fos/*metabolism ; Rats ; Transcription, Genetic ; Transfection
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  • 13
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    Efficient persistence of extrachromosomal KSHV DNA mediated by latency-associated nuclear antigen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Primary effusion lymphoma (PEL) cells harbor Kaposi's sarcoma-associated herpesvirus (KSHV) episomes and express a KSHV-encoded latency-associated nuclear antigen (LANA). In PEL cells, LANA and KSHV DNA colocalized in dots in interphase nuclei and along mitotic chromosomes. In the absence of KSHV DNA, LANA was diffusely distributed in the nucleus or on mitotic chromosomes. In lymphoblasts, LANA was necessary and sufficient for the persistence of episomes containing a specific KSHV DNA fragment. Furthermore, LANA colocalized with the artificial KSHV DNA episomes in nuclei and along mitotic chromosomes. These results support a model in which LANA tethers KSHV DNA to chromosomes during mitosis to enable the efficient segregation of KSHV episomes to progeny cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballestas, M E -- Chatis, P A -- Kaye, K M -- CA67380-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213686" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis/genetics/metabolism ; Cell Nucleus/chemistry ; Chromosomes/chemistry/*metabolism ; Cosmids ; DNA, Viral/analysis/genetics/*metabolism ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Interphase ; Lymphocytes/chemistry ; Microscopy, Confocal ; *Mitosis ; Nuclear Proteins/analysis/genetics/*metabolism ; *Plasmids ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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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
    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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  • 15
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    Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanagisawa, J -- Yanagi, Y -- Masuhiro, Y -- Suzawa, M -- Watanabe, M -- Kashiwagi, K -- Toriyabe, T -- Kawabata, M -- Miyazono, K -- Kato, S -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1317-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/pharmacology ; COS Cells ; Calcitriol/*metabolism/pharmacology ; Cell Nucleus/metabolism ; DNA-Binding Proteins/*metabolism ; Histone Acetyltransferases ; Ligands ; Nuclear Receptor Coactivator 1 ; Phosphorylation ; Receptor Cross-Talk ; Receptors, Calcitriol/*metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Receptors, Retinoic Acid/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Smad3 Protein ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Beta-defensins: linking innate and adaptive immunity through dendritic and T cell CCR6 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human beta-defensins are also chemotactic for immature dendritic cells and memory T cells. Human beta-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The beta-defensin-induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by beta-defensin. Thus, beta-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, D -- Chertov, O -- Bykovskaia, S N -- Chen, Q -- Buffo, M J -- Shogan, J -- Anderson, M -- Schroder, J M -- Wang, J M -- Howard, O M -- Oppenheim, J J -- N01-CO-56000/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunoregulation, Division of Basic Sciences, Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521347" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/immunology ; Binding, Competitive ; Cell Line ; Chemokine CCL20 ; Chemokines, CC/metabolism/pharmacology ; Chemotaxis ; Chemotaxis, Leukocyte ; Defensins ; Dendritic Cells/*immunology ; Humans ; *Immunity, Active ; *Immunity, Innate ; Immunologic Memory ; *Macrophage Inflammatory Proteins ; Pertussis Toxin ; Proteins/pharmacology/*physiology ; Receptors, CCR6 ; Receptors, Chemokine/genetics/*metabolism ; Recombinant Proteins/pharmacology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virulence Factors, Bordetella/pharmacology ; *beta-Defensins
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  • 17
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    Positive and negative regulation of IkappaB kinase activity through IKKbeta subunit phosphorylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: IkappaB [inhibitor of nuclear factor kappaB (NF-kappaB)] kinase (IKK) phosphorylates IkappaB inhibitory proteins, causing their degradation and activation of transcription factor NF-kappaB, a master activator of inflammatory responses. IKK is composed of three subunits-IKKalpha and IKKbeta, which are highly similar protein kinases, and IKKgamma, a regulatory subunit. In mammalian cells, phosphorylation of two sites at the activation loop of IKKbeta was essential for activation of IKK by tumor necrosis factor and interleukin-1. Elimination of equivalent sites in IKKalpha, however, did not interfere with IKK activation. Thus, IKKbeta, not IKKalpha, is the target for proinflammatory stimuli. Once activated, IKKbeta autophosphorylated at a carboxyl-terminal serine cluster. Such phosphorylation decreased IKK activity and may prevent prolonged activation of the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delhase, M -- Hayakawa, M -- Chen, Y -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):309-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195894" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; HeLa Cells ; Helix-Loop-Helix Motifs ; Humans ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Leucine Zippers ; *MAP Kinase Kinase Kinase 1 ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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  • 20
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    Action of DNA repair endonuclease ERCC1/XPF in living cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: To study the nuclear organization and dynamics of nucleotide excision repair (NER), the endonuclease ERCC1/XPF (for excision repair cross complementation group 1/xeroderma pigmentosum group F) was tagged with green fluorescent protein and its mobility was monitored in living Chinese hamster ovary cells. In the absence of DNA damage, the complex moved freely through the nucleus, with a diffusion coefficient (15 +/- 5 square micrometers per second) consistent with its molecular size. Ultraviolet light-induced DNA damage caused a transient dose-dependent immobilization of ERCC1/XPF, likely due to engagement of the complex in a single repair event. After 4 minutes, the complex regained mobility. These results suggest (i) that NER operates by assembly of individual NER factors at sites of DNA damage rather than by preassembly of holocomplexes and (ii) that ERCC1/XPF participates in repair of DNA damage in a distributive fashion rather than by processive scanning of large genome segments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houtsmuller, A B -- Rademakers, S -- Nigg, A L -- Hoogstraten, D -- Hoeijmakers, J H -- Vermeulen, W -- New York, N.Y. -- Science. 1999 May 7;284(5416):958-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology (Josephine Nefkens Institute, Erasmus University, Post Office Box 1738, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Cricetinae ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/*metabolism ; Diffusion ; Endonucleases/*metabolism ; Fluorescence ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Luminescent Proteins ; Microscopy, Confocal ; Microscopy, Fluorescence ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Ultraviolet Rays
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  • 21
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    Replication of subgenomic hepatitis C virus RNAs in a hepatoma cell line (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: An estimated 170 million persons worldwide are infected with hepatitis C virus (HCV), a major cause of chronic liver disease. Despite increasing knowledge of genome structure and individual viral proteins, studies on virus replication and pathogenesis have been hampered by the lack of reliable and efficient cell culture systems. A full-length consensus genome was cloned from viral RNA isolated from an infected human liver and used to construct subgenomic selectable replicons. Upon transfection into a human hepatoma cell line, these RNAs were found to replicate to high levels, permitting metabolic radiolabeling of viral RNA and proteins. This work defines the structure of HCV replicons functional in cell culture and provides the basis for a long-sought cellular system that should allow detailed molecular studies of HCV and the development of antiviral drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lohmann, V -- Korner, F -- Koch, J -- Herian, U -- Theilmann, L -- Bartenschlager, R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Virology, Johannes-Gutenberg University Mainz, Obere Zahlbacher Strasse 67, 55131 Mainz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390360" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Hepatocellular ; Cloning, Molecular ; Drug Resistance ; *Genome, Viral ; Gentamicins/pharmacology ; Hepacivirus/genetics/*physiology ; Hepatitis C/virology ; Humans ; Liver Neoplasms ; RNA, Viral/*biosynthesis/genetics ; *Replicon ; Transfection ; Tumor Cells, Cultured/*virology ; Viral Nonstructural Proteins/analysis/genetics ; Virus Cultivation ; *Virus Replication
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  • 22
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    Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-01-05
    Description: Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bosch, F -- Miksa, M -- Bittigau, P -- Vockler, J -- Dikranian, K -- Tenkova, T I -- Stefovska, V -- Turski, L -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):70-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/*cytology/drug effects/embryology/growth & development ; Calcium Channel Blockers/pharmacology ; Dizocilpine Maleate/pharmacology ; Dopamine Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Fetus ; Haloperidol/pharmacology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Electron ; Muscarinic Antagonists/pharmacology ; *Nerve Degeneration ; Neurons/*cytology/drug effects/metabolism ; Quinoxalines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/metabolism ; Scopolamine Hydrobromide/pharmacology
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  • 23
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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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  • 24
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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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  • 25
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    A molecular mechanism for electrical tuning of cochlear hair cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Cochlear frequency selectivity in lower vertebrates arises in part from electrical tuning intrinsic to the sensory hair cells. The resonant frequency is determined largely by the gating kinetics of calcium-activated potassium (BK) channels encoded by the slo gene. Alternative splicing of slo from chick cochlea generated kinetically distinct BK channels. Combination with accessory beta subunits slowed the gating kinetics of alpha splice variants but preserved relative differences between them. In situ hybridization showed that the beta subunit is preferentially expressed by low-frequency (apical) hair cells in the avian cochlea. Interaction of beta with alpha splice variants could provide the kinetic range needed for electrical tuning of cochlear hair cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanathan, K -- Michael, T H -- Jiang, G J -- Hiel, H -- Fuchs, P A -- DC00276/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Hearing Sciences, Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880252" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Calcium/metabolism ; Cell Line ; Electrophysiology ; Gene Expression ; Hair Cells, Auditory/*physiology ; Humans ; In Situ Hybridization ; *Ion Channel Gating ; Kinetics ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Potentials ; Patch-Clamp Techniques ; Potassium Channels/genetics/*physiology ; *Potassium Channels, Calcium-Activated ; Quail ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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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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    Erythropoietin receptor activation by a ligand-induced conformation change (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: Erythropoietin and other cytokine receptors are thought to be activated through hormone-induced dimerization and autophosphorylation of JAK kinases associated with the receptor intracellular domains. An in vivo protein fragment complementation assay was used to obtain evidence for an alternative mechanism in which unliganded erythropoietin receptor dimers exist in a conformation that prevents activation of JAK2 but then undergo a ligand-induced conformation change that allows JAK2 to be activated. These results are consistent with crystallographic evidence of distinct dimeric configurations for unliganded and ligand-bound forms of the erythropoietin receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Remy, I -- Wilson, I A -- Michnick, S W -- GM49497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):990-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Biochimie, Universite de Montreal, Casier Postal 6128, succursale Centre-ville, Montreal, Quebec, H3C 3J7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9974393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; COS Cells ; Cricetinae ; Dimerization ; Erythropoietin/metabolism ; Flow Cytometry ; Fluoresceins/metabolism ; Janus Kinase 2 ; Ligands ; Methotrexate/analogs & derivatives/metabolism ; Microscopy, Fluorescence ; Peptides, Cyclic/metabolism ; *Protein Conformation ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Erythropoietin/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Tetrahydrofolate Dehydrogenase/chemistry/metabolism ; Transfection
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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    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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    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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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
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    Stem cells as potential nerve therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):650-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Diffuse Cerebral Sclerosis of Schilder/*therapy ; Embryo, Mammalian/cytology ; Financing, Government ; Germany ; Humans ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/physiology/transplantation ; Rats ; Research Support as Topic ; Spinal Cord ; Stem Cells/*cytology/physiology
    Print ISSN: 0036-8075
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    PEG antibodies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorsky, R -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites, Antibody ; Biological Availability ; Half-Life ; Immunoglobulin Fab Fragments/*immunology/*metabolism ; Male ; Polyethylene Glycols/*metabolism ; Rats ; Rats, Wistar
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    BRCA1 inhibition of estrogen receptor signaling in transfected cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, S -- Wang, J -- Yuan, R -- Ma, Y -- Meng, Q -- Erdos, M R -- Pestell, R G -- Yuan, F -- Auborn, K J -- Goldberg, I D -- Rosen, E M -- R01-CA75503/CA/NCI NIH HHS/ -- R01-ES09169/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, 270-05 76th Avenue, New Hyde Park, NY 11040, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334989" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*physiology ; Breast/cytology ; Breast Neoplasms/etiology ; Cell Division ; Enhancer Elements, Genetic ; Epithelial Cells/cytology ; Estradiol/metabolism ; Estrogen Receptor alpha ; Female ; Genes, BRCA1 ; Genes, Reporter ; Humans ; Ligands ; Male ; Receptors, Estrogen/*metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    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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    The role of CCR7 in TH1 and TH2 cell localization and delivery of B cell help in vivo (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Subsets of murine CD4+ T cells localize to different areas of the spleen after adoptive transfer. Naive and T helper 1 (TH1) cells, which express the chemokine receptor CCR7, are home to the periarteriolar lymphoid sheath, whereas activated TH2 cells, which lack CCR7, form rings at the periphery of the T cell zones near B cell follicles. Retroviral transduction of TH2 cells with CCR7 forces them to localize in a TH1-like pattern and inhibits their participation in B cell help in vivo but not in vitro. Thus, differential expression of chemokine receptors results in unique cellular migration patterns that are important for effective immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randolph, D A -- Huang, G -- Carruthers, C J -- Bromley, L E -- Chaplin, D D -- AI34580/AI/NIAID NIH HHS/ -- T32 GM07200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2159-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Allergy and Immunology, Department of Internal Medicine, Center for Immunology, Washington University School of Medicine. Howard Hughes Medical Institute, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591648" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/*immunology ; Calcium/metabolism ; Cell Movement ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, CCR7 ; Receptors, Chemokine/*immunology/metabolism ; Signal Transduction ; Spleen/*immunology ; Th1 Cells/*immunology/metabolism ; Th2 Cells/*immunology/metabolism ; Transfection
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    Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2alpha, a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, D R -- Shi, S T -- Romano, P R -- Barber, G N -- Lai, M M -- AI 40038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology and Immunology and Howard Hughes Medical Institute, University of Southern California, School of Medicine, Los Angeles, CA 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390359" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chloramphenicol O-Acetyltransferase/biosynthesis ; Drug Resistance, Microbial ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Eukaryotic Initiation Factor-2/chemistry/metabolism ; HeLa Cells ; *Hepacivirus/drug effects ; Humans ; Interferon-alpha/*pharmacology ; Phosphorylation ; Protein Biosynthesis ; Recombinant Fusion Proteins/metabolism/pharmacology ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Transfection ; Transformation, Genetic ; Viral Envelope Proteins/chemistry/metabolism/pharmacology/*physiology ; eIF-2 Kinase/*antagonists & inhibitors/chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prevention of constitutive TNF receptor 1 signaling by silencer of death domains (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: Tumor necrosis factor receptor type 1 (TNF-R1) contains a cytoplasmic death domain that is required for the signaling of TNF activities such as apoptosis and nuclear factor kappa B (NF-kappaB) activation. Normally, these signals are generated only after TNF-induced receptor aggregation. However, TNF-R1 self-associates and signals independently of ligand when overexpressed. This apparent paradox may be explained by silencer of death domains (SODD), a widely expressed approximately 60-kilodalton protein that was found to be associated with the death domain of TNF-R1. TNF treatment released SODD from TNF-R1, permitting the recruitment of proteins such as TRADD and TRAF2 to the active TNF-R1 signaling complex. SODD also interacted with death receptor-3 (DR3), another member of the TNF receptor superfamily. Thus, SODD association may be representative of a general mechanism for preventing spontaneous signaling by death domain-containing receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Y -- Woronicz, J D -- Liu, W -- Goeddel, D V -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):543-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915703" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Antigens, CD/chemistry/genetics/*metabolism ; Apoptosis ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Jurkat Cells ; Molecular Sequence Data ; Mutation ; NF-kappa B/metabolism ; Protein Binding ; Proteins/metabolism ; Receptor Aggregation ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Member 25 ; Receptors, Tumor Necrosis Factor, Type I ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; U937 Cells
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    Potential target found for antimetastasis drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Cloning, Molecular ; *Glucuronidase ; Glycoside Hydrolases/*antagonists & inhibitors/*genetics/isolation & ; purification/metabolism ; Humans ; Mice ; Neoplasm Metastasis/*prevention & control ; Rats ; Tumor Cells, Cultured
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  • 40
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    Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: The Ras-dependent activation of mitogen-activated protein (MAP) kinase pathways by many receptors coupled to heterotrimeric guanine nucleotide binding proteins (G proteins) requires the activation of Src family tyrosine kinases. Stimulation of beta2 adrenergic receptors resulted in the assembly of a protein complex containing activated c-Src and the receptor. Src recruitment was mediated by beta-arrestin, which functions as an adapter protein, binding both c-Src and the agonist-occupied receptor. beta-Arrestin 1 mutants, impaired either in c-Src binding or in the ability to target receptors to clathrin-coated pits, acted as dominant negative inhibitors of beta2 adrenergic receptor-mediated activation of the MAP kinases Erk1 and Erk2. These data suggest that beta-arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal transduction in which the "desensitized" receptor functions as a critical structural component of a mitogenic signaling complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ferguson, S S -- Daaka, Y -- Miller, W E -- Maudsley, S -- Della Rocca, G J -- Lin, F -- Kawakatsu, H -- Owada, K -- Luttrell, D K -- Caron, M G -- Lefkowitz, R J -- DK02352/DK/NIDDK NIH HHS/ -- DK55524/DK/NIDDK NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):655-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, 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/9924018" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cell Membrane/metabolism ; Enzyme Activation ; GTP-Binding Proteins/metabolism ; Humans ; Isoproterenol/metabolism/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Models, Biological ; Phosphorylation ; Point Mutation ; Precipitin Tests ; Proto-Oncogene Proteins pp60(c-src)/*metabolism ; Receptor Cross-Talk ; Receptors, Adrenergic, beta-2/*metabolism ; Receptors, Cell Surface/metabolism ; *Signal Transduction ; Transfection ; src Homology Domains
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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
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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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    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
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  • 45
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    Odor response properties of rat olfactory receptor neurons (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-06-26
    Description: Molecular biology studies of olfaction have identified a multigene family of molecular receptors that are likely to be involved in odor transduction mechanisms. However, because previous functional data on peripheral coding were mainly collected from inferior vertebrates, it has been difficult to document the degree of specificity of odor interaction mechanisms. As a matter of fact, studies of the functional expression of olfactory receptors have not demonstrated the low or high specificity of olfactory receptors. In this study, the selectivity of olfactory receptor neurons was investigated in the rat at the cellular level under physiological conditions by unitary extracellular recordings. Individual olfactory receptor neurons were broadly responsive to qualitatively distinct odor compounds. We conclude that peripheral coding is based on activated arrays of olfactory receptor cells with overlapping tuning profiles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duchamp-Viret, P -- Chaput, M A -- Duchamp, A -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Neurosciences et Systemes Sensoriels, CNRS, UMR, Universite Claude Bernard, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne cedex, France. pduchamp@olfac.univ-lyon1.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381881" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones ; Action Potentials ; Animals ; Anisoles ; Benzaldehydes ; Camphor ; Cyclohexenes ; *Odors ; Olfactory Receptor Neurons/*physiology ; Pentanols ; Rats ; Rats, Wistar ; Receptors, Odorant/genetics/*physiology ; Terpenes
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    Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: BRCA1 encodes a tumor suppressor that is mutated in familial breast and ovarian cancers. Here, it is shown that BRCA1 interacts in vitro and in vivo with hRad50, which forms a complex with hMre11 and p95/nibrin. Upon irradiation, BRCA1 was detected in discrete foci in the nucleus, which colocalize with hRad50. Formation of irradiation-induced foci positive for BRCA1, hRad50, hMre11, or p95 was dramatically reduced in HCC/1937 breast cancer cells carrying a homozygous mutation in BRCA1 but was restored by transfection of wild-type BRCA1. Ectopic expression of wild-type, but not mutated, BRCA1 in these cells rendered them less sensitive to the DNA damage agent, methyl methanesulfonate. These data suggest that BRCA1 is important for the cellular responses to DNA damage that are mediated by the hRad50-hMre11-p95 complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Q -- Chen, C F -- Li, S -- Chen, Y -- Wang, C C -- Xiao, J -- Chen, P L -- Sharp, Z D -- Lee, W H -- CA 30195/CA/NCI NIH HHS/ -- CA 58183/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):747-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, San Antonio, TX 78245, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426999" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*metabolism ; Cell Cycle Proteins/*metabolism ; Cell Nucleus/*metabolism ; Cell Survival ; *DNA Damage ; *DNA Repair Enzymes ; DNA-Binding Proteins/*metabolism ; Gamma Rays ; Genes, BRCA1 ; Humans ; Methyl Methanesulfonate/pharmacology ; Mutagens/pharmacology ; Mutation ; *Nuclear Proteins ; Rad51 Recombinase ; Recombination, Genetic ; Transfection ; Tumor Cells, Cultured
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    Identification of a nuclear receptor for bile acids (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-05-21
    Description: Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, M -- Okamoto, A Y -- Repa, J J -- Tu, H -- Learned, R M -- Luk, A -- Hull, M V -- Lustig, K D -- Mangelsdorf, D J -- Shan, B -- New York, N.Y. -- Science. 1999 May 21;284(5418):1362-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/*metabolism ; Biological Transport ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/metabolism ; Cholesterol 7-alpha-Hydroxylase/*genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Histone Acetyltransferases ; Homeostasis ; Humans ; *Hydroxysteroid Dehydrogenases ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
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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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    Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Extracellular signals often result in simultaneous activation of both the Raf-MEK-ERK and PI3K-Akt pathways (where ERK is extracellular-regulated kinase, MEK is mitogen-activated protein kinase or ERK kinase, and PI3K is phosphatidylinositol 3-kinase). However, these two signaling pathways were shown to exert opposing effects on muscle cell hypertrophy. Furthermore, the PI3K-Akt pathway was shown to inhibit the Raf-MEK-ERK pathway; this cross-regulation depended on the differentiation state of the cell: Akt activation inhibited the Raf-MEK-ERK pathway in differentiated myotubes, but not in their myoblast precursors. The stage-specific inhibitory action of Akt correlated with its stage-specific ability to form a complex with Raf, suggesting the existence of differentially expressed mediators of an inhibitory Akt-Raf complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rommel, C -- Clarke, B A -- Zimmermann, S -- Nunez, L -- Rossman, R -- Reid, K -- Moelling, K -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Signaling System/drug effects ; Mice ; Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism ; Muscle, Skeletal/*cytology/*metabolism ; Myogenin/genetics ; Phenotype ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-raf/*antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection ; Transgenes
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  • 50
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    Molecular identification of a eukaryotic, stretch-activated nonselective cation channel (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: Calcium-permeable, stretch-activated nonselective cation (SA Cat) channels mediate cellular responses to mechanical stimuli. However, genes encoding such channels have not been identified in eukaryotes. The yeast MID1 gene product (Mid1) is required for calcium influx in the yeast Saccharomyces cerevisiae. Functional expression of Mid1 in Chinese hamster ovary cells conferred sensitivity to mechanical stress that resulted in increases in both calcium conductance and the concentration of cytosolic free calcium. These increases were dependent on the presence of extracellular calcium and were reduced by gadolinium, a blocker of SA Cat channels. Single-channel analyses with cell-attached patches revealed that Mid1 acts as a calcium-permeable, cation-selective stretch-activated channel with a conductance of 32 picosiemens at 150 millimolar cesium chloride in the pipette. Thus, Mid1 appears to be a eukaryotic, SA Cat channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanzaki, M -- Nagasawa, M -- Kojima, I -- Sato, C -- Naruse, K -- Sokabe, M -- Iida, H -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):882-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CHO Cells ; Calcium/metabolism ; Calcium Channels/chemistry/genetics/*metabolism ; Cations/*metabolism ; Cell Membrane/metabolism ; Cell Membrane Permeability ; Cesium/metabolism ; Chlorides/pharmacology ; Cricetinae ; Fungal Proteins/chemistry/genetics/*metabolism ; Gadolinium/pharmacology ; Ion Channels/chemistry/genetics/*metabolism ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Membrane Potentials ; Molecular Sequence Data ; Patch-Clamp Techniques ; Pressure ; Saccharomyces cerevisiae/genetics/metabolism ; *Saccharomyces cerevisiae Proteins ; Stress, Mechanical ; Transfection ; Zinc Compounds/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Light-dependent sequestration of TIMELESS by CRYPTOCHROME (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Most organisms have circadian clocks consisting of negative feedback loops of gene regulation that facilitate adaptation to cycles of light and darkness. In this study, CRYPTOCHROME (CRY), a protein involved in circadian photoperception in Drosophila, is shown to block the function of PERIOD/TIMELESS (PER/TIM) heterodimeric complexes in a light-dependent fashion. TIM degradation does not occur under these conditions; thus, TIM degradation is uncoupled from abrogation of its function by light. CRY and TIM are part of the same complex and directly interact in yeast in a light-dependent fashion. PER/TIM and CRY influence the subcellular distribution of these protein complexes, which reside primarily in the nucleus after the perception of a light signal. Thus, CRY acts as a circadian photoreceptor by directly interacting with core components of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ceriani, M F -- Darlington, T K -- Staknis, D -- Mas, P -- Petti, A A -- Weitz, C J -- Kay, S A -- MH-51573/MH/NIMH NIH HHS/ -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):553-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and NSF Center for Biological Timing, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Clocks ; Cell Line ; Cell Nucleus/metabolism ; *Circadian Rhythm ; Cryptochromes ; Cytoplasm/metabolism ; Darkness ; Dimerization ; Drosophila ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/genetics/*metabolism ; Green Fluorescent Proteins ; Insect Proteins/genetics/*metabolism ; *Light ; Luminescent Proteins ; Mutation ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Recombinant Fusion Proteins/metabolism ; Transfection ; Yeasts/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
    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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    Transduction of human CD34+ cells that mediate long-term engraftment of NOD/SCID mice by HIV vectors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: Efficient gene transfer into human hematopoietic stem cells (HSCs) is an important goal in the study of the hematopoietic system as well as for gene therapy of hematopoietic disorders. A lentiviral vector based on the human immunodeficiency virus (HIV) was able to transduce human CD34+ cells capable of stable, long-term reconstitution of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. High-efficiency transduction occurred in the absence of cytokine stimulation and resulted in transgene expression in multiple lineages of human hematopoietic cells for up to 22 weeks after transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, H -- Smith, K A -- Mosier, D E -- Verma, I M -- Torbett, B E -- CA44360/CA/NCI NIH HHS/ -- DK49886/DK/NIDDK NIH HHS/ -- HL53670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):682-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Division ; Cell Survival ; Colony-Forming Units Assay ; Gene Expression ; *Gene Transfer Techniques ; *Genetic Vectors ; Green Fluorescent Proteins ; HIV/*genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; *Hematopoietic Stem Cells/cytology/immunology ; Humans ; Leukemia Virus, Murine/genetics ; Luminescent Proteins/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Promoter Regions, Genetic ; Transfection ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    HIV vaccines. Magic of the occult? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montefiori, D -- Moore, J P -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):336-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for AIDS Research, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA. monte005@mc.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; COS Cells ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/*immunology ; HIV Envelope Protein gp120/immunology ; HIV Envelope Protein gp41/immunology ; HIV-1/*immunology/physiology ; Mice ; Neutralization Tests ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    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
    Print ISSN: 0036-8075
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    Light-independent role of CRY1 and CRY2 in the mammalian circadian clock (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cryptochrome (CRY), a photoreceptor for the circadian clock in Drosophila, binds to the clock component TIM in a light-dependent fashion and blocks its function. In mammals, genetic evidence suggests a role for CRYs within the clock, distinct from hypothetical photoreceptor functions. Mammalian CRY1 and CRY2 are here shown to act as light-independent inhibitors of CLOCK-BMAL1, the activator driving Per1 transcription. CRY1 or CRY2 (or both) showed light-independent interactions with CLOCK and BMAL1, as well as with PER1, PER2, and TIM. Thus, mammalian CRYs act as light-independent components of the circadian clock and probably regulate Per1 transcriptional cycling by contacting both the activator and its feedback inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, E A Jr -- Staknis, D -- Weitz, C J -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/10531061" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Dimerization ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/metabolism/*physiology ; *Gene Expression Regulation ; Genes, Reporter ; Helix-Loop-Helix Motifs ; Humans ; Intracellular Signaling Peptides and Proteins ; *Light ; Mice ; Nuclear Proteins/antagonists & inhibitors/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/antagonists & inhibitors/metabolism ; Transcription Factors/antagonists & inhibitors/metabolism ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cloning genes encoding MHC class II-restricted antigens: mutated CDC27 as a tumor antigen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: In an effort to identify tumor-specific antigens recognized by CD4(+) T cells, an approach was developed that allows the screening of an invariant chain-complementary DNA fusion library in a genetically engineered cell line expressing the essential components of the major histocompatibility complex (MHC) class II processing and presentation pathway. This led to the identification of a mutated form of human CDC27, which gave rise to an HLA-DR4-restricted melanoma antigen. A mutated form of triosephosphate isomerase, isolated by a biochemical method, was also identified as an HLA-DR1-restricted antigen. Thus, this approach may be generally applicable to the identification of antigens recognized by CD4(+) T cells, which could aid the development of strategies for the treatment of patients with cancer, autoimmune diseases, or infectious diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, R F -- Wang, X -- Atwood, A C -- Topalian, S L -- Rosenberg, S A -- New York, N.Y. -- Science. 1999 May 21;284(5418):1351-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, National Cancer Institute, National Institutes of Health, Building 10/2B42, 9000 Rockville Pike, Bethesda, MD 20892, USA. rongfu@pop.nci.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334988" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation ; Antigens, Differentiation, B-Lymphocyte/genetics/immunology ; Antigens, Neoplasm/*immunology ; Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome ; CD4-Positive T-Lymphocytes/immunology ; Cell Cycle Proteins/*genetics/*immunology ; Cell Line, Transformed ; *Cloning, Molecular ; Epitopes/immunology ; HLA-DR1 Antigen/immunology ; HLA-DR4 Antigen/immunology ; Histocompatibility Antigens Class II/genetics/*immunology ; Humans ; Lymphocytes, Tumor-Infiltrating/*immunology ; Melanoma/immunology ; Point Mutation ; Recombinant Fusion Proteins ; Transfection ; Triose-Phosphate Isomerase/genetics/immunology
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeling, J M -- Miller, J R -- Gil, R -- Moon, R T -- White, R -- Virshup, D M -- 3P30CA42014/CA/NCI NIH HHS/ -- R01 CA71074/CA/NCI NIH HHS/ -- T32CA09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092233" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/genetics/*metabolism ; Down-Regulation ; Genes, Reporter ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/metabolism ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Phosphatase 2 ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; *Trans-Activators ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Wnt Proteins ; Xenopus ; Xenopus Proteins ; *Zebrafish Proteins ; beta Catenin
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Role of heteromer formation in GABAB receptor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
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    STAT5 interaction with the T cell receptor complex and stimulation of T cell proliferation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: The role of STAT (signal transducer and activator of transcription) proteins in T cell receptor (TCR) signaling was analyzed. STAT5 became immediately and transiently phosphorylated on tyrosine 694 in response to TCR stimulation. Expression of the protein tyrosine kinase Lck, a key signaling protein in the TCR complex, activated DNA binding of transfected STAT5A and STAT5B to specific STAT inducible elements. The role of Lck in STAT5 activation was confirmed in a Lck-deficient T cell line in which the activation of STAT5 by TCR stimulation was abolished. Expression of Lck induced specific interaction of STAT5 with the subunits of the TCR, indicating that STAT5 may be directly involved in TCR signaling. Stimulation of T cell clones and primary T cell lines also induced the association of STAT5 with the TCR complex. Inhibition of STAT5 function by expression of a dominant negative mutant STAT5 reduced antigen-stimulated proliferation of T cells. Thus, TCR stimulation appears to directly activate STAT5, which may participate in the regulation of gene transcription and T cell proliferation during immunological responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welte, T -- Leitenberg, D -- Dittel, B N -- al-Ramadi, B K -- Xie, B -- Chin, Y E -- Janeway, C A Jr -- Bothwell, A L -- Bottomly, K -- Fu, X Y -- AI34522/AI/NIAID NIH HHS/ -- GM46367/GM/NIGMS NIH HHS/ -- GM55590/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):222-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigen-Presenting Cells/immunology ; Antigens/immunology ; Cell Division ; Cell Line ; DNA-Binding Proteins/genetics/*metabolism ; Interferon-gamma/pharmacology ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/genetics/immunology/metabolism ; Mice ; Mice, Transgenic ; *Milk Proteins ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Antigen, T-Cell/genetics/immunology/*metabolism ; STAT5 Transcription Factor ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology/metabolism ; Th2 Cells/immunology/metabolism ; Trans-Activators/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Probing alcoholism's 'dark side' (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1473.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498528" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/cerebrospinal fluid/*metabolism ; Animals ; Brain/*metabolism ; Corticotropin-Releasing Hormone/cerebrospinal fluid/*metabolism ; Dopamine/metabolism ; Humans ; Rats ; Substance Withdrawal Syndrome/metabolism/prevention & control
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    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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    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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    Tbx5 and the retinotectum projection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Dorsal and ventral aspects of the eye are distinct from the early stages of development. The developing eye cup grows dorsally, and the choroidal fissure is formed on its ventral side. Retinal axons from the dorsal and ventral retina project to the ventral and dorsal tectum, respectively. Misexpression of the Tbx5 gene induced dorsalization of the ventral side of the eye and altered projections of retinal ganglion cell axons. Thus, Tbx5 is involved in eye morphogenesis and is a topographic determinant of the visual projections between retina and tectum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshiba-Takeuchi, K -- Takeuchi, J K -- Matsumoto, K -- Momose, T -- Uno, K -- Hoepker, V -- Ogura, K -- Takahashi, N -- Nakamura, H -- Yasuda, K -- Ogura, T -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara, Japan 630-0101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Avian Proteins ; Axons/*ultrastructure ; Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/genetics/physiology ; Chick Embryo ; DNA-Binding Proteins/genetics ; Electroporation ; Ephrin-B1 ; Ephrin-B2 ; Eye/*embryology ; Gene Expression ; Homeodomain Proteins/genetics ; Membrane Proteins/genetics/physiology ; Morphogenesis ; PAX2 Transcription Factor ; Pigment Epithelium of Eye/embryology/metabolism ; Retina/*embryology/metabolism ; Retinal Ganglion Cells/ultrastructure ; Superior Colliculi/*embryology ; T-Box Domain Proteins/genetics/*physiology ; Transcription Factors/genetics ; Transfection ; Transgenes
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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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    A mammalian H+ channel generated through alternative splicing of the NADPH oxidase homolog NOH-1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Voltage-gated proton (H+) channels are found in many human and animal tissues and play an important role in cellular defense against acidic stress. However, a molecular identification of these unique ion conductances has so far not been achieved. A 191-amino acid protein is described that, upon heterologous expression, has properties indistinguishable from those of native H+ channels. This protein is generated through alternative splicing of messenger RNA derived from the gene NOH-1 (NADPH oxidase homolog 1, where NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banfi, B -- Maturana, A -- Jaconi, S -- Arnaudeau, S -- Laforge, T -- Sinha, B -- Ligeti, E -- Demaurex, N -- Krause, K H -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):138-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology of Aging Laboratory, Department of Geriatrics, Geneva University Hospitals, Geneva Medical School, CH-1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615049" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Cell Line ; Cytosol/metabolism ; Electric Conductivity ; Electron Transport ; Expressed Sequence Tags ; Humans ; Hydrogen/*metabolism ; Hydrogen-Ion Concentration ; Ion Channel Gating ; Ion Channels/chemistry/*genetics/metabolism ; Membrane Glycoproteins/chemistry/*genetics ; Molecular Sequence Data ; NADPH Oxidase/chemistry/*genetics ; Patch-Clamp Techniques ; Protons ; Transfection ; Tumor Cells, Cultured ; Zinc/pharmacology
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    Lentiviral vectors--the promise of gene therapy within reach? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amado, R G -- Chen, I S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):674-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, UCLA School of Medicine and UCLA AIDS Institute, Los Angeles, CA 90095, USA. ramado@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Gene Transfer Techniques ; Genes, Viral ; *Genetic Therapy ; *Genetic Vectors ; HIV/*genetics/physiology ; HIV Infections/therapy/virology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/physiology ; Humans ; Lentivirus/*genetics/physiology ; Mutagenesis, Insertional ; Plasmids ; Recombination, Genetic ; Retinitis Pigmentosa/therapy ; Transfection ; Virus Replication
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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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    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
    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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    Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, S -- Groh, V -- Wu, J -- Steinle, A -- Phillips, J H -- Lanier, L L -- Spies, T -- P01 CA18221/CA/NCI NIH HHS/ -- R01 AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):727-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426993" target="_blank"〉PubMed〈/a〉
    Keywords: Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology/metabolism ; Humans ; Jurkat Cells ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Lymphocyte Subsets/immunology ; Membrane Proteins/metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Immunologic/chemistry/genetics/*immunology/metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; Tumor Cells, Cultured
    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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    Neuronal activity-dependent cell survival mediated by transcription factor MEF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: During mammalian development, electrical activity promotes the calcium-dependent survival of neurons that have made appropriate synaptic connections. However, the mechanisms by which calcium mediates neuronal survival during development are not well characterized. A transcription-dependent mechanism was identified by which calcium influx into neurons promoted cell survival. The transcription factor MEF2 was selectively expressed in newly generated postmitotic neurons and was required for the survival of these neurons. Calcium influx into cerebellar granule neurons led to activation of p38 mitogen-activated protein kinase-dependent phosphorylation and activation of MEF2. Once activated, MEF2 regulated neuronal survival by stimulating MEF2-dependent gene transcription. These findings demonstrate that MEF2 is a calcium-regulated transcription factor and define a function for MEF2 during nervous system development that is distinct from previously well-characterized functions of MEF2 during muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Z -- Bonni, A -- Xia, F -- Nadal-Vicens, M -- Greenberg, M E -- 5T32NS07112/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):785-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Department of Neurology, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/embryology/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dimerization ; Immunohistochemistry ; MEF2 Transcription Factors ; Mitogen-Activated Protein Kinases/metabolism ; Mitosis ; Mutation ; Myogenic Regulatory Factors ; Neurons/*cytology/*metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; p38 Mitogen-Activated Protein Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    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
    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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  • 79
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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    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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  • 81
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    Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Smad proteins mediate transforming growth factor-beta (TGF-beta) signaling to regulate cell growth and differentiation. The SnoN oncoprotein was found to interact with Smad2 and Smad4 and to repress their abilities to activate transcription through recruitment of the transcriptional corepressor N-CoR. Immediately after TGF-beta stimulation, SnoN is rapidly degraded by the nuclear accumulation of Smad3, allowing the activation of TGF-beta target genes. By 2 hours, TGF-beta induces a marked increase in SnoN expression, resulting in termination of Smad-mediated transactivation. Thus, SnoN maintains the repressed state of TGF-beta-responsive genes in the absence of ligand and participates in negative feedback regulation of TGF-beta signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stroschein, S L -- Wang, W -- Zhou, S -- Zhou, Q -- Luo, K -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):771-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Division, Lawrence Berkeley National Laboratory, and Department of Molecular and Cell Biology, University of California, Berkeley, 229 Stanley Hall, Mail Code 3206, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531062" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Cell Nucleus/metabolism ; DNA/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Feedback ; *Gene Expression Regulation ; Humans ; Intracellular Signaling Peptides and Proteins ; Nuclear Proteins/metabolism ; Nuclear Receptor Co-Repressor 1 ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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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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  • 83
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    Turning thoughts into actions (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):888-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Computer Systems ; Cybernetics ; Electrodes, Implanted ; Electroencephalography ; Female ; Humans ; Male ; Models, Neurological ; Motivation ; Motor Cortex/physiology ; Paralysis/*rehabilitation ; Prostheses and Implants ; Psychomotor Performance/*physiology ; Rats ; *Robotics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    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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  • 85
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    Processing of the notch ligand delta by the metalloprotease Kuzbanian (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Signaling by the Notch surface receptor controls cell fate determination in a broad spectrum of tissues. This signaling is triggered by the interaction of the Notch protein with what, so far, have been thought to be transmembrane ligands expressed on adjacent cells. Here biochemical and genetic analyses show that the ligand Delta is cleaved on the surface, releasing an extracellular fragment capable of binding to Notch and acting as an agonist of Notch activity. The ADAM disintegrin metalloprotease Kuzbanian is required for this processing event. These observations raise the possibility that Notch signaling in vivo is modulated by soluble forms of the Notch ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qi, H -- Rand, M D -- Wu, X -- Sestan, N -- Wang, W -- Rakic, P -- Xu, T -- Artavanis-Tsakonas, S -- NS14841/NS/NINDS NIH HHS/ -- NS26084/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):91-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536-0812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872749" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Disintegrins/genetics/*metabolism ; Drosophila/embryology/genetics/metabolism ; *Drosophila Proteins ; Female ; Intracellular Signaling Peptides and Proteins ; Ligands ; Male ; Membrane Proteins/genetics/*metabolism ; Metalloendopeptidases/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Neurons/cytology ; Protein Processing, Post-Translational ; Receptors, Notch ; Signal Transduction ; Transfection
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  • 86
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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  • 87
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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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  • 88
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Synergy between tumor suppressor APC and the beta-catenin-Tcf4 target Tcf1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1. The most abundant Tcf1 isoforms lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roose, J -- Huls, G -- van Beest, M -- Moerer, P -- van der Horn, K -- Goldschmeding, R -- Logtenberg, T -- Clevers, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1923-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Center for Biomedical Genetics, Department of Pathology, University Medical Center Utrecht, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein ; Animals ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Intestinal Neoplasms/genetics/metabolism/pathology ; Lymphoid Enhancer-Binding Factor 1 ; Male ; Mammary Neoplasms, Experimental/genetics/metabolism/pathology ; Mice ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic ; T Cell Transcription Factor 1 ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*genetics/*metabolism ; Transfection ; Tumor Cells, Cultured ; beta Catenin
    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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    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
    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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  • 91
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    Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease. Abeta generation depends on proteolytic cleavage of the amyloid precursor protein (APP) by two unknown proteases: beta-secretase and gamma-secretase. These proteases are prime therapeutic targets. A transmembrane aspartic protease with all the known characteristics of beta-secretase was cloned and characterized. Overexpression of this protease, termed BACE (for beta-site APP-cleaving enzyme) increased the amount of beta-secretase cleavage products, and these were cleaved exactly and only at known beta-secretase positions. Antisense inhibition of endogenous BACE messenger RNA decreased the amount of beta-secretase cleavage products, and purified BACE protein cleaved APP-derived substrates with the same sequence specificity as beta-secretase. Finally, the expression pattern and subcellular localization of BACE were consistent with that expected for beta-secretase. Future development of BACE inhibitors may prove beneficial for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassar, R -- Bennett, B D -- Babu-Khan, S -- Kahn, S -- Mendiaz, E A -- Denis, P -- Teplow, D B -- Ross, S -- Amarante, P -- Loeloff, R -- Luo, Y -- Fisher, S -- Fuller, J -- Edenson, S -- Lile, J -- Jarosinski, M A -- Biere, A L -- Curran, E -- Burgess, T -- Louis, J C -- Collins, F -- Treanor, J -- Rogers, G -- Citron, M -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):735-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen, Inc., One Amgen Center Drive, M/S 29-2-B, Thousand Oaks, CA 91320-1799, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531052" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/*enzymology ; Amino Acid Motifs ; Amino Acid Sequence ; Amyloid Precursor Protein Secretases ; Amyloid beta-Peptides/*biosynthesis ; Amyloid beta-Protein Precursor/*metabolism ; Animals ; Aspartic Acid Endopeptidases/chemistry/genetics/*isolation & ; purification/*metabolism ; Binding Sites ; Brain/enzymology/metabolism ; Cell Line ; Cloning, Molecular ; Endopeptidases ; Endosomes/enzymology ; Gene Expression ; Gene Library ; Golgi Apparatus/enzymology ; Humans ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Peptides/metabolism ; Protease Inhibitors/pharmacology ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; 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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  • 92
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Perspectives: neurobiology. Cranking it up a notch (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chenn, A -- Walsh, C A -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA. shoogasmax@netzero.net〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577225" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Count ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebral Cortex/cytology/metabolism ; Humans ; Ligands ; Membrane Proteins/*metabolism ; Neurites/*physiology ; Neurons/*cytology/metabolism ; Receptor, Notch1 ; Receptor, Notch2 ; Receptors, Cell Surface/*metabolism ; *Signal Transduction ; Stem Cells/cytology/metabolism ; *Transcription Factors ; Transcriptional Activation ; 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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    Evidence for autoregulation of cystathionine gamma-synthase mRNA stability in Arabidopsis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: Control of messenger RNA (mRNA) stability serves as an important mechanism for regulating gene expression. Analysis of Arabidopsis mutants that overaccumulate soluble methionine (Met) revealed that the gene for cystathionine gamma-synthase (CGS), the key enzyme in Met biosynthesis, is regulated at the level of mRNA stability. Transfection experiments with wild-type and mutant forms of the CGS gene suggest that an amino acid sequence encoded by the first exon of CGS acts in cis to destabilize its own mRNA in a process that is activated by Met or one of its metabolites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiba, Y -- Ishikawa, M -- Kijima, F -- Tyson, R H -- Kim, J -- Yamamoto, A -- Nambara, E -- Leustek, T -- Wallsgrove, R M -- Naito, S -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1371-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/*enzymology/genetics ; Carbon-Oxygen Lyases/chemistry/*genetics/metabolism ; Exons ; Gene Expression Regulation, Enzymologic ; *Gene Expression Regulation, Plant ; Genes, Plant ; Genes, Reporter ; Kinetics ; Methionine/metabolism ; Molecular Sequence Data ; Mutation ; RNA, Messenger/genetics/*metabolism ; Sequence Alignment ; 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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  • 95
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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
    Print ISSN: 0036-8075
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    Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Expression of Q205L Galphao (Galphao*), an alpha subunit of heterotrimeric guanine nucleotide-binding proteins (G proteins) that lacks guanosine triphosphatase (GTPase) activity in NIH-3T3 cells, results in transformation. Expression of Galphao* in NIH-3T3 cells activated signal transducer and activator of transcription 3 (Stat3) but not mitogen-activated protein (MAP) kinases 1 or 2. Coexpression of dominant negative Stat3 inhibited Galphao*-induced transformation of NIH-3T3 cells and activation of endogenous Stat3. Furthermore, Galphao* expression increased activity of the tyrosine kinase c-Src, and the Galphao*-induced activation of Stat3 was blocked by expression of Csk (carboxyl-terminal Src kinase), which inactivates c-Src. The results indicate that Stat3 can function as a downstream effector for Galphao* and mediate its biological effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ram, P T -- Horvath, C M -- Iyengar, R -- 1F32 CA79134-01/CA/NCI NIH HHS/ -- DK-38671/DK/NIDDK NIH HHS/ -- GM-54508/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):142-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Immunobiology Center, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA. ramp01@doc.mssm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615050" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line, Transformed ; *Cell Transformation, Neoplastic ; DNA-Binding Proteins/*metabolism ; Enzyme Activation ; GTP-Binding Protein alpha Subunits ; Genes, Reporter ; Heterotrimeric GTP-Binding Proteins/genetics/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neurites/physiology ; Neuronal Plasticity ; Neurons/metabolism/physiology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/*metabolism ; Transfection ; src-Family Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Imaging protein kinase Calpha activation in cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Spatially resolved fluorescence resonance energy transfer (FRET) measured by fluorescence lifetime imaging microscopy (FLIM), provides a method for tracing the catalytic activity of fluorescently tagged proteins inside live cell cultures and enables determination of the functional state of proteins in fixed cells and tissues. Here, a dynamic marker of protein kinase Calpha (PKCalpha) activation is identified and exploited. Activation of PKCalpha is detected through the binding of fluorescently tagged phosphorylation site-specific antibodies; the consequent FRET is measured through the donor fluorophore on PKCalpha by FLIM. This approach enabled the imaging of PKCalpha activation in live and fixed cultured cells and was also applied to pathological samples.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, T -- Squire, A -- Hansra, G -- Bornancin, F -- Prevostel, C -- Hanby, A -- Harris, W -- Barnes, D -- Schmidt, S -- Mellor, H -- Bastiaens, P I -- Parker, P J -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2085-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Phosphorylation Laboratory and Cell Biophysics Laboratory, Imperial Cancer Research Fund (ICRF), 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Breast Neoplasms/enzymology ; COS Cells ; Catalysis ; Cytoplasm/enzymology ; Endoplasmic Reticulum/enzymology ; Energy Transfer ; Enzyme Activation ; Fluorescence ; Fluorescent Dyes ; Golgi Apparatus/enzymology ; Green Fluorescent Proteins ; Humans ; Immune Sera ; Isoenzymes/immunology/*metabolism ; Luminescent Proteins ; Mice ; *Microscopy, Fluorescence ; Phosphorylation ; Phosphothreonine/immunology/metabolism ; Protein Kinase C/immunology/*metabolism ; Protein Kinase C-alpha ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Control of mRNA decay by heat shock-ubiquitin-proteasome pathway (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-16
    Description: Cytokine and proto-oncogene messenger RNAs (mRNAs) are rapidly degraded through AU-rich elements in the 3' untranslated region. Rapid decay involves AU-rich binding protein AUF1, which complexes with heat shock proteins hsc70-hsp70, translation initiation factor eIF4G, and poly(A) binding protein. AU-rich mRNA decay is associated with displacement of eIF4G from AUF1, ubiquitination of AUF1, and degradation of AUF1 by proteasomes. Induction of hsp70 by heat shock, down-regulation of the ubiquitin-proteasome network, or inactivation of ubiquitinating enzyme E1 all result in hsp70 sequestration of AUF1 in the perinucleus-nucleus, and all three processes block decay of AU-rich mRNAs and AUF1 protein. These results link the rapid degradation of cytokine mRNAs to the ubiquitin-proteasome pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laroia, G -- Cuesta, R -- Brewer, G -- Schneider, R J -- CA42357/CA/NCI NIH HHS/ -- CA52443/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):499-502.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Biochemistry, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10205060" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Carrier Proteins/metabolism ; Cell Nucleus/metabolism ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoplasm/metabolism ; Eukaryotic Initiation Factor-4G ; Granulocyte-Macrophage Colony-Stimulating Factor/*genetics ; HSC70 Heat-Shock Proteins ; HSP70 Heat-Shock Proteins/*metabolism ; HeLa Cells ; *Heat-Shock Response ; *Heterogeneous-Nuclear Ribonucleoprotein D ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/*metabolism ; Peptide Initiation Factors/metabolism ; Poly(A)-Binding Proteins ; Proteasome Endopeptidase Complex ; Protein Binding ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/*metabolism ; Transfection ; Ubiquitins/*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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  • 99
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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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  • 100
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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
    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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