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  • Animals  (6.040)
  • Female  (1.472)
  • American Association for the Advancement of Science (AAAS)  (6.653)
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  • 11
    Publikationsdatum: 1998-12-16
    Beschreibung: A peripheral membrane protein that is interactive with lymphocytic choriomeningitis virus (LCMV) was purified from cells permissive to infection. Tryptic peptides from this protein were determined to be alpha-dystroglycan (alpha-DG). Several strains of LCMV and other arenaviruses, including Lassa fever virus (LFV), Oliveros, and Mobala, bound to purified alpha-DG protein. Soluble alpha-DG blocked both LCMV and LFV infection. Cells bearing a null mutation of the gene encoding DG were resistant to LCMV infection, and reconstitution of DG expression in null mutant cells restored susceptibility to LCMV infection. Thus, alpha-DG is a cellular receptor for both LCMV and LFV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, W -- Henry, M D -- Borrow, P -- Yamada, H -- Elder, J H -- Ravkov, E V -- Nichol, S T -- Compans, R W -- Campbell, K P -- Oldstone, M B -- AG 00080/AG/NIA NIH HHS/ -- AI 09484/AI/NIAID NIH HHS/ -- DK09712/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2079-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Neuropharmacology, 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/9851928" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Arenavirus/metabolism ; Cell Line ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; Dystroglycans ; Lassa virus/*metabolism/physiology ; Lymphocytic choriomeningitis virus/*metabolism/physiology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, Virus/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Virus Replication
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-09-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1432-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750111" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chromosome Mapping ; *Chromosomes, Human ; Gene Expression ; *Genome ; *Genome, Human ; Hominidae/*genetics ; *Human Characteristics ; Humans ; Mutation ; Pan troglodytes/genetics ; *Sequence Analysis, DNA ; Sialic Acids/chemistry/physiology ; Species Specificity
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-04-29
    Beschreibung: After the vertebrate lens is induced from head ectoderm, lens-specific genes are expressed. Transcriptional regulation of the lens-specific alphaA-crystallin gene is controlled by an enhancer element, alphaCE2. A gene encoding an alphaCE2-binding protein, L-maf(lens-specific maf), was isolated. L-maf expression is initiated in the lens placode and is restricted to lens cells. The gene product L-Maf regulates the expression of multiple genes expressed in the lens, and ectopic expression of this transcription factor converts chick embryonic ectodermal cells and cultured cells into lens fibers. Thus, vertebrate lens induction and differentiation can be triggered by the activation of L-Maf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogino, H -- Yasuda, K -- New York, N.Y. -- Science. 1998 Apr 3;280(5360):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9525857" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Basic-Leucine Zipper Transcription Factors ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Crystallins/genetics ; DNA, Complementary ; DNA-Binding Proteins/chemistry/genetics ; Ectoderm ; Enhancer Elements, Genetic ; Eye Proteins/genetics ; G-Box Binding Factors ; *Gene Expression Regulation, Developmental ; Genes, Reporter ; Intermediate Filament Proteins/genetics ; Lens, Crystalline/*cytology/*embryology/metabolism ; Maf Transcription Factors ; Molecular Sequence Data ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 14
    Publikationsdatum: 1998-08-07
    Beschreibung: The small guanosine triphosphatases (GTPases) Cdc42 and Rac1 regulate E-cadherin-mediated cell-cell adhesion. IQGAP1, a target of Cdc42 and Rac1, was localized with E-cadherin and beta-catenin at sites of cell-cell contact in mouse L fibroblasts expressing E-cadherin (EL cells), and interacted with E-cadherin and beta-catenin both in vivo and in vitro. IQGAP1 induced the dissociation of alpha-catenin from a cadherin-catenin complex in vitro and in vivo. Overexpression of IQGAP1 in EL cells, but not in L cells expressing an E-cadherin-alpha-catenin chimeric protein, resulted in a decrease in E-cadherin-mediated cell-cell adhesive activity. Thus, IQGAP1, acting downstream of Cdc42 and Rac1, appears to regulate cell-cell adhesion through the cadherin-catenin pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroda, S -- Fukata, M -- Nakagawa, M -- Fujii, K -- Nakamura, T -- Ookubo, T -- Izawa, I -- Nagase, T -- Nomura, N -- Tani, H -- Shoji, I -- Matsuura, Y -- Yonehara, S -- Kaibuchi, K -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):832-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694656" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cadherins/*metabolism ; *Cell Adhesion ; Cell Cycle Proteins/*metabolism ; Cell Membrane/metabolism ; Cytoskeletal Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; L Cells (Cell Line) ; Mice ; Mutation ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; *Trans-Activators ; alpha Catenin ; beta Catenin ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-02-07
    Beschreibung: The Son of Sevenless (Sos) proteins control receptor-mediated activation of Ras by catalyzing the exchange of guanosine diphosphate for guanosine triphosphate on Ras. The NH2-terminal region of Sos contains a Dbl homology (DH) domain in tandem with a pleckstrin homology (PH) domain. In COS-1 cells, the DH domain of Sos stimulated guanine nucleotide exchange on Rac but not Cdc42 in vitro and in vivo. The tandem DH-PH domain of Sos (DH-PH-Sos) was defective in Rac activation but regained Rac stimulating activity when it was coexpressed with activated Ras. Ras-mediated activation of DH-PH-Sos did not require activation of mitogen-activated protein kinase but it was dependent on activation of phosphoinositide 3-kinase. These results reveal a potential mechanism for coupling of Ras and Rac signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimnual, A S -- Yatsula, B A -- Bar-Sagi, D -- CA09176/CA/NCI NIH HHS/ -- CA28146/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438849" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/metabolism ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; Membrane Proteins/chemistry/*metabolism ; *Mitogen-Activated Protein Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins ; Recombinant Fusion Proteins/metabolism ; Retroviridae Proteins, Oncogenic/chemistry ; Signal Transduction ; Son of Sevenless Proteins ; Transfection ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 16
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-05-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1998 May 1;280(5364):677-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599145" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Behavior, Animal ; Female ; *Hylobates ; Male ; *Sexual Behavior, Animal ; *Social Behavior
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-09-22
    Beschreibung: The mechanisms underlying visual motion detection can be studied simultaneously in different cell compartments in vivo by using calcium as a reporter of the spatiotemporal activity distribution in single motion-sensitive cells of the fly. As predicted by the Reichardt model, local dendritic calcium signals are found to indicate the direction and velocity of pattern motion but are corrupted by spatial pattern properties. The latter are canceled out by spatial integration, thus leading to a purely directional selective output signal in the axon. These findings attribute a specific computational task to the dendrites of visual interneurons and imply a functional interpretation of dendritic morphology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Single, S -- Borst, A -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1848-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich-Miescher-Laboratory of the Max-Planck-Society, Spemannstrasse 37-39, D-72076 Tuebingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743497" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Axons/metabolism/physiology ; Calcium/*metabolism ; Calcium Channels/metabolism ; Dendrites/metabolism/*physiology/ultrastructure ; Diptera/physiology ; Female ; Interneurons/physiology ; Membrane Potentials ; *Motion Perception ; Photoreceptor Cells, Invertebrate/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 18
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-05-09
    Beschreibung: Current evidence suggests that the nucleus has a distinct substructure, albeit one that is dynamic rather than a rigid framework. Viral infection, oncogene expression, and inherited human disorders can each cause profound and specific changes in nuclear organization. This review summarizes recent progress in understanding nuclear organization, highlighting in particular the dynamic aspects of nuclear structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamond, A I -- Earnshaw, W C -- 073915/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):547-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Dundee, Dundee DD1 4HN, Scotland, UK. a.i.lamond@dundee.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554838" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Nucleolus/physiology/ultrastructure ; Cell Nucleus/chemistry/*physiology/*ultrastructure ; Chromatin/physiology ; Chromosomes/physiology ; *Drosophila Proteins ; Euchromatin ; Gene Expression Regulation ; Heterochromatin/physiology ; Humans ; Insect Proteins/chemistry/physiology ; Interphase ; Neoplasm Proteins/chemistry/physiology ; *Nuclear Proteins ; Polycomb Repressive Complex 1 ; Polycomb-Group Proteins ; Repressor Proteins/chemistry/physiology ; Ribonucleoproteins, Small Nuclear/analysis/physiology ; Transcription Factors/chemistry/physiology ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 19
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-05-09
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1998 Apr 17;280(5362):380-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9575083" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Anthropology, Physical ; Biological Evolution ; Brain/*anatomy & histology ; Computer Simulation ; DNA, Mitochondrial/genetics ; Female ; *Genetics, Population ; *Hinduism/history ; History, Ancient ; Hominidae/*anatomy & histology ; Humans ; India ; Male ; Models, Anatomic ; Y Chromosome/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 20
    Publikationsdatum: 1998-08-07
    Beschreibung: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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