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  • Binding Sites  (52)
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  • American Association for the Advancement of Science (AAAS)  (95)
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  • 1
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    Genome-wide location and function of DNA binding proteins (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-23
    Beschreibung: Understanding how DNA binding proteins control global gene expression and chromosomal maintenance requires knowledge of the chromosomal locations at which these proteins function in vivo. We developed a microarray method that reveals the genome-wide location of DNA-bound proteins and used this method to monitor binding of gene-specific transcription activators in yeast. A combination of location and expression profiles was used to identify genes whose expression is directly controlled by Gal4 and Ste12 as cells respond to changes in carbon source and mating pheromone, respectively. The results identify pathways that are coordinately regulated by each of the two activators and reveal previously unknown functions for Gal4 and Ste12. Genome-wide location analysis will facilitate investigation of gene regulatory networks, gene function, and genome maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, B -- Robert, F -- Wyrick, J J -- Aparicio, O -- Jennings, E G -- Simon, I -- Zeitlinger, J -- Schreiber, J -- Hannett, N -- Kanin, E -- Volkert, T L -- Wilson, C J -- Bell, S P -- Young, R A -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2306-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125145" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Binding Sites ; Cell Cycle ; DNA, Fungal/genetics/metabolism ; DNA-Binding Proteins/*metabolism ; Fungal Proteins/*metabolism ; Galactose/metabolism ; *Gene Expression Profiling ; *Gene Expression Regulation, Fungal ; Genes, Fungal ; *Genome, Fungal ; Oligonucleotide Array Sequence Analysis ; Peptides/pharmacology ; Promoter Regions, Genetic ; Saccharomyces cerevisiae/*genetics/metabolism/physiology ; *Saccharomyces cerevisiae Proteins ; Transcription Factors/*metabolism ; Transcriptional Activation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Identification of HE1 as the second gene of Niemann-Pick C disease (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-23
    Beschreibung: Niemann-Pick type C2 disease (NP-C2) is a fatal hereditary disorder of unknown etiology characterized by defective egress of cholesterol from lysosomes. Here we show that the disease is caused by a deficiency in HE1, a ubiquitously expressed lysosomal protein identified previously as a cholesterol-binding protein. HE1 was undetectable in fibroblasts from NP-C2 patients but present in fibroblasts from unaffected controls and NP-C1 patients. Mutations in the HE1 gene, which maps to chromosome 14q24.3, were found in NP-C2 patients but not in controls. Treatment of NP-C2 fibroblasts with exogenous recombinant HE1 protein ameliorated lysosomal accumulation of low density lipoprotein-derived cholesterol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naureckiene, S -- Sleat, D E -- Lackland, H -- Fensom, A -- Vanier, M T -- Wattiaux, R -- Jadot, M -- Lobel, P -- DK45992/DK/NIDDK NIH HHS/ -- DK54317/DK/NIDDK NIH HHS/ -- NS37918/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2298-301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ, 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125141" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Biological Transport ; CHO Cells ; *Carrier Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; Cholesterol/*metabolism ; Cricetinae ; Culture Media, Conditioned ; Fibroblasts/metabolism ; Glycoproteins/chemistry/*genetics/*metabolism/pharmacology ; Humans ; Lysosomes/*metabolism ; Molecular Sequence Data ; Mutation ; Niemann-Pick Diseases/*genetics/metabolism ; Rats ; Receptor, IGF Type 2/metabolism ; Recombinant Proteins/metabolism/pharmacology ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Global analysis of the genetic network controlling a bacterial cell cycle (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-16
    Beschreibung: This report presents full-genome evidence that bacterial cells use discrete transcription patterns to control cell cycle progression. Global transcription analysis of synchronized Caulobacter crescentus cells was used to identify 553 genes (19% of the genome) whose messenger RNA levels varied as a function of the cell cycle. We conclude that in bacteria, as in yeast, (i) genes involved in a given cell function are activated at the time of execution of that function, (ii) genes encoding proteins that function in complexes are coexpressed, and (iii) temporal cascades of gene expression control multiprotein structure biogenesis. A single regulatory factor, the CtrA member of the two-component signal transduction family, is directly or indirectly involved in the control of 26% of the cell cycle-regulated genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laub, M T -- McAdams, H H -- Feldblyum, T -- Fraser, C M -- Shapiro, L -- GM32506/GM/NIGMS NIH HHS/ -- GM51426/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2144-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Beckman Center, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118148" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Bacterial Proteins/genetics/metabolism ; Binding Sites ; Caulobacter crescentus/*cytology/*genetics/growth & development/physiology ; Cell Cycle/*genetics ; Chemotaxis/genetics ; *DNA-Binding Proteins ; DNA-Directed RNA Polymerases/genetics ; Fimbriae Proteins ; Flagella/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; Interphase ; Membrane Proteins/genetics ; Oligonucleotide Array Sequence Analysis ; RNA, Bacterial/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; S Phase ; Signal Transduction ; *Transcription Factors ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Down-regulation of the macrophage lineage through interaction with OX2 (CD200) (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-02
    Beschreibung: OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoek, R M -- Ruuls, S R -- Murphy, C A -- Wright, G J -- Goddard, R -- Zurawski, S M -- Blom, B -- Homola, M E -- Streit, W J -- Brown, M H -- Barclay, A N -- Sedgwick, J D -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099416" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD ; Antigens, Surface/*metabolism ; Arthritis, Experimental/immunology/pathology ; Cell Lineage ; Central Nervous System/immunology/pathology ; Denervation ; *Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/pathology ; Facial Nerve ; Gene Targeting ; Joints/immunology/pathology ; Lymph Nodes/cytology ; Macrophage Activation ; Macrophages/cytology/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Microglia/physiology ; Neurons/physiology ; Rats ; Receptors, Immunologic/metabolism ; Spleen/cytology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Biochemical basis of oxidative protein folding in the endoplasmic reticulum (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-11-25
    Beschreibung: The endoplasmic reticulum (ER) supports disulfide bond formation by a poorly understood mechanism requiring protein disulfide isomerase (PDI) and ERO1. In yeast, Ero1p-mediated oxidative folding was shown to depend on cellular flavin adenine dinucleotide (FAD) levels but not on ubiquinone or heme, and Ero1p was shown to be a FAD-binding protein. We reconstituted efficient oxidative folding in vitro using FAD, PDI, and Ero1p. Disulfide formation proceeded by direct delivery of oxidizing equivalents from Ero1p to folding substrates via PDI. This kinetic shuttling of oxidizing equivalents could allow the ER to support rapid disulfide formation while maintaining the ability to reduce and rearrange incorrect disulfide bonds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tu, B P -- Ho-Schleyer, S C -- Travers, K J -- Weissman, J S -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1571-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090354" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Binding Sites ; Carboxypeptidases/chemistry/metabolism ; Cathepsin A ; Chemistry, Physical ; Disulfides/chemistry ; Endoplasmic Reticulum/*metabolism ; Flavin-Adenine Dinucleotide/*metabolism ; Glutathione/metabolism ; Glycoproteins/*metabolism ; Microsomes/metabolism ; Mutation ; Oxidation-Reduction ; Oxidoreductases Acting on Sulfur Group Donors ; Physicochemical Phenomena ; Protein Disulfide-Isomerases/genetics/*metabolism ; *Protein Folding ; Ribonuclease, Pancreatic/chemistry/metabolism ; Saccharomyces cerevisiae/metabolism ; *Saccharomyces cerevisiae Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-11-25
    Beschreibung: beta-Arrestins, originally discovered in the context of heterotrimeric guanine nucleotide binding protein-coupled receptor (GPCR) desensitization, also function in internalization and signaling of these receptors. We identified c-Jun amino-terminal kinase 3 (JNK3) as a binding partner of beta-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells. The upstream JNK activators apoptosis signal-regulating kinase 1 (ASK1) and mitogen-activated protein kinase (MAPK) kinase 4 were also found in complex with beta-arrestin 2. Cellular transfection of beta-arrestin 2 caused cytosolic retention of JNK3 and enhanced JNK3 phosphorylation stimulated by ASK1. Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles. Thus, beta-arrestin 2 acts as a scaffold protein, which brings the spatial distribution and activity of this MAPK module under the control of a GPCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, P H -- Chow, C W -- Miller, W E -- Laporte, S A -- Field, M E -- Lin, F T -- Davis, R J -- Lefkowitz, R J -- CA65861/CA/NCI NIH HHS/ -- CA85422/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090355" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Angiotensin II/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; COS Cells ; Cell Line ; Cell Nucleus/metabolism ; Cytosol/enzymology/metabolism ; Endosomes/enzymology/metabolism ; Enzyme Activation ; Humans ; *MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinase 5 ; MAP Kinase Kinase Kinases/*metabolism ; *MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 10 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Rats ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Two-Hybrid System Techniques
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    PSD-95 involvement in maturation of excitatory synapses (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-11-18
    Beschreibung: PSD-95 is a neuronal PDZ protein that associates with receptors and cytoskeletal elements at synapses, but whose function is uncertain. We found that overexpression of PSD-95 in hippocampal neurons can drive maturation of glutamatergic synapses. PSD-95 expression enhanced postsynaptic clustering and activity of glutamate receptors. Postsynaptic expression of PSD-95 also enhanced maturation of the presynaptic terminal. These effects required synaptic clustering of PSD-95 but did not rely on its guanylate kinase domain. PSD-95 expression also increased the number and size of dendritic spines. These results demonstrate that PSD-95 can orchestrate synaptic development and are suggestive of roles for PSD-95 in synapse stabilization and plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉El-Husseini, A E -- Schnell, E -- Chetkovich, D M -- Nicoll, R A -- Bredt, D S -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1364-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082065" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cells, Cultured ; Dendrites/ultrastructure ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; Interneurons/cytology/metabolism/*physiology ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Nerve Tissue Proteins/chemistry/genetics/metabolism/*physiology ; Patch-Clamp Techniques ; Presynaptic Terminals/physiology ; Protein Structure, Tertiary ; Pyramidal Cells/cytology/metabolism/*physiology ; Rats ; Receptor Aggregation ; Receptors, AMPA/metabolism ; Receptors, Glutamate/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Synaptic Vesicles/physiology ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Allosteric effects of Pit-1 DNA sites on long-term repression in cell type specification (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-11-10
    Beschreibung: Reciprocal gene activation and restriction during cell type differentiation from a common lineage is a hallmark of mammalian organogenesis. A key question, then, is whether a critical transcriptional activator of cell type-specific gene targets can also restrict expression of the same genes in other cell types. Here, we show that whereas the pituitary-specific POU domain factor Pit-1 activates growth hormone gene expression in one cell type, the somatotrope, it restricts its expression from a second cell type, the lactotrope. This distinction depends on a two-base pair spacing in accommodation of the bipartite POU domains on a conserved growth hormone promoter site. The allosteric effect on Pit-1, in combination with other DNA binding factors, results in the recruitment of a corepressor complex, including nuclear receptor corepressor N-CoR, which, unexpectedly, is required for active long-term repression of the growth hormone gene in lactotropes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scully, K M -- Jacobson, E M -- Jepsen, K -- Lunyak, V -- Viadiu, H -- Carriere, C -- Rose, D W -- Hooshmand, F -- Aggarwal, A K -- Rosenfeld, M G -- R01 DK18477/DK/NIDDK NIH HHS/ -- R01 DK54802/DK/NIDDK NIH HHS/ -- R01 GM49327/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1127-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Endocrinology and Metabolism, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073444" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Allosteric Regulation ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; Conserved Sequence ; Crystallization ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Female ; *Gene Expression Regulation ; Genes, Reporter ; Growth Hormone/*genetics ; Male ; Mice ; Mice, Transgenic ; Models, Molecular ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Nuclear Receptor Co-Repressor 1 ; Pituitary Gland/cytology/*metabolism ; Prolactin/*genetics ; Promoter Regions, Genetic ; Protein Conformation ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/genetics/*metabolism ; Transcription Factor Pit-1 ; Transcription Factors/chemistry/genetics/*metabolism ; Transcriptional Activation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Integration of multiple signals through cooperative regulation of the N-WASP-Arp2/3 complex (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-10-29
    Beschreibung: The protein N-WASP [a homolog to the Wiskott-Aldrich syndrome protein (WASP)] regulates actin polymerization by stimulating the actin-nucleating activity of the actin-related protein 2/3 (Arp2/3) complex. N-WASP is tightly regulated by multiple signals: Only costimulation by Cdc42 and phosphatidylinositol (4,5)-bisphosphate (PIP2) yields potent polymerization. We found that regulation requires N-WASP's constitutively active output domain (VCA) and two regulatory domains: a Cdc42-binding domain and a previously undescribed PIP(2)-binding domain. In the absence of stimuli, the regulatory modules together hold the VCA-Arp2/3 complex in an inactive "closed" conformation. In this state, both the Cdc42- and PIP2-binding sites are masked. Binding of either input destabilizes the closed state and enhances binding of the other input. This cooperative activation mechanism shows how combinations of simple binding domains can be used to integrate and amplify coincident signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prehoda, K E -- Scott, J A -- Mullins, R D -- Lim, W A -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):801-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052943" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actin Cytoskeleton/metabolism ; Actin-Related Protein 2 ; Actin-Related Protein 3 ; Actins/*metabolism ; Amino Acid Motifs ; Binding Sites ; Biopolymers ; *Cytoskeletal Proteins ; GTP Phosphohydrolases/metabolism ; Humans ; Models, Biological ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Thermodynamics ; Wiskott-Aldrich Syndrome Protein, Neuronal ; cdc42 GTP-Binding Protein/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Learning-induced LTP in neocortex (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-10-20
    Beschreibung: The hypothesis that learning occurs through long-term potentiation (LTP)- and long-term depression (LTD)-like mechanisms is widely held but unproven. This hypothesis makes three assumptions: Synapses are modifiable, they modify with learning, and they strengthen through an LTP-like mechanism. We previously established the ability for synaptic modification and a synaptic strengthening with motor skill learning in horizontal connections of the rat motor cortex (MI). Here we investigated whether learning strengthened these connections through LTP. We demonstrated that synapses in the trained MI were near the ceiling of their modification range, compared with the untrained MI, but the range of synaptic modification was not affected by learning. In the trained MI, LTP was markedly reduced and LTD was enhanced. These results are consistent with the use of LTP to strengthen synapses during learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rioult-Pedotti, M S -- Friedman, D -- Donoghue, J P -- NS27164/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):533-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Brown University, Providence, RI 02912, USA. mengia_rioult@brown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039938" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Electric Stimulation ; Female ; Learning/*physiology ; Long-Term Potentiation/*physiology ; Models, Neurological ; Motor Cortex/*physiology ; Motor Skills ; Neuronal Plasticity ; Rats ; Rats, Sprague-Dawley ; Synapses/*physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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