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  • Rats  (57)
  • Engineering
  • American Association for the Advancement of Science (AAAS)  (61)
  • 2005-2009  (61)
  • 2006  (61)
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  • 2005-2009  (61)
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  • 1
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    Characterization of the piRNA complex from rat testes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Small noncoding RNAs regulate processes essential for cell growth and development, including mRNA degradation, translational repression, and transcriptional gene silencing (TGS). During a search for candidate mammalian factors for TGS, we purified a complex that contains small RNAs and Riwi, the rat homolog to human Piwi. The RNAs, frequently 29 to 30 nucleotides in length, are called Piwi-interacting RNAs (piRNAs), 94% of which map to 100 defined (〈 or = 101 kb) genomic regions. Within these regions, the piRNAs generally distribute across only one genomic strand or distribute on two strands but in a divergent, nonoverlapping manner. Preparations of piRNA complex (piRC) contain rRecQ1, which is homologous to qde-3 from Neurospora, a gene implicated in silencing pathways. Piwi has been genetically linked to TGS in flies, and slicer activity cofractionates with the purified complex. These results are consistent with a gene-silencing role for piRC in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lau, Nelson C -- Seto, Anita G -- Kim, Jinkuk -- Kuramochi-Miyagawa, Satomi -- Nakano, Toru -- Bartel, David P -- Kingston, Robert E -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):363-7. Epub 2006 Jun 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778019" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/isolation & purification/metabolism ; Animals ; Chromosomes, Mammalian ; Conserved Sequence ; DNA Helicases/isolation & purification/metabolism ; Gene Library ; Genome ; Male ; Mice ; Proteins/isolation & purification/*metabolism ; *RNA Interference ; RNA, Untranslated/chemistry/genetics/isolation & purification/*metabolism ; Rats ; Rats, Sprague-Dawley ; RecQ Helicases ; Ribonucleoproteins/chemistry/isolation & purification/*metabolism ; Testis/*chemistry ; Transcription, Genetic
    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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    A clamping mechanism involved in SNARE-dependent exocytosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: During neurotransmitter release at the synapse, influx of calcium ions stimulates the release of neurotransmitter. However, the mechanism by which synaptic vesicle fusion is coupled to calcium has been unclear, despite the identification of both the core fusion machinery [soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)] and the principal calcium sensor (synaptotagmin). Here, we describe what may represent a basic principle of the coupling mechanism: a reversible clamping protein (complexin) that can freeze the SNAREpin, an assembled fusion-competent intermediate en route to fusion. When calcium binds to the calcium sensor synaptotagmin, the clamp would then be released. SNARE proteins, and key regulators like synaptotagmin and complexin, can be ectopically expressed on the cell surface. Cells expressing such "flipped" synaptic SNAREs fuse constitutively, but when we coexpressed complexin, fusion was blocked. Adding back calcium triggered fusion from this intermediate in the presence of synaptotagmin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giraudo, Claudio G -- Eng, William S -- Melia, Thomas J -- Rothman, James E -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):676-80. Epub 2006 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cellular Biophysics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794037" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Vesicular Transport ; Animals ; Calcium/metabolism ; Cell Membrane/metabolism ; *Exocytosis ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Nerve Tissue Proteins/*metabolism ; Rats ; Recombinant Proteins/metabolism ; SNARE Proteins/*metabolism ; Synaptotagmin I/metabolism ; Synaptotagmins/metabolism ; Type C Phospholipases/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    A virulence locus of Pseudomonas aeruginosa encodes a protein secretion apparatus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-10
    Description: Bacterial pathogens frequently use protein secretion to mediate interactions with their hosts. Here we found that a virulence locus (HSI-I) of Pseudomonas aeruginosa encodes a protein secretion apparatus. The apparatus assembled in discrete subcellular locations and exported Hcp1, a hexameric protein that forms rings with a 40 angstrom internal diameter. Regulatory patterns of HSI-I suggested that the apparatus functions during chronic infections. We detected Hcp1 in pulmonary secretions of cystic fibrosis (CF) patients and Hcp1-specific antibodies in their sera. Thus, HSI-I likely contributes to the pathogenesis of P. aeruginosa in CF patients. HSI-I-related loci are widely distributed among bacterial pathogens and may play a general role in mediating host interactions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2800167/" 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/PMC2800167/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mougous, Joseph D -- Cuff, Marianne E -- Raunser, Stefan -- Shen, Aimee -- Zhou, Min -- Gifford, Casey A -- Goodman, Andrew L -- Joachimiak, Grazyna -- Ordonez, Claudia L -- Lory, Stephen -- Walz, Thomas -- Joachimiak, Andrzej -- Mekalanos, John J -- AI21451/AI/NIAID NIH HHS/ -- AI26289/AI/NIAID NIH HHS/ -- GM074942/GM/NIGMS NIH HHS/ -- GM62414/GM/NIGMS NIH HHS/ -- P50 GM062414/GM/NIGMS NIH HHS/ -- P50 GM062414-02/GM/NIGMS NIH HHS/ -- U54 GM074942/GM/NIGMS NIH HHS/ -- U54 GM074942-04S2/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 9;312(5779):1526-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16763151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/*genetics/physiology/secretion ; Crystallography, X-Ray ; Cystic Fibrosis/complications/microbiology ; Humans ; Models, Molecular ; Protein Conformation ; Pseudomonas Infections/complications/microbiology ; Pseudomonas aeruginosa/*genetics/pathogenicity ; Rats ; Recombinant Fusion Proteins ; Sequence Alignment ; Virulence/genetics
    Print ISSN: 0036-8075
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  • 4
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    American Society for Cell Biology. Sprayed-on growth factors guide stem cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1865.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/*pharmacology ; Bone and Bones/*cytology ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Extracellular Matrix ; Myoblasts/cytology ; Rats ; Stem Cells/*cytology
    Print ISSN: 0036-8075
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  • 5
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    Evolution of hormone-receptor complexity by molecular exploitation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: According to Darwinian theory, complexity evolves by a stepwise process of elaboration and optimization under natural selection. Biological systems composed of tightly integrated parts seem to challenge this view, because it is not obvious how any element's function can be selected for unless the partners with which it interacts are already present. Here we demonstrate how an integrated molecular system-the specific functional interaction between the steroid hormone aldosterone and its partner the mineralocorticoid receptor-evolved by a stepwise Darwinian process. Using ancestral gene resurrection, we show that, long before the hormone evolved, the receptor's affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular exploitation-recruitment of an older molecule, previously constrained for a different role, into a new functional complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridgham, Jamie T -- Carroll, Sean M -- Thornton, Joseph W -- F32-GM074398/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):97-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Ecology and Evolutionary Biology, University of Oregon, Eugene, OR 97403, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601189" target="_blank"〉PubMed〈/a〉
    Keywords: Aldosterone/chemistry/*metabolism ; Amino Acid Substitution ; Animals ; Bayes Theorem ; Binding Sites ; Desoxycorticosterone/metabolism ; *Evolution, Molecular ; Gene Duplication ; Hagfishes ; Hydrocortisone/metabolism ; Lampreys ; Ligands ; Mutation ; Perciformes ; Phylogeny ; Rats ; Receptors, Glucocorticoid/chemistry/genetics/metabolism ; Receptors, Mineralocorticoid/chemistry/*genetics/*metabolism ; Receptors, Steroid/chemistry/*genetics/*metabolism ; Skates (Fish)
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  • 6
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    Cortex is driven by weak but synchronously active thalamocortical synapses (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Sensory stimuli reach the brain via the thalamocortical projection, a group of axons thought to be among the most powerful in the neocortex. Surprisingly, these axons account for only approximately 15% of synapses onto cortical neurons. The thalamocortical pathway might thus achieve its effectiveness via high-efficacy thalamocortical synapses or via amplification within cortical layer 4. In rat somatosensory cortex, we measured in vivo the excitatory postsynaptic potential evoked by a single synaptic connection and found that thalamocortical synapses have low efficacy. Convergent inputs, however, are both numerous and synchronous, and intracortical amplification is not required. Our results suggest a mechanism of cortical activation by which thalamic input alone can drive cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruno, Randy M -- Sakmann, Bert -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1622-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology, Max Planck Institute for Medical Research, Jahnstrasse 29, 69120 Heidelberg, Germany. bruno@mpimf-heidelberg.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778049" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Dendrites/physiology ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Membrane Potentials ; Neural Pathways ; Neurons/*physiology ; Rats ; Rats, Wistar ; Somatosensory Cortex/cytology/*physiology ; Synapses/*physiology ; *Synaptic Transmission ; Thalamus/cytology/*physiology ; Vibrissae/innervation/physiology
    Print ISSN: 0036-8075
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  • 7
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    Ca2+ entry through plasma membrane IP3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: Inositol 1,4,5-trisphosphate receptors (IP3Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane (PM) channels in cells lacking IP3R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP3Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP3Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellis, Olivier -- Dedos, Skarlatos G -- Tovey, Stephen C -- Taufiq-Ur-Rahman -- Dubel, Stefan J -- Taylor, Colin W -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):229-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Bungarotoxins/metabolism/pharmacology ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling ; Cell Membrane/*metabolism ; Cells, Cultured ; Chickens ; Electric Conductivity ; Endoplasmic Reticulum/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; *Ion Channel Gating ; Mice ; Nuclear Envelope/metabolism ; Patch-Clamp Techniques ; Point Mutation ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/*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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  • 8
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    The high cost of coming to America (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teich, Al -- White, Wendy D -- New York, N.Y. -- Science. 2006 May 5;312(5774):657.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675666" target="_blank"〉PubMed〈/a〉
    Keywords: Engineering ; *Foreign Professional Personnel ; Humans ; *International Cooperation ; *Security Measures ; *Students ; Travel ; United States
    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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    Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(Met/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. When placed in stressful settings, BDNF(Met/Met) mice exhibited increased anxiety-related behaviors that were not normalized by the antidepressant, fluoxetine. A variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880880/" 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/PMC1880880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhe-Yu -- Jing, Deqiang -- Bath, Kevin G -- Ieraci, Alessandro -- Khan, Tanvir -- Siao, Chia-Jen -- Herrera, Daniel G -- Toth, Miklos -- Yang, Chingwen -- McEwen, Bruce S -- Hempstead, Barbara L -- Lee, Francis S -- MH060478/MH/NIMH NIH HHS/ -- MH068850/MH/NIMH NIH HHS/ -- NS052819/NS/NINDS NIH HHS/ -- NS30687/NS/NINDS NIH HHS/ -- R01 NS052819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10021, USA. zheyuchen@sdu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023662" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anxiety/drug therapy/*genetics ; Behavior, Animal ; Brain-Derived Neurotrophic Factor/*genetics/*physiology ; Conditioning (Psychology) ; Dendrites/ultrastructure ; Dentate Gyrus/cytology ; Fear ; Fluoxetine/administration & dosage/pharmacology ; Hippocampus/anatomy & histology/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/cytology/metabolism ; Organ Size ; *Polymorphism, Single Nucleotide ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors/administration & dosage/pharmacology
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  • 10
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    Applied physics. High-speed atomic force microscopy (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansma, Paul K -- Schitter, Georg -- Fantner, Georg E -- Prater, Craig -- GM 65354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):601-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of California, Santa Barbara, CA 93106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068247" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Collagen/ultrastructure ; Electronics ; *Microscopy, Atomic Force/instrumentation/methods ; Rats ; Time Factors
    Print ISSN: 0036-8075
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  • 11
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    Neuroscience. Neurons find strength through synchrony in the brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonso, Jose-Manuel -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1604-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, State University of New York College of Optometry, New York, NY 10036, USA. jalonso@sunyopt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Excitatory Postsynaptic Potentials ; Mice ; Neural Pathways ; Neurons/*physiology ; Rats ; Somatosensory Cortex/*physiology ; Synapses/*physiology ; *Synaptic Transmission ; Thalamus/*physiology
    Print ISSN: 0036-8075
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  • 12
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    Alterations in 5-HT1B receptor function by p11 in depression-like states (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Chergui, Karima -- Rachleff, Ilan -- Flajolet, Marc -- Zhang, Xiaoqun -- El Yacoubi, Malika -- Vaugeois, Jean-Marie -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):77-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400147" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Electroconvulsive Therapy ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Neurons/metabolism ; Rats ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism/physiology ; Signal Transduction ; Two-Hybrid System Techniques
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  • 13
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    Chemistry. Toward molecular imaging with xenon MRI (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Driehuys, Bastiaan -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):432-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiology, Center for In Vivo Microscopy, Duke University Medical Center, Durham, NC 27710, USA. driehuys@orion.duhs.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053138" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atherosclerosis/diagnosis/physiopathology ; *Biosensing Techniques ; Humans ; Lung/anatomy & histology ; Magnetic Resonance Imaging/*methods ; Magnetic Resonance Spectroscopy ; Rats ; Sensitivity and Specificity ; *Xenon Isotopes
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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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    Excitatory effect of GABAergic axo-axonic cells in cortical microcircuits (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-18
    Description: Axons in the cerebral cortex receive synaptic input at the axon initial segment almost exclusively from gamma-aminobutyric acid-releasing (GABAergic) axo-axonic cells (AACs). The axon has the lowest threshold for action potential generation in neurons; thus, AACs are considered to be strategically placed inhibitory neurons controlling neuronal output. However, we found that AACs can depolarize pyramidal cells and can initiate stereotyped series of synaptic events in rat and human cortical networks because of a depolarized reversal potential for axonal relative to perisomatic GABAergic inputs. Excitation and signal propagation initiated by AACs is supported by the absence of the potassium chloride cotransporter 2 in the axon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szabadics, Janos -- Varga, Csaba -- Molnar, Gabor -- Olah, Szabolcs -- Barzo, Pal -- Tamas, Gabor -- N535915/PHS HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 13;311(5758):233-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Comparative Physiology, University of Szeged, Kozep fasor 52, Szeged, H-6726, Hungary.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410524" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/*physiology ; Cerebral Cortex/*cytology/physiology ; Excitatory Postsynaptic Potentials ; Humans ; In Vitro Techniques ; Middle Aged ; Neural Inhibition ; Neurons/*physiology ; Pyramidal Cells/physiology ; Rats ; Rats, Wistar ; Symporters/metabolism ; gamma-Aminobutyric Acid/physiology
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  • 15
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    Conjunctive representation of position, direction, and velocity in entorhinal cortex (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-05-06
    Description: Grid cells in the medial entorhinal cortex (MEC) are part of an environment-independent spatial coordinate system. To determine how information about location, direction, and distance is integrated in the grid-cell network, we recorded from each principal cell layer of MEC in rats that explored two-dimensional environments. Whereas layer II was predominated by grid cells, grid cells colocalized with head-direction cells and conjunctive grid x head-direction cells in the deeper layers. All cell types were modulated by running speed. The conjunction of positional, directional, and translational information in a single MEC cell type may enable grid coordinates to be updated during self-motion-based navigation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sargolini, Francesca -- Fyhn, Marianne -- Hafting, Torkel -- McNaughton, Bruce L -- Witter, Menno P -- Moser, May-Britt -- Moser, Edvard I -- New York, N.Y. -- Science. 2006 May 5;312(5774):758-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for the Biology of Memory, Norwegian University of Science and Technology, 7489 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophysiology ; Entorhinal Cortex/*cytology/*physiology ; Exploratory Behavior ; Locomotion ; Male ; Nerve Net/*physiology ; Neurons/*physiology ; *Orientation ; Rats ; Rats, Long-Evans ; *Space Perception
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  • 16
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    Escherichia coli induces DNA double-strand breaks in eukaryotic cells (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-12
    Description: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
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  • 17
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    An architectural framework that may lie at the core of the postsynaptic density (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-01-28
    Description: The postsynaptic density (PSD) is a complex assembly of proteins associated with the postsynaptic membrane that organizes neurotransmitter receptors, signaling pathways, and regulatory elements within a cytoskeletal matrix. Here we show that the sterile alpha motif domain of rat Shank3/ProSAP2, a master scaffolding protein located deep within the PSD, can form large sheets composed of helical fibers stacked side by side. Zn2+, which is found in high concentrations in the PSD, binds tightly to Shank3 and may regulate assembly. Sheets of the Shank protein could form a platform for the construction of the PSD complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baron, Marisa K -- Boeckers, Tobias M -- Vaida, Bianca -- Faham, Salem -- Gingery, Mari -- Sawaya, Michael R -- Salyer, Danielle -- Gundelfinger, Eckart D -- Bowie, James U -- R01 CA081000/CA/NCI NIH HHS/ -- R01 GM063919/GM/NIGMS NIH HHS/ -- R01 GM063919-07/GM/NIGMS NIH HHS/ -- R01 GM063919-08/GM/NIGMS NIH HHS/ -- R01 GM075922/GM/NIGMS NIH HHS/ -- R01 GM075922-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 27;311(5760):531-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, Molecular Biology Institute, University of California, Los Angeles, 611 Charles E. Young Drive East, Los Angeles, CA 90095-1570, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439662" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/analysis/*chemistry/genetics/metabolism ; Animals ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Hippocampus/chemistry ; Microscopy, Electron ; Models, Molecular ; Mutation ; Nerve Tissue Proteins ; Neurons/chemistry ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Rats ; Recombinant Fusion Proteins/analysis ; Solubility ; Synapses/*chemistry ; Zinc/metabolism
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  • 18
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    Activity-dependent regulation of MEF2 transcription factors suppresses excitatory synapse number (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-02-18
    Description: In the mammalian nervous system, neuronal activity regulates the strength and number of synapses formed. The genetic program that coordinates this process is poorly understood. We show that myocyte enhancer factor 2 (MEF2) transcription factors suppressed excitatory synapse number in a neuronal activity- and calcineurin-dependent manner as hippocampal neurons formed synapses. In response to increased neuronal activity, calcium influx into neurons induced the activation of the calcium/calmodulin-regulated phosphatase calcineurin, which dephosphorylated and activated MEF2. When activated, MEF2 promoted the transcription of a set of genes, including arc and synGAP, that restrict synapse number. These findings define an activity-dependent transcriptional program that may control synapse number during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flavell, Steven W -- Cowan, Christopher W -- Kim, Tae-Kyung -- Greer, Paul L -- Lin, Yingxi -- Paradis, Suzanne -- Griffith, Eric C -- Hu, Linda S -- Chen, Chinfei -- Greenberg, Michael E -- AG05870/AG/NIA NIH HHS/ -- HD18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- R01 EY013613/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1008-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Program, Children's Hospital, and Departments of Neurology and 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/16484497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cytoskeletal Proteins/genetics ; Dendrites/physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; GTPase-Activating Proteins/genetics ; Gene Expression Regulation ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; MEF2 Transcription Factors ; Mutation ; Myogenic Regulatory Factors/genetics/*physiology ; Nerve Tissue Proteins/genetics ; Neurons/*physiology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; RNA Interference ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Transcription, Genetic ; Transfection
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  • 19
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    BKCa-Cav channel complexes mediate rapid and localized Ca2+-activated K+ signaling (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-10-28
    Description: Large-conductance calcium- and voltage-activated potassium channels (BKCa) are dually activated by membrane depolarization and elevation of cytosolic calcium ions (Ca2+). Under normal cellular conditions, BKCa channel activation requires Ca2+ concentrations that typically occur in close proximity to Ca2+ sources. We show that BKCa channels affinity-purified from rat brain are assembled into macromolecular complexes with the voltage-gated calcium channels Cav1.2 (L-type), Cav2.1 (P/Q-type), and Cav2.2 (N-type). Heterologously expressed BKCa-Cav complexes reconstitute a functional "Ca2+ nanodomain" where Ca2+ influx through the Cav channel activates BKCa in the physiological voltage range with submillisecond kinetics. Complex formation with distinct Cav channels enables BKCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkefeld, Henrike -- Sailer, Claudia A -- Bildl, Wolfgang -- Rohde, Volker -- Thumfart, Jorg-Oliver -- Eble, Silke -- Klugbauer, Norbert -- Reisinger, Ellen -- Bischofberger, Josef -- Oliver, Dominik -- Knaus, Hans-Gunther -- Schulte, Uwe -- Fakler, Bernd -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):615-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, University of Freiburg, Hermann-Herder-Strasse 7, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain Chemistry ; CHO Cells ; Calcium/*metabolism ; Calcium Channels, L-Type/drug effects/isolation & purification/*metabolism ; Calcium Channels, N-Type/drug effects/isolation & purification/*metabolism ; Calcium Signaling ; Chromaffin Cells/drug effects/metabolism ; Cricetinae ; Cricetulus ; Egtazic Acid/analogs & derivatives/pharmacology ; Large-Conductance Calcium-Activated Potassium Channels/drug effects/isolation & ; purification/*metabolism ; Membrane Potentials/drug effects ; Molecular Sequence Data ; Patch-Clamp Techniques ; Potassium/*metabolism ; Rats ; *Signal Transduction ; Transfection ; Xenopus
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  • 20
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    Protrudin induces neurite formation by directional membrane trafficking (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-11-04
    Description: Guanosine triphosphatases of the Rab family are key regulators of membrane trafficking, with Rab11 playing a specific role in membrane recycling. We identified a mammalian protein, protrudin, that promoted neurite formation through interaction with the guanosine diphosphate (GDP)-bound form of Rab11. Phosphorylation of protrudin by extracellular signal-regulated kinase (ERK) in response to nerve growth factor promoted protrudin association with Rab11-GDP. Down-regulation of protrudin by RNA interference induced membrane extension in all directions and inhibited neurite formation. Thus, protrudin regulates Rab11-dependent membrane recycling to promote the directional membrane trafficking required for neurite formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirane, Michiko -- Nakayama, Keiichi I -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082457" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Guanosine Diphosphate/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1/metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology/physiology ; Neurites/*physiology ; PC12 Cells ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Vesicular Transport Proteins ; rab GTP-Binding Proteins/metabolism
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  • 21
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    Reward timing in the primary visual cortex (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-18
    Description: We discovered that when adult rats experience an association between visual stimuli and subsequent rewards, the responses of a substantial fraction of neurons in the primary visual cortex evolve from those that relate solely to the physical attributes of the stimuli to those that accurately predict the timing of reward. In addition to revealing a remarkable type of response plasticity in adult V1, these data demonstrate that reward-timing activity-a "higher" brain function-can occur very early in sensory-processing paths. These findings challenge the traditional interpretation of activity in the primary visual cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shuler, Marshall G -- Bear, Mark F -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1606-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543459" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cues ; Dominance, Ocular ; Evoked Potentials, Visual ; Male ; Neurons/*physiology ; Photic Stimulation ; Rats ; Rats, Long-Evans ; *Reward ; Time Perception/*physiology ; Visual Cortex/*physiology
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  • 22
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    Synaptic amplifier of inflammatory pain in the spinal dorsal horn (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-06-17
    Description: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
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  • 23
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    Odorant receptor-derived cAMP signals direct axonal targeting (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-09-23
    Description: In mammals, odorant receptors (ORs) direct the axons of olfactory sensory neurons (OSNs) toward targets in the olfactory bulb. We show that cyclic adenosine monophosphate (cAMP) signals that regulate the expression of axon guidance molecules are essential for the OR-instructed axonal projection. Genetic manipulations of ORs, stimulatory G protein, cAMP-dependent protein kinase, and cAMP response element-binding protein shifted the axonal projection sites along the anteriorposterior axis in the olfactory bulb. Thus, it is the OR-derived cAMP signals, rather than direct action of OR molecules, that determine the target destinations of OSNs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Takeshi -- Suzuki, Misao -- Sakano, Hitoshi -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):657-61. Epub 2006 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Axons/*physiology ; Cyclic AMP/*metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; GTP-Binding Protein alpha Subunits, Gs/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Neuropilin-1/genetics/metabolism ; Olfactory Bulb/cytology/*physiology ; Olfactory Receptor Neurons/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Rats, Wistar ; Receptors, Odorant/*metabolism ; *Signal Transduction ; Transcription, Genetic
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  • 24
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    Caspase-10 in mouse or not? (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janicke, Reiner U -- Sohn, Dennis -- Totzke, Gudrun -- Schulze-Osthoff, Klaus -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1874.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*immunology ; Antibody Specificity ; Caspase 10 ; Caspases/*genetics/immunology/*metabolism ; Humans ; Mice/*genetics ; Oligopeptides/metabolism ; Rats ; Species Specificity
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  • 25
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    Causal reasoning in rats (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-02-18
    Description: Empirical research with nonhuman primates appears to support the view that causal reasoning is a key cognitive faculty that divides humans from animals. The claim is that animals approximate causal learning using associative processes. The present results cast doubt on that conclusion. Rats made causal inferences in a basic task that taps into core features of causal reasoning without requiring complex physical knowledge. They derived predictions of the outcomes of interventions after passive observational learning of different kinds of causal models. These competencies cannot be explained by current associative theories but are consistent with causal Bayes net theories.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blaisdell, Aaron P -- Sawa, Kosuke -- Leising, Kenneth J -- Waldmann, Michael R -- MH12531/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1020-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of California, Los Angeles, CA 90095, USA. blaisdell@psych.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association Learning ; Bayes Theorem ; *Cognition ; Comprehension ; Forecasting ; Male ; Rats ; Rats, Long-Evans
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    Archaeology. Dates revise Easter Island history (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1360.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Chronology as Topic ; Conservation of Natural Resources ; Emigration and Immigration/*history ; *Environment ; History, Ancient ; Humans ; Polynesia ; Rats ; Trees
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    N- to C-terminal SNARE complex assembly promotes rapid membrane fusion (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-05
    Description: Assembly of the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) syntaxin 1, SNAP-25, and synaptobrevin 2 is thought to be the driving force for the exocytosis of synaptic vesicles. However, whereas exocytosis is triggered at a millisecond time scale, the SNARE-mediated fusion of liposomes requires hours for completion, which challenges the idea of a key role for SNAREs in the final steps of exocytosis. We found that liposome fusion was dramatically accelerated when a stabilized syntaxin/SNAP-25 acceptor complex was used. Thus, SNAREs do have the capacity to execute fusion at a speed required for neuronal secretion, demonstrating that the maintenance of acceptor complexes is a critical step in biological fusion reactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pobbati, Ajaybabu V -- Stein, Alexander -- Fasshauer, Dirk -- P01 GM072694/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):673-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888141" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Circular Dichroism ; Dimerization ; Exocytosis ; Liposomes/*chemistry ; *Membrane Fusion ; Molecular Sequence Data ; Peptide Fragments/chemistry/metabolism ; Protein Binding ; Protein Folding ; Protein Structure, Secondary ; Qa-SNARE Proteins/chemistry/*metabolism ; R-SNARE Proteins/chemistry/metabolism ; Rats ; Synaptosomal-Associated Protein 25/chemistry/*metabolism
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    Role of leucine in regulating food intake (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laviano, Alessandro -- Meguid, Michael M -- Inui, Akio -- Rossi-Fanelli, Filippo -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1236-8; author reply 1236-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Appetite ; Brain/metabolism ; *Eating ; Humans ; Leucine/*administration & dosage/*physiology ; *Protein Biosynthesis ; Protein Kinases/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases
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    Hypothalamic mTOR signaling regulates food intake (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-13
    Description: The mammalian Target of Rapamycin (mTOR) protein is a serine-threonine kinase that regulates cell-cycle progression and growth by sensing changes in energy status. We demonstrated that mTOR signaling plays a role in the brain mechanisms that respond to nutrient availability, regulating energy balance. In the rat, mTOR signaling is controlled by energy status in specific regions of the hypothalamus and colocalizes with neuropeptide Y and proopiomelanocortin neurons in the arcuate nucleus. Central administration of leucine increases hypothalamic mTOR signaling and decreases food intake and body weight. The hormone leptin increases hypothalamic mTOR activity, and the inhibition of mTOR signaling blunts leptin's anorectic effect. Thus, mTOR is a cellular fuel sensor whose hypothalamic activity is directly tied to the regulation of energy intake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cota, Daniela -- Proulx, Karine -- Smith, Kathi A Blake -- Kozma, Sara C -- Thomas, George -- Woods, Stephen C -- Seeley, Randy J -- DK 17844/DK/NIDDK NIH HHS/ -- DK 54080/DK/NIDDK NIH HHS/ -- DK 54890/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 May 12;312(5775):927-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Cincinnati, Genome Research Institute, 2170 East Galbraith Road, Cincinnati, OH 45237, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arcuate Nucleus of Hypothalamus/cytology/enzymology/metabolism ; *Eating ; *Energy Intake ; *Energy Metabolism ; Fasting ; Hypothalamus/enzymology/*metabolism ; Injections, Intraventricular ; Leptin/pharmacology ; Leucine/*administration & dosage/pharmacology ; Neurons/enzymology/*metabolism ; Neuropeptide Y/genetics/metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Rats ; Rats, Long-Evans ; Ribosomal Protein S6/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; STAT3 Transcription Factor/metabolism ; *Signal Transduction ; Sirolimus/administration & dosage/pharmacology ; TOR Serine-Threonine Kinases ; Valine/administration & dosage/pharmacology ; Weight Loss
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    Learning induces long-term potentiation in the hippocampus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Years of intensive investigation have yielded a sophisticated understanding of long-term potentiation (LTP) induced in hippocampal area CA1 by high-frequency stimulation (HFS). These efforts have been motivated by the belief that similar synaptic modifications occur during memory formation, but it has never been shown that learning actually induces LTP in CA1. We found that one-trial inhibitory avoidance learning in rats produced the same changes in hippocampal glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the amplitude of evoked synaptic transmission in CA1 in vivo. Because the learning-induced synaptic potentiation occluded HFS-induced LTP, we conclude that inhibitory avoidance training induces LTP in CA1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitlock, Jonathan R -- Heynen, Arnold J -- Shuler, Marshall G -- Bear, Mark F -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1093-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/*physiology ; Conditioning (Psychology) ; Electric Stimulation ; Electrodes, Implanted ; Excitatory Postsynaptic Potentials ; Hippocampus/*physiology ; Long-Term Potentiation/*physiology ; Male ; Memory/*physiology ; Phosphorylation ; Phosphoserine/metabolism ; Rats ; Rats, Long-Evans ; Receptors, AMPA/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission
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    Epilepsy-related ligand/receptor complex LGI1 and ADAM22 regulate synaptic transmission (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
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    Environmental restoration. Big dams ready for teardown (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):584.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources ; *Ecosystem ; Engineering ; *Environment ; Geologic Sediments ; *Rivers ; *Salmon ; Trees ; Washington
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    Human lineage-specific amplification, selection, and neuronal expression of DUF1220 domains (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: Extreme gene duplication is a major source of evolutionary novelty. A genome-wide survey of gene copy number variation among human and great ape lineages revealed that the most striking human lineage-specific amplification was due to an unknown gene, MGC8902, which is predicted to encode multiple copies of a protein domain of unknown function (DUF1220). Sequences encoding these domains are virtually all primate-specific, show signs of positive selection, and are increasingly amplified generally as a function of a species' evolutionary proximity to humans, where the greatest number of copies (212) is found. DUF1220 domains are highly expressed in brain regions associated with higher cognitive function, and in brain show neuron-specific expression preferentially in cell bodies and dendrites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popesco, Magdalena C -- Maclaren, Erik J -- Hopkins, Janet -- Dumas, Laura -- Cox, Michael -- Meltesen, Lynne -- McGavran, Loris -- Wyckoff, Gerald J -- Sikela, James M -- AA11853/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1304-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Medical Genetics, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946073" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; Brain/*metabolism ; Cognition ; Exons ; *Gene Amplification ; Gene Dosage ; Gene Duplication ; Gene Expression ; Genome, Human ; Humans ; Macaca mulatta/genetics ; Mice ; Molecular Sequence Data ; Neocortex/metabolism ; Neurons/*metabolism ; Pan troglodytes/genetics ; Phylogeny ; Polymerase Chain Reaction ; *Protein Structure, Tertiary ; Proteins/*chemistry/genetics ; Rats ; *Selection, Genetic
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    Long-term potentiation of neuron-glia synapses mediated by Ca2+-permeable AMPA receptors (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-06-10
    Description: Interactions between neurons and glial cells in the brain may serve important functions in the development, maintenance, and plasticity of neural circuits. Fast neuron-glia synaptic transmission has been found between hippocampal neurons and NG2 cells, a distinct population of macroglia-like cells widely distributed in the brain. We report that these neuron-glia synapses undergo activity-dependent modifications analogous to long-term potentiation (LTP) at excitatory synapses, a hallmark of neuronal plasticity. However, unlike the induction of LTP at many neuron-neuron synapses, both induction and expression of LTP at neuron-NG2 synapses involve Ca2+-permeable AMPA receptors on NG2 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ge, Woo-Ping -- Yang, Xiu-Juan -- Zhang, Zhijun -- Wang, Hui-Kun -- Shen, Wanhua -- Deng, Qiu-Dong -- Duan, Shumin -- New York, N.Y. -- Science. 2006 Jun 9;312(5779):1533-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience and Key Laboratory of Neurobiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. shumin@ion.ac.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16763153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; In Vitro Techniques ; *Long-Term Potentiation ; Neuroglia/*physiology ; Neurons/*physiology ; Rats ; Receptors, AMPA/*physiology ; Synapses/*physiology
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    Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-06-24
    Description: Alpha-synuclein (alphaSyn) misfolding is associated with several devastating neurodegenerative disorders, including Parkinson's disease (PD). In yeast cells and in neurons alphaSyn accumulation is cytotoxic, but little is known about its normal function or pathobiology. The earliest defect following alphaSyn expression in yeast was a block in endoplasmic reticulum (ER)-to-Golgi vesicular trafficking. In a genomewide screen, the largest class of toxicity modifiers were proteins functioning at this same step, including the Rab guanosine triphosphatase Ypt1p, which associated with cytoplasmic alphaSyn inclusions. Elevated expression of Rab1, the mammalian YPT1 homolog, protected against alphaSyn-induced dopaminergic neuron loss in animal models of PD. Thus, synucleinopathies may result from disruptions in basic cellular functions that interface with the unique biology of particular neurons to make them especially vulnerable.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1983366/" 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/PMC1983366/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooper, Antony A -- Gitler, Aaron D -- Cashikar, Anil -- Haynes, Cole M -- Hill, Kathryn J -- Bhullar, Bhupinder -- Liu, Kangning -- Xu, Kexiang -- Strathearn, Katherine E -- Liu, Fang -- Cao, Songsong -- Caldwell, Kim A -- Caldwell, Guy A -- Marsischky, Gerald -- Kolodner, Richard D -- Labaer, Joshua -- Rochet, Jean-Christophe -- Bonini, Nancy M -- Lindquist, Susan -- P50 NS038372/NS/NINDS NIH HHS/ -- R01-HG002923/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):324-8. Epub 2006 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Missouri-Kansas City, Kansas City, MO 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Dopamine/physiology ; Drosophila ; Endoplasmic Reticulum/*metabolism ; Gene Expression ; Gene Library ; Golgi Apparatus/*metabolism ; Humans ; Mice ; Nerve Degeneration ; Neurons/cytology/*physiology ; Parkinsonian Disorders/metabolism/pathology/*physiopathology ; Proteasome Endopeptidase Complex/metabolism ; Protein Folding ; *Protein Transport ; Proteins/chemistry/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; alpha-Synuclein/chemistry/genetics/*metabolism ; rab GTP-Binding Proteins/genetics/metabolism ; rab1 GTP-Binding Proteins/genetics/*metabolism
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    Rats smell in stereo (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-02-04
    Description: It has been hypothesized that rats and other mammals can use stereo cues to localize odor sources, but there is limited behavioral evidence to support this hypothesis. We found that rats trained on an odor-localization task can localize odors accurately in one or two sniffs. Bilateral sampling was essential for accurate odor localization, with internasal intensity and timing differences as directional cues. If the stimulus arrived at the correct point of the respiration cycle, internasal timing differences as short as 50 milliseconds sufficed. Neuronal recordings show that bulbar neurons responded differentially to stimuli from the left and stimuli from the right.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajan, Raghav -- Clement, James P -- Bhalla, Upinder S -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):666-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Centre for Biological Sciences, University of Agricultural Science-Gandhi Krishi Vignan Kendra Campus, Bellary Road, Bangalore, Karnataka 560065, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Cues ; Electrophysiology ; Female ; Male ; Nasal Cavity/innervation/physiology ; Neurons/physiology ; Nose/anatomy & histology/*physiology ; Odors ; Olfactory Bulb/physiology ; Olfactory Pathways/*physiology ; Olfactory Receptor Neurons/physiology ; Phenylethyl Alcohol ; Random Allocation ; Rats ; Rats, Wistar ; Respiration ; Smell/*physiology ; Trigeminal Nerve/physiology
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    Neuroscience. Adam finds an exciting mate (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snyder, Solomon H -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1744-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA. ssnyder@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990538" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/*metabolism ; Animals ; Brain/cytology/metabolism/physiopathology ; Epilepsy/metabolism/*physiopathology ; Humans ; Intracellular Signaling Peptides and Proteins/*metabolism ; Ligands ; Membrane Proteins/*metabolism ; Neurons/metabolism ; Protein Binding ; Rats ; Receptors, AMPA/*metabolism ; Synapses/*metabolism ; Synaptic Membranes/metabolism ; *Synaptic Transmission
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    Neuroscience. ZAP and ZIP, a story to forget (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bliss, Tim V P -- Collingridge, Graham L -- Laroche, Serge -- MC_U117512674/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1058-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurophysiology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. tbliss@nimr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/physiology ; Dentate Gyrus/physiology ; Electric Stimulation ; Heat-Shock Proteins/pharmacology ; Hippocampus/*physiology ; *Long-Term Potentiation/drug effects ; Long-Term Synaptic Depression/physiology ; Memory/*physiology ; Models, Neurological ; Neurons/physiology ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Receptors, AMPA/metabolism ; Synapses/*physiology ; Transcription, Genetic
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    Activity- and mTOR-dependent suppression of Kv1.1 channel mRNA translation in dendrites (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-d-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raab-Graham, Kimberly F -- Haddick, Patrick C G -- Jan, Yuh Nung -- Jan, Lily Yeh -- MH13010/MH/NIMH NIH HHS/ -- MH65334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):144-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023663" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cells, Cultured ; Dendrites/drug effects/*metabolism ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; Kv1.1 Potassium Channel/*biosynthesis/*genetics ; Neuronal Plasticity ; Neurons/metabolism/virology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; Protein Biosynthesis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinases/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Recombinant Fusion Proteins/metabolism ; Sindbis Virus/physiology ; Sirolimus/pharmacology ; Synapses/physiology ; TOR Serine-Threonine Kinases
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    Environmental restoration. Restoring Yosemite's twin (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):582-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068234" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Conservation of Natural Resources ; *Ecosystem ; Engineering ; *Environment ; *Fresh Water ; Plant Development ; Rivers ; Water Movements ; Water Supply
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Bioengineering. Artificial arrays could help submarines make like a fish (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, Briahna -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1382-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Science Disciplines ; *Biomimetic Materials ; Biomimetics ; Computer Simulation ; Engineering ; *Fishes/physiology ; Interdisciplinary Communication ; Mathematics ; Pressure ; *Sense Organs/physiology
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    Human catechol-O-methyltransferase haplotypes modulate protein expression by altering mRNA secondary structure (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-23
    Description: Catechol-O-methyltransferase (COMT) is a key regulator of pain perception, cognitive function, and affective mood. Three common haplotypes of the human COMT gene, divergent in two synonymous and one nonsynonymous position, code for differences in COMT enzymatic activity and are associated with pain sensitivity. Haplotypes divergent in synonymous changes exhibited the largest difference in COMT enzymatic activity, due to a reduced amount of translated protein. The major COMT haplotypes varied with respect to messenger RNA local stem-loop structures, such that the most stable structure was associated with the lowest protein levels and enzymatic activity. Site-directed mutagenesis that eliminated the stable structure restored the amount of translated protein. These data highlight the functional significance of synonymous variations and suggest the importance of haplotypes over single-nucleotide polymorphisms for analysis of genetic variations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nackley, A G -- Shabalina, S A -- Tchivileva, I E -- Satterfield, K -- Korchynskyi, O -- Makarov, S S -- Maixner, W -- Diatchenko, L -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1930-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurosensory Disorders, University of North Carolina, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185601" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Base Pairing ; Base Sequence ; Catechol O-Methyltransferase/*biosynthesis/*genetics/metabolism ; *Haplotypes ; Humans ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; *Nucleic Acid Conformation ; PC12 Cells ; Pain/genetics ; Phenotype ; Polymorphism, Single Nucleotide ; RNA Stability ; RNA, Messenger/*chemistry/genetics/metabolism ; Rats ; Transfection
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    Invasive species. The Galapagos Islands kiss their goat problem goodbye (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Jerry -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1567.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; Cats ; Conservation of Natural Resources ; Culicidae/virology ; *Ecosystem ; Ecuador ; *Goats ; Plant Development ; Population Dynamics ; Rats ; West Nile virus
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    Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: TFII-I is a transcription factor and a target of phosphorylation by Bruton's tyrosine kinase. In humans, deletions spanning the TFII-I locus are associated with a cognitive defect, the Williams-Beuren cognitive profile. We report an unanticipated role of TFII-I outside the nucleus as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation of TRPC3 (transient receptor potential C3) channels. Inhibition of ACE by TFII-I requires phosphotyrosine residues that engage the SH2 (Src-homology 2) domains of phospholipase C-g (PLC-g) and an interrupted, pleckstrin homology (PH)-like domain that binds the split PH domain of PLC-g. Our observations suggest a model in which TFII-I suppresses ACE by competing with TRPC3 for binding to PLC-g.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caraveo, Gabriela -- van Rossum, Damian B -- Patterson, Randen L -- Snyder, Solomon H -- Desiderio, Stephen -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Institute for Cell 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/17023658" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bradykinin/pharmacology ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Humans ; Models, Biological ; Molecular Sequence Data ; PC12 Cells ; Phospholipase C gamma/chemistry/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Rats ; TRPC Cation Channels/*metabolism ; Transcription Factors, TFII/chemistry/*metabolism ; Uridine Triphosphate/pharmacology ; src Homology Domains
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    Molecular biology. A new RNA dimension to genome control (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carthew, Richard W -- R01 GM068743/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):305-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208, USA. r-carthew@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Complementary ; Drosophila/genetics ; Drosophila melanogaster/genetics/metabolism ; Female ; *Gene Expression Regulation ; *Genome ; Germ Cells/metabolism/physiology ; Male ; Mice ; RNA/chemistry/*genetics/isolation & purification/*metabolism ; *RNA Interference ; RNA, Antisense/chemistry/metabolism ; RNA, Untranslated/chemistry/genetics/*metabolism ; Rats ; Retroelements ; Ribonucleoproteins/chemistry/isolation & purification/metabolism ; Spermatids/metabolism ; Spermatogenesis ; Testis/chemistry/cytology ; Transcription, Genetic
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    Humanization of yeast to produce complex terminally sialylated glycoproteins (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-09
    Description: Yeast is a widely used recombinant protein expression system. We expanded its utility by engineering the yeast Pichia pastoris to secrete human glycoproteins with fully complex terminally sialylated N-glycans. After the knockout of four genes to eliminate yeast-specific glycosylation, we introduced 14 heterologous genes, allowing us to replicate the sequential steps of human glycosylation. The reported cell lines produce complex glycoproteins with greater than 90% terminal sialylation. Finally, to demonstrate the utility of these yeast strains, functional recombinant erythropoietin was produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, Stephen R -- Davidson, Robert C -- Sethuraman, Natarajan -- Nett, Juergen H -- Jiang, Youwei -- Rios, Sandra -- Bobrowicz, Piotr -- Stadheim, Terrance A -- Li, Huijuan -- Choi, Byung-Kwon -- Hopkins, Daniel -- Wischnewski, Harry -- Roser, Jessica -- Mitchell, Teresa -- Strawbridge, Rendall R -- Hoopes, Jack -- Wildt, Stefan -- Gerngross, Tillman U -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1441-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GlycoFi Inc., 21 Lafayette Street, Suite 200, Lebanon, NH 03766, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16960007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; Cytidine Monophosphate N-Acetylneuraminic Acid/metabolism ; Erythropoietin/chemistry/genetics/*metabolism ; Genetic Vectors ; Glycosylation ; Humans ; Pichia/*genetics/metabolism ; *Protein Engineering ; Rats ; Recombinant Proteins/biosynthesis/chemistry ; Sialic Acids/metabolism ; Sialoglycoproteins/*biosynthesis/chemistry/genetics ; Transformation, Genetic
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    SV2 is the protein receptor for botulinum neurotoxin A (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: How the widely used botulinum neurotoxin A (BoNT/A) recognizes and enters neurons is poorly understood. We found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C). Fragments of SV2 that harbor the toxin interaction domain inhibited BoNT/A from binding to neurons. BoNT/A binding to SV2A and SV2B knockout hippocampal neurons was abolished and was restored by expressing SV2A, SV2B, or SV2C. Reduction of SV2 expression in PC12 and Neuro-2a cells also inhibited entry of BoNT/A, which could be restored by expressing SV2 isoforms. Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, Min -- Yeh, Felix -- Tepp, William H -- Dean, Camin -- Johnson, Eric A -- Janz, Roger -- Chapman, Edwin R -- R01 EY016452/EY/NEI NIH HHS/ -- R01 EY016452-03/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):592-6. Epub 2006 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543415" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Botulinum Toxins, Type A/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endocytosis ; Hippocampus/cytology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neuromuscular Junction/metabolism ; Neurons/*metabolism ; PC12 Cells ; Protein Binding ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; R-SNARE Proteins/metabolism ; Rats ; Synaptic Vesicles/*metabolism ; Synaptotagmins/metabolism
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    Combined analog and action potential coding in hippocampal mossy fibers (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-04
    Description: In the mammalian cortex, it is generally assumed that the output information of neurons is encoded in the number and the timing of action potentials. Here, we show, by using direct patchclamp recordings from presynaptic hippocampal mossy fiber boutons, that axons transmit analog signals in addition to action potentials. Excitatory presynaptic potentials result from subthreshold dendritic synaptic inputs, which propagate several hundreds of micrometers along the axon and modulate action potential-evoked transmitter release at the mossy fiber-CA3 synapse. This combined analog and action potential coding represents an additional mechanism for information transmission in a major hippocampal pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alle, Henrik -- Geiger, Jorg R P -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1290-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Independent Hertie Research Group, Max Planck Institute for Brain Research, D-60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513983" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Action Potentials ; Animals ; Calcium Signaling ; Dendrites/physiology ; Dentate Gyrus/cytology/*physiology ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; In Vitro Techniques ; Models, Neurological ; Mossy Fibers, Hippocampal/*physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Receptors, AMPA/antagonists & inhibitors/metabolism ; Regression Analysis ; Synapses/physiology ; *Synaptic Transmission
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    The polarity protein Par-3 directly interacts with p75NTR to regulate myelination (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: Cell polarity is critical in various cellular processes ranging from cell migration to asymmetric cell division and axon and dendrite specification. Similarly, myelination by Schwann cells is polarized, but the mechanisms involved remain unclear. Here, we show that the polarity protein Par-3 localizes asymmetrically in Schwann cells at the axon-glial junction and that disruption of Par-3 localization, by overexpression and knockdown, inhibits myelination. Additionally, we show that Par-3 directly associates and recruits the p75 neurotrophin receptor to the axon-glial junction, forming a complex necessary for myelination. Together, these results point to a critical role in the establishment of cell polarity for myelination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Jonah R -- Jolicoeur, Christine -- Yamauchi, Junji -- Elliott, Jimmy -- Fawcett, James P -- Ng, Benjamin K -- Cayouette, Michel -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):832-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Neurobiology, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles 90089, USA. jonah.chan@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082460" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Axons/chemistry/ultrastructure ; Brain-Derived Neurotrophic Factor/physiology ; Carrier Proteins/analysis/chemistry/genetics/*metabolism ; *Cell Polarity ; Cells, Cultured ; Coculture Techniques ; Ganglia, Spinal/ultrastructure ; Intercellular Junctions/chemistry ; Mice ; Myelin Sheath/*physiology ; Nerve Tissue Proteins/chemistry/*metabolism ; Protein Structure, Tertiary ; Rats ; Receptors, Growth Factor/chemistry/*metabolism ; Schwann Cells/cytology/*physiology/ultrastructure
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    Ischemia opens neuronal gap junction hemichannels (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-05-13
    Description: Neuronal excitotoxicity during stroke is caused by activation of unidentified large-conductance channels, leading to swelling and calcium dysregulation. We show that ischemic-like conditions [O(2)/glucose deprivation (OGD)] open hemichannels, or half gap junctions, in neurons. Hemichannel opening was indicated by a large linear current and flux across the membrane of small fluorescent molecules. Single-channel openings of hemichannels (530 picosiemens) were observed in OGD. Both the current and dye flux were blocked by inhibitors of hemichannels. Therefore, hemichannel opening contributes to the profound ionic dysregulation during stroke and may be a ubiquitous component of ischemic neuronal death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Roger J -- Zhou, Ning -- MacVicar, Brian A -- New York, N.Y. -- Science. 2006 May 12;312(5775):924-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690868" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Brain Ischemia/pathology/*physiopathology ; Carbenoxolone/pharmacology ; Cell Hypoxia ; Cell Membrane Permeability ; Connexins ; Fluoresceins/metabolism ; Gap Junctions/drug effects/*physiology ; Glucose/deficiency/metabolism ; Hippocampus/cytology ; In Vitro Techniques ; Ion Channels/drug effects/*physiology ; Lanthanum/pharmacology ; Membrane Potentials ; Mice ; Necrosis ; Nerve Tissue Proteins/*physiology ; Neurons/pathology/*physiology/ultrastructure ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Rhodamines/metabolism ; Stroke/pathology/physiopathology
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    Drug trials. Violent reaction to monoclonal antibody therapy remains a mystery (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, Eliot -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1688-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/*adverse ; effects/immunology/metabolism ; Antigens, CD28/metabolism ; *Clinical Trials as Topic ; Humans ; *Lymphocyte Activation ; Macaca fascicularis ; Mice ; Rats ; T-Lymphocytes, Regulatory/*immunology
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    Neuroscience. The map in the brain: grid cells may help us navigate (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyman, Karen -- New York, N.Y. -- Science. 2006 May 5;312(5774):680-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675676" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Entorhinal Cortex/*cytology/*physiology ; Exploratory Behavior ; Hippocampus/cytology/physiology ; Locomotion ; Nerve Net/*physiology ; Neurons/*physiology ; *Orientation ; Rats ; *Space Perception
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    Maternal oxytocin triggers a transient inhibitory switch in GABA signaling in the fetal brain during delivery (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-16
    Description: We report a signaling mechanism in rats between mother and fetus aimed at preparing fetal neurons for delivery. In immature neurons, gamma-aminobutyric acid (GABA) is the primary excitatory neurotransmitter. We found that, shortly before delivery, there is a transient reduction in the intracellular chloride concentration and an excitatory-to-inhibitory switch of GABA actions. These events were triggered by oxytocin, an essential maternal hormone for labor. In vivo administration of an oxytocin receptor antagonist before delivery prevented the switch of GABA actions in fetal neurons and aggravated the severity of anoxic episodes. Thus, maternal oxytocin inhibits fetal neurons and increases their resistance to insults during delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyzio, Roman -- Cossart, Rosa -- Khalilov, Ilgam -- Minlebaev, Marat -- Hubner, Christian A -- Represa, Alfonso -- Ben-Ari, Yehezkel -- Khazipov, Rustem -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1788-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Neurobiologie de la Mediterranee, INSERM U29, Universite de la Mediterranee, Campus Scientifique de Luminy, Boite Postale 13, 13273 Marseille Cedex 09, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170309" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Animals, Newborn ; Benzamides/pharmacology ; Chlorides/metabolism ; Female ; Fetal Hypoxia/physiopathology ; Fetus/*physiology ; GABA-A Receptor Agonists ; GABA-A Receptor Antagonists ; Hippocampus/cytology/*embryology/physiology ; In Vitro Techniques ; Indoles/pharmacology ; Maternal-Fetal Exchange ; *Neural Inhibition ; Neurons/*physiology ; Oxytocin/pharmacology/*physiology ; *Parturition ; Patch-Clamp Techniques ; Pregnancy ; Rats ; Rats, Wistar ; Receptors, GABA-A/physiology ; Receptors, Oxytocin/antagonists & inhibitors ; Signal Transduction ; Sodium Potassium Chloride Symporter Inhibitors ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Vasotocin/analogs & derivatives/pharmacology ; gamma-Aminobutyric Acid/*physiology
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    Graded regulation of the Kv2.1 potassium channel by variable phosphorylation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-19
    Description: Dynamic modulation of ion channels by phosphorylation underlies neuronal plasticity. The Kv2.1 potassium channel is highly phosphorylated in resting mammalian neurons. Activity-dependent Kv2.1 dephosphorylation by calcineurin induces graded hyperpolarizing shifts in voltage-dependent activation, causing suppression of neuronal excitability. Mass spectrometry-SILAC (stable isotope labeling with amino acids in cell culture) identified 16 Kv2.1 phosphorylation sites, of which 7 were dephosphorylated by calcineurin. Mutation of individual calcineurin-regulated sites to alanine produced incremental shifts mimicking dephosphorylation, whereas mutation to aspartate yielded equivalent resistance to calcineurin. Mutations at multiple sites were additive, showing that variable phosphorylation of Kv2.1 at a large number of sites allows graded activity-dependent regulation of channel gating and neuronal firing properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Kang-Sik -- Mohapatra, Durga P -- Misonou, Hiroaki -- Trimmer, James S -- NS42225/NS/NINDS NIH HHS/ -- R01 NS042225/NS/NINDS NIH HHS/ -- R01 NS042225-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):976-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917065" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/genetics/metabolism ; Alkaline Phosphatase/metabolism ; Animals ; Aspartic Acid/genetics/metabolism ; Brain/metabolism ; Calcineurin/metabolism ; Calcium/metabolism ; Cell Line ; Chromatography, Liquid ; Humans ; *Ion Channel Gating ; Ionomycin/pharmacology ; Mass Spectrometry ; Mutation ; Neurons/physiology ; Patch-Clamp Techniques ; Phosphorylation ; Phosphoserine/metabolism ; Phosphothreonine/metabolism ; Point Mutation ; Rats ; Recombinant Proteins/metabolism ; Serine/genetics ; Shab Potassium Channels/*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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    Storage of spatial information by the maintenance mechanism of LTP (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Analogous to learning and memory storage, long-term potentiation (LTP) is divided into induction and maintenance phases. Testing the hypothesis that the mechanism of LTP maintenance stores information requires reversing this mechanism in vivo and finding out whether long-term stored information is lost. This was not previously possible. Recently however, persistent phosphorylation by the atypical protein kinase C isoform, protein kinase Mzeta (PKMz), has been found to maintain late LTP in hippocampal slices. Here we show that a cell-permeable PKMz inhibitor, injected in the rat hippocampus, both reverses LTP maintenance in vivo and produces persistent loss of 1-day-old spatial information. Thus, the mechanism maintaining LTP sustains spatial memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastalkova, Eva -- Serrano, Peter -- Pinkhasova, Deana -- Wallace, Emma -- Fenton, Andre Antonio -- Sacktor, Todd Charlton -- MH57068/MH/NIMH NIH HHS/ -- R01 MH53576/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1141-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Physiology, Pharmacology, and Neurology, Robert F. Furchgott Center for Neural and Behavioral Science, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931766" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning ; Conditioning (Psychology) ; Dentate Gyrus/drug effects/physiology ; Electric Stimulation ; Excitatory Postsynaptic Potentials/drug effects ; Heat-Shock Proteins/administration & dosage/pharmacology ; Hippocampus/drug effects/*physiology ; Long-Term Potentiation/drug effects/*physiology ; Male ; Memory/drug effects/*physiology ; Perforant Pathway ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Rats, Long-Evans ; Staurosporine/pharmacology ; Time 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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    Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Coordinated control of energy metabolism and glucose homeostasis requires communication between organs and tissues. We identified a neuronal pathway that participates in the cross talk between the liver and adipose tissue. By studying a mouse model, we showed that adenovirus-mediated expression of peroxisome proliferator-activated receptor (PPAR)-g2 in the liver induces acute hepatic steatosis while markedly decreasing peripheral adiposity. These changes were accompanied by increased energy expenditure and improved systemic insulin sensitivity. Hepatic vagotomy and selective afferent blockage of the hepatic vagus revealed that the effects on peripheral tissues involve the afferent vagal nerve. Furthermore, an antidiabetic thiazolidinedione, a PPARg agonist, enhanced this pathway. This neuronal pathway from the liver may function to protect against metabolic perturbation induced by excessive energy storage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uno, Kenji -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Ogihara, Takehide -- Imai, Junta -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Iwasaki, Hiroko -- Ishihara, Hisamitsu -- Sasano, Hironobu -- Inukai, Kouichi -- Mizuguchi, Hiroyuki -- Asano, Tomoichiro -- Shiota, Masakazu -- Nakazato, Masamitsu -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778057" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/innervation/*metabolism ; Afferent Pathways/physiology ; Animals ; Blood Glucose/analysis ; Dietary Fats/administration & dosage ; Efferent Pathways/physiology ; *Energy Metabolism ; Fatty Liver/pathology ; Glucose/metabolism ; Glucose Tolerance Test ; Hypoglycemic Agents/pharmacology ; Insulin/blood/*physiology ; Insulin Resistance ; Lipolysis ; Liver/*innervation/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Oxygen Consumption ; PPAR gamma/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Sympathetic Nervous System/physiology ; Vagotomy ; Vagus Nerve/*physiology ; Weight Gain
    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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  • 57
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    Detection, stimulation, and inhibition of neuronal signals with high-density nanowire transistor arrays (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: We report electrical properties of hybrid structures consisting of arrays of nanowire field-effect transistors integrated with the individual axons and dendrites of live mammalian neurons, where each nanoscale junction can be used for spatially resolved, highly sensitive detection, stimulation, and/or inhibition of neuronal signal propagation. Arrays of nanowire-neuron junctions enable simultaneous measurement of the rate, amplitude, and shape of signals propagating along individual axons and dendrites. The configuration of nanowire-axon junctions in arrays, as both inputs and outputs, makes possible controlled studies of partial to complete inhibition of signal propagation by both local electrical and chemical stimuli. In addition, nanowire-axon junction arrays were integrated and tested at a level of at least 50 "artificial synapses" per neuron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patolsky, Fernando -- Timko, Brian P -- Yu, Guihua -- Fang, Ying -- Greytak, Andrew B -- Zheng, Gengfeng -- Lieber, Charles M -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1100-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931757" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Cells, Cultured ; Dendrites/physiology ; Electric Conductivity ; Electric Stimulation ; Electrophysiology/instrumentation/*methods ; Microelectrodes ; *Nanostructures ; *Neural Inhibition ; Neurites/physiology ; Neurons/*physiology ; Rats ; Rats, Inbred F344 ; Rats, Sprague-Dawley ; Silicon ; Synapses/physiology ; *Transistors, Electronic
    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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    Opposing activities protect against age-onset proteotoxicity (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-08-12
    Description: Aberrant protein aggregation is a common feature of late-onset neurodegenerative diseases, including Alzheimer's disease, which is associated with the misassembly of the Abeta(1-42) peptide. Aggregation-mediated Abeta(1-42) toxicity was reduced in Caenorhabditis elegans when aging was slowed by decreased insulin/insulin growth factor-1-like signaling (IIS). The downstream transcription factors, heat shock factor 1, and DAF-16 regulate opposing disaggregation and aggregation activities to promote cellular survival in response to constitutive toxic protein aggregation. Because the IIS pathway is central to the regulation of longevity and youthfulness in worms, flies, and mammals, these results suggest a mechanistic link between the aging process and aggregation-mediated proteotoxicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Ehud -- Bieschke, Jan -- Perciavalle, Rhonda M -- Kelly, Jeffery W -- Dillin, Andrew -- DK 46335/DK/NIDDK NIH HHS/ -- NS 50636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1604-10. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, 10010 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/16902091" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amyloid beta-Peptides/chemistry/*metabolism ; Animals ; Biopolymers/chemistry/metabolism ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Survival ; Forkhead Transcription Factors ; Humans ; Insulin-Like Growth Factor I/metabolism ; Models, Biological ; Molecular Weight ; Movement ; Muscles/metabolism/physiology ; PC12 Cells ; Peptide Fragments/chemistry/*metabolism ; RNA Interference ; Rats ; Receptor, Insulin/genetics/metabolism ; Signal Transduction ; Transcription Factors/genetics/*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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  • 59
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    A calcium-regulated MEF2 sumoylation switch controls postsynaptic differentiation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Postsynaptic differentiation of dendrites is an essential step in synapse formation. We report here a requirement for the transcription factor myocyte enhancer factor 2A (MEF2A) in the morphogenesis of postsynaptic granule neuron dendritic claws in the cerebellar cortex. A transcriptional repressor form of MEF2A that is sumoylated at lysine-403 promoted dendritic claw differentiation. Activity-dependent calcium signaling induced a calcineurin-mediated dephosphorylation of MEF2A at serine-408 and, thereby, promoted a switch from sumoylation to acetylation at lysine-403, which led to inhibition of dendritic claw differentiation. Our findings define a mechanism underlying postsynaptic differentiation that may modulate activity-dependent synapse development and plasticity in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shalizi, Aryaman -- Gaudilliere, Brice -- Yuan, Zengqiang -- Stegmuller, Judith -- Shirogane, Takahiro -- Ge, Qingyuan -- Tan, Yi -- Schulman, Brenda -- Harper, J Wade -- Bonni, Azad -- AG11085/AG/NIA NIH HHS/ -- NS41021/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1012-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Louis Pasteur Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484498" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Calcineurin/metabolism ; Calcium/*metabolism ; Calcium Signaling ; Cell Differentiation ; Cell Line ; Cerebellar Cortex/cytology/*physiology ; Dendrites/physiology/*ultrastructure ; Electroporation ; Humans ; In Vitro Techniques ; MEF2 Transcription Factors ; Morphogenesis ; Myogenic Regulatory Factors/genetics/*metabolism ; Neurons/*cytology/physiology ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/metabolism ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Synapses/*physiology ; 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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    Neuroscience. SUMO wrestles the synapse (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beg, Asim A -- Scheiffele, Peter -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):962-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA. ab2516@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*physiology ; Calcium/metabolism ; Calcium Signaling ; Cerebellum/cytology/physiology ; Dendrites/physiology/ultrastructure ; Hippocampus/cytology/physiology ; MEF2 Transcription Factors ; Myogenic Regulatory Factors/genetics/*physiology ; Neurons/*physiology ; Phosphorylation ; RNA Interference ; Rats ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Synapses/*physiology ; *Transcription, Genetic
    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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    Neuroscience. Regulating energy balance: the substrate strikes back (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, Jeffrey S -- New York, N.Y. -- Science. 2006 May 12;312(5775):861-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA 02215, USA. jflier@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690851" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases ; Animals ; Appetite ; Body Weight ; Diet ; *Eating ; *Energy Metabolism ; Homeostasis ; Hypothalamus/enzymology/*metabolism ; Leptin/physiology ; Leucine/*administration & dosage/physiology ; Multienzyme Complexes/metabolism ; Neural Pathways/physiology ; Neurons/enzymology ; Obesity ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Ribosomal Protein S6 Kinases/metabolism ; *Signal Transduction ; Sirolimus/pharmacology ; Starvation ; TOR Serine-Threonine Kinases ; Thinness
    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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