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  • Articles  (33)
  • Cells, Cultured
  • 2005-2009  (33)
  • 1980-1984
  • 2005  (33)
  • Computer Science  (33)
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  • Articles  (33)
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  • 2005-2009  (33)
  • 1980-1984
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  • 1
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    Equivalent effects of snake PLA2 neurotoxins and lysophospholipid-fatty acid mixtures (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-13
    Description: Snake presynaptic phospholipase A2 neurotoxins (SPANs) paralyze the neuromuscular junction (NMJ). Upon intoxication, the NMJ enlarges and has a reduced content of synaptic vesicles, and primary neuronal cultures show synaptic swelling with surface exposure of the lumenal domain of the synaptic vesicle protein synaptotagmin I. Concomitantly, these neurotoxins induce exocytosis of neurotransmitters. We found that an equimolar mixture of lysophospholipids and fatty acids closely mimics all of the biological effects of SPANs. These results draw attention to the possible role of local lipid changes in synaptic vesicle release and provide new tools for the study of exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rigoni, Michela -- Caccin, Paola -- Gschmeissner, Steve -- Koster, Grielof -- Postle, Anthony D -- Rossetto, Ornella -- Schiavo, Giampietro -- Montecucco, Cesare -- GP0272Y01/Telethon/Italy -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1678-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences and Consiglio Nazionale Ricerche Institute of Neuroscience, University of Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Elapid Venoms/toxicity ; Esterification ; Exocytosis ; Fatty Acids/*metabolism/toxicity ; Glutamic Acid/metabolism ; Hydrolysis ; Kinetics ; Lipid Bilayers ; Lysophospholipids/*metabolism/toxicity ; Male ; Mass Spectrometry ; Membrane Fusion ; Membrane Lipids/metabolism ; Mice ; Neuromuscular Junction/drug effects/metabolism/physiology ; Neurons/drug effects/metabolism/ultrastructure ; Neurotoxins/*metabolism/toxicity ; Neurotransmitter Agents/metabolism ; Phospholipases A/*metabolism/toxicity ; Phospholipases A2 ; Synapses/drug effects/ultrastructure ; Synaptic Membranes/metabolism/*physiology ; Synaptic Vesicles/drug effects/physiology/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Nucleus accumbens long-term depression and the expression of behavioral sensitization (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-29
    Description: Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brebner, Karen -- Wong, Tak Pan -- Liu, Lidong -- Liu, Yitao -- Campsall, Paul -- Gray, Sarah -- Phelps, Lindsay -- Phillips, Anthony G -- Wang, Yu Tian -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1340-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/16311338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Behavior, Animal/*drug effects ; Cells, Cultured ; Clathrin/physiology ; Dextroamphetamine/*administration & dosage/pharmacology ; Dynamins/pharmacology ; Endocytosis ; Excitatory Postsynaptic Potentials ; *Long-Term Synaptic Depression/drug effects ; Male ; Membrane Potentials ; Models, Animal ; Motor Activity/*drug effects ; Nucleus Accumbens/drug effects/*physiology ; Patch-Clamp Techniques ; Peptides/pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Recombinant Fusion Proteins/pharmacology ; Stereotyped Behavior/*drug effects ; Synaptic Transmission/drug effects ; Ventral Tegmental Area/drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Glial membranes at the node of Ranvier prevent neurite outgrowth (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Altered TCR signaling from geometrically repatterned immunological synapses (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: The immunological synapse is a specialized cell-cell junction that is defined by large-scale spatial patterns of receptors and signaling molecules yet remains largely enigmatic in terms of formation and function. We used supported bilayer membranes and nanometer-scale structures fabricated onto the underlying substrate to impose geometric constraints on immunological synapse formation. Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse. These results are consistent with a model of the synapse in which spatial translocation of TCRs represents a direct mechanism of signal regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mossman, Kaspar D -- Campi, Gabriele -- Groves, Jay T -- Dustin, Michael L -- GM64900/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1191-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigen-Presenting Cells/metabolism ; Cells, Cultured ; Lipid Bilayers ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell/chemistry/*metabolism ; *Signal Transduction ; Structure-Activity Relationship ; T-Lymphocytes/immunology/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: Blood calcium concentration is maintained within a narrow range despite large variations in dietary input and body demand. The Transient Receptor Potential ion channel TRPV5 has been implicated in this process. We report here that TRPV5 is stimulated by the mammalian hormone klotho. Klotho, a beta-glucuronidase, hydrolyzes extracellular sugar residues on TRPV5, entrapping the channel in the plasma membrane. This maintains durable calcium channel activity and membrane calcium permeability in kidney. Thus, klotho activates a cell surface channel by hydrolysis of its extracellular N-linked oligosaccharides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Q -- Hoefs, S -- van der Kemp, A W -- Topala, C N -- Bindels, R J -- Hoenderop, J G -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Glucuronidase/antagonists & inhibitors/metabolism ; Glycosylation ; Humans ; Hydrolysis ; Kidney/cytology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Patch-Clamp Techniques ; Protein Transport ; Rabbits ; Sodium/metabolism ; TRPV Cation Channels/genetics/*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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  • 6
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    Neurodegeneration. Huntington's research points to possible new therapies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Astrocytic purinergic signaling coordinates synaptic networks (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: To investigate the role of astrocytes in regulating synaptic transmission, we generated inducible transgenic mice that express a dominant-negative SNARE domain selectively in astrocytes to block the release of transmitters from these glial cells. By releasing adenosine triphosphate, which accumulates as adenosine, astrocytes tonically suppressed synaptic transmission, thereby enhancing the dynamic range for long-term potentiation and mediated activity-dependent, heterosynaptic depression. These results indicate that astrocytes are intricately linked in the regulation of synaptic strength and plasticity and provide a pathway for synaptic cross-talk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascual, Olivier -- Casper, Kristen B -- Kubera, Cathryn -- Zhang, Jing -- Revilla-Sanchez, Raquel -- Sul, Jai-Yoon -- Takano, Hajime -- Moss, Stephen J -- McCarthy, Ken -- Haydon, Philip G -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Conte Center for Integration at the Tripartite Synapse, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210541" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Adenosine A1 Receptor Antagonists ; Adenosine Triphosphatases/antagonists & inhibitors ; Adenosine Triphosphate/analogs & derivatives/metabolism/pharmacology ; Animals ; Astrocytes/drug effects/*physiology ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Purinergic P1 Receptor Antagonists ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A1/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Receptors, Purinergic P1/metabolism ; Receptors, Purinergic P2/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Xanthines/pharmacology
    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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  • 8
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    Neuroscience. Cancer drugs may help injured nerve cells regrow their axons (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*pharmacology ; Axons/drug effects/*physiology ; Cells, Cultured ; Erlotinib Hydrochloride ; Mice ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurons/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Quinazolines/*pharmacology ; Rats ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/metabolism ; Signal Transduction/*drug effects ; Spinal Cord Injuries/drug therapy
    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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  • 9
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    EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in the adult central nervous system (CNS), but the underlying signaling mechanisms of regeneration inhibition are not fully understood. Here, we show that suppressing the kinase function of the epidermal growth factor receptor (EGFR) blocks the activities of both myelin inhibitors and chondroitin sulfate proteoglycans in inhibiting neurite outgrowth. In addition, regeneration inhibitors trigger the phosphorylation of EGFR in a calcium-dependent manner. Local administration of EGFR inhibitors promotes significant regeneration of injured optic nerve fibers, pointing to a promising therapeutic avenue for enhancing axon regeneration after CNS injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koprivica, Vuk -- Cho, Kin-Sang -- Park, Jong Bae -- Yiu, Glenn -- Atwal, Jasvinder -- Gore, Bryan -- Kim, Jieun A -- Lin, Estelle -- Tessier-Lavigne, Marc -- Chen, Dong Feng -- He, Zhigang -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):106-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/*physiology ; Calcium/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/*metabolism ; Enzyme Inhibitors/pharmacology ; Erlotinib Hydrochloride ; GPI-Linked Proteins ; Humans ; Mice ; Myelin Proteins/*metabolism/pharmacology ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurites/drug effects/physiology ; Optic Nerve/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Phosphorylation ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*metabolism ; Receptors, Cell Surface/metabolism ; Retinal Ganglion Cells/drug effects/physiology ; Signal Transduction/drug effects ; Tyrphostins/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Stem cells. Scientists chase after immortality in a petri dish (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):1982-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Embryo, Mammalian/*cytology ; Female ; Genomic Imprinting ; Humans ; Male ; Meiosis ; *Oocytes/cytology/physiology ; Ovary/cytology/physiology ; *Spermatozoa/cytology/physiology ; *Stem Cells/cytology/physiology ; Testis/cytology/physiology
    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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