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  • 1
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*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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  • 2
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    Prevention of cardiac hypertrophy in mice by calcineurin inhibition (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Hypertrophic cardiomyopathy (HCM) is an inherited form of heart disease that affects 1 in 500 individuals. Here it is shown that calcineurin, a calcium-regulated phosphatase, plays a critical role in the pathogenesis of HCM. Administration of the calcineurin inhibitors cyclosporin and FK506 prevented disease in mice that were genetically predisposed to develop HCM as a result of aberrant expression of tropomodulin, myosin light chain-2, or fetal beta-tropomyosin in the heart. Cyclosporin had a similar effect in a rat model of pressure-overload hypertrophy. These results suggest that calcineurin inhibitors merit investigation as potential therapeutics for certain forms of human heart disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sussman, M A -- Lim, H W -- Gude, N -- Taigen, T -- Olson, E N -- Robbins, J -- Colbert, M C -- Gualberto, A -- Wieczorek, D F -- Molkentin, J D -- HL58224-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733519" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; *Cardiac Myosins ; Cardiomegaly/metabolism/pathology/*prevention & control ; Cardiomyopathy, Dilated/pathology/*prevention & control ; Cardiomyopathy, Hypertrophic/genetics/metabolism/pathology/*prevention & control ; Carrier Proteins/genetics ; Cyclosporine/*pharmacology ; Female ; Mice ; Mice, Transgenic ; *Microfilament Proteins ; Models, Cardiovascular ; Myocardium/*metabolism/pathology ; Myosin Light Chains/genetics/metabolism ; Rats ; Signal Transduction ; Tacrolimus/*pharmacology ; Tropomodulin ; Tropomyosin/genetics
    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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    Proteolytic inactivation of MAP-kinase-kinase by anthrax lethal factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Anthrax lethal toxin, produced by the bacterium Bacillus anthracis, is the major cause of death in animals infected with anthrax. One component of this toxin, lethal factor (LF), is suspected to be a metalloprotease, but no physiological substrates have been identified. Here it is shown that LF is a protease that cleaves the amino terminus of mitogen-activated protein kinase kinases 1 and 2 (MAPKK1 and MAPKK2) and that this cleavage inactivates MAPKK1 and inhibits the MAPK signal transduction pathway. The identification of a cleavage site for LF may facilitate the development of LF inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duesbery, N S -- Webb, C P -- Leppla, S H -- Gordon, V M -- Klimpel, K R -- Copeland, T D -- Ahn, N G -- Oskarsson, M K -- Fukasawa, K -- Paull, K D -- Vande Woude, G F -- New York, N.Y. -- Science. 1998 May 1;280(5364):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced BioScience Laboratories-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Post Office Box B, Frederick, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9563949" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Bacterial ; *Bacillus anthracis/enzymology ; Bacterial Toxins/metabolism/*toxicity ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cell Line, Transformed ; Enzyme Activation ; Enzyme Inhibitors/toxicity ; Humans ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 2 ; Metalloendopeptidases/metabolism/toxicity ; Mice ; *Mitogen-Activated Protein Kinase Kinases ; Myelin Basic Protein/metabolism ; Oocytes/physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Xenopus laevis
    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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    DARPP-32: regulator of the efficacy of dopaminergic neurotransmission (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Dopaminergic neurons exert a major modulatory effect on the forebrain. Dopamine and adenosine 3',5'-monophosphate-regulated phosphoprotein (32 kilodaltons) (DARPP-32), which is enriched in all neurons that receive a dopaminergic input, is converted in response to dopamine into a potent protein phosphatase inhibitor. Mice generated to contain a targeted disruption of the DARPP-32 gene showed profound deficits in their molecular, electrophysiological, and behavioral responses to dopamine, drugs of abuse, and antipsychotic medication. The results show that DARPP-32 plays a central role in regulating the efficacy of dopaminergic neurotransmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fienberg, A A -- Hiroi, N -- Mermelstein, P G -- Song, W -- Snyder, G L -- Nishi, A -- Cheramy, A -- O'Callaghan, J P -- Miller, D B -- Cole, D G -- Corbett, R -- Haile, C N -- Cooper, D C -- Onn, S P -- Grace, A A -- Ouimet, C C -- White, F J -- Hyman, S E -- Surmeier, D J -- Girault, J -- Nestler, E J -- Greengard, P -- DA 08227/DA/NIDA NIH HHS/ -- DA10044/DA/NIDA NIH HHS/ -- F31 DA005794/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):838-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694658" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamines/pharmacology ; Animals ; Behavior, Animal/drug effects ; Calcium/metabolism ; Cocaine/pharmacology ; Corpus Striatum/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dopamine/pharmacology/*physiology ; Dopamine Agents/pharmacology ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Female ; Gene Expression Regulation ; Gene Targeting ; Genes, fos ; Glutamic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics/*metabolism ; Neurons/*metabolism ; Phosphoprotein Phosphatases/metabolism ; *Phosphoproteins ; Phosphorylation ; Raclopride ; Receptors, Dopamine D1/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Salicylamides/pharmacology ; Sodium-Potassium-Exchanging ATPase/metabolism ; *Synaptic Transmission ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Role of IQGAP1, a target of the small GTPases Cdc42 and Rac1, in regulation of E-cadherin- mediated cell-cell adhesion (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The small guanosine triphosphatases (GTPases) Cdc42 and Rac1 regulate E-cadherin-mediated cell-cell adhesion. IQGAP1, a target of Cdc42 and Rac1, was localized with E-cadherin and beta-catenin at sites of cell-cell contact in mouse L fibroblasts expressing E-cadherin (EL cells), and interacted with E-cadherin and beta-catenin both in vivo and in vitro. IQGAP1 induced the dissociation of alpha-catenin from a cadherin-catenin complex in vitro and in vivo. Overexpression of IQGAP1 in EL cells, but not in L cells expressing an E-cadherin-alpha-catenin chimeric protein, resulted in a decrease in E-cadherin-mediated cell-cell adhesive activity. Thus, IQGAP1, acting downstream of Cdc42 and Rac1, appears to regulate cell-cell adhesion through the cadherin-catenin pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroda, S -- Fukata, M -- Nakagawa, M -- Fujii, K -- Nakamura, T -- Ookubo, T -- Izawa, I -- Nagase, T -- Nomura, N -- Tani, H -- Shoji, I -- Matsuura, Y -- Yonehara, S -- Kaibuchi, K -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):832-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694656" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/*metabolism ; *Cell Adhesion ; Cell Cycle Proteins/*metabolism ; Cell Membrane/metabolism ; Cytoskeletal Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; L Cells (Cell Line) ; Mice ; Mutation ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; *Trans-Activators ; alpha Catenin ; beta Catenin ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    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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    Impaired locomotion and dopamine signaling in retinoid receptor mutant mice (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krezel, W -- Ghyselinck, N -- Samad, T A -- Dupe, V -- Kastner, P -- Borrelli, E -- Chambon, P -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):863-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS, INSERM, Universite Louis Pasteur, College de France, Boite Postale 163, 67404 Illkirch Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/pharmacology ; Corpus Striatum/*metabolism ; Dimerization ; Dopamine/*metabolism ; Locomotion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Motor Activity/drug effects ; Muscle, Skeletal/physiology ; Parkinson Disease/etiology ; Peripheral Nervous System/physiology ; Receptors, Dopamine D1/genetics/metabolism ; Receptors, Dopamine D2/genetics/metabolism ; Receptors, Retinoic Acid/genetics/*physiology ; Retinoid X Receptors ; Schizophrenia/etiology ; *Signal Transduction ; Transcription Factors/genetics/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Increased vascularization in mice overexpressing angiopoietin-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: The angiopoietins and members of the vascular endothelial growth factor (VEGF) family are the only growth factors thought to be largely specific for vascular endothelial cells. Targeted gene inactivation studies in mice have shown that VEGF is necessary for the early stages of vascular development and that angiopoietin-1 is required for the later stages of vascular remodeling. Here it is shown that transgenic overexpression of angiopoietin-1 in the skin of mice produces larger, more numerous, and more highly branched vessels. These results raise the possibility that angiopoietins can be used, alone or in combination with VEGF, to promote therapeutic angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suri, C -- McClain, J -- Thurston, G -- McDonald, D M -- Zhou, H -- Oldmixon, E H -- Sato, T N -- Yancopoulos, G D -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774272" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Capillaries/anatomy & histology/ultrastructure ; Endothelial Growth Factors/genetics/physiology ; Endothelium, Vascular/ultrastructure ; Gene Expression ; Keratinocytes/metabolism ; Lymphokines/genetics/physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; *Neovascularization, Physiologic ; Skin/*blood supply/metabolism ; Transgenes ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/ultrastructure
    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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    Role of the CLOCK protein in the mammalian circadian mechanism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The mouse Clock gene encodes a bHLH-PAS protein that regulates circadian rhythms and is related to transcription factors that act as heterodimers. Potential partners of CLOCK were isolated in a two-hybrid screen, and one, BMAL1, was coexpressed with CLOCK and PER1 at known circadian clock sites in brain and retina. CLOCK-BMAL1 heterodimers activated transcription from E-box elements, a type of transcription factor-binding site, found adjacent to the mouse per1 gene and from an identical E-box known to be important for per gene expression in Drosophila. Mutant CLOCK from the dominant-negative Clock allele and BMAL1 formed heterodimers that bound DNA but failed to activate transcription. Thus, CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gekakis, N -- Staknis, D -- Nguyen, H B -- Davis, F C -- Wilsbacher, L D -- King, D P -- Takahashi, J S -- Weitz, C J -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1564-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston MA 02115, USA. 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616112" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/genetics/*physiology ; Cloning, Molecular ; Cricetinae ; DNA/metabolism ; Dimerization ; Feedback ; Gene Expression ; Helix-Loop-Helix Motifs ; Male ; Mesocricetus ; Mice ; Mutation ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation
    Print ISSN: 0036-8075
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  • 9
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    Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: The calcium-calmodulin-dependent kinase II (CaMKII) is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its calcium-calmodulin (CaM)-dependent activity, CaMKII can undergo autophosphorylation, resulting in CaM-independent activity. A point mutation was introduced into the alphaCaMKII gene that blocked the autophosphorylation of threonine at position 286 (Thr286) of this kinase without affecting its CaM-dependent activity. The mutant mice had no N-methyl-D-aspartate receptor-dependent LTP in the hippocampal CA1 area and showed no spatial learning in the Morris water maze. Thus, the autophosphorylation of alphaCaMKII at Thr286 appears to be required for LTP and learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giese, K P -- Fedorov, N B -- Filipkowski, R K -- Silva, A J -- AG13622/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):870-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452388" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Calmodulin/metabolism ; Gene Targeting ; Hippocampus/metabolism/*physiology ; *Long-Term Potentiation/drug effects ; *Maze Learning ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Patch-Clamp Techniques ; Phosphorylation ; Phosphothreonine/metabolism ; Picrotoxin/pharmacology ; Point Mutation ; Pyramidal Cells/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
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  • 10
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    Axonal swellings and degeneration in mice lacking the major proteolipid of myelin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: Glial cells produce myelin and contribute to axonal morphology in the nervous system. Two myelin membrane proteolipids, PLP and DM20, were shown to be essential for the integrity of myelinated axons. In the absence of PLP-DM20, mice assembled compact myelin sheaths but subsequently developed widespread axonal swellings and degeneration, associated predominantly with small-caliber nerve fibers. Similar swellings were absent in dysmyelinated shiverer mice, which lack myelin basic protein (MBP), but recurred in MBP*PLP double mutants. Thus, fiber degeneration, which was probably secondary to impaired axonal transport, could indicate that myelinated axons require local oligodendroglial support.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, I -- Klugmann, M -- Anderson, T -- Yool, D -- Thomson, C -- Schwab, M H -- Schneider, A -- Zimmermann, F -- McCulloch, M -- Nadon, N -- Nave, K A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Neurobiology Group, Department of Veterinary Clinical Studies, University of Glasgow, Glasgow G61 1QH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616125" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Axons/*physiology/*ultrastructure ; Cell Communication ; Central Nervous System/*ultrastructure ; Female ; Mice ; Mice, Neurologic Mutants ; Models, Neurological ; Motor Activity ; Myelin Proteolipid Protein/analysis/genetics/*physiology ; Myelin Sheath/chemistry/physiology/ultrastructure ; Nerve Degeneration/*pathology ; *Nerve Tissue Proteins ; Oligodendroglia/physiology ; Optic Nerve/ultrastructure ; Organelles/ultrastructure ; Spinal Cord/ultrastructure ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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