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  • Mice, Inbred C57BL  (6)
  • 2020-2024
  • 2020-2022
  • 2000-2004  (6)
  • 2003  (6)
  • 1
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    Modification of ocular defects in mouse developmental glaucoma models by tyrosinase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: Mutations in the cytochrome P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene are a common cause of human primary congenital glaucoma (PCG). Here we show that Cyp1b1-/- mice have ocular drainage structure abnormalities resembling those reported in human PCG patients. Using Cyp1b1-/- mice, we identified the tyrosinase gene (Tyr) as a modifier of the drainage structure phenotype, with Tyr deficiency increasing the magnitude of dysgenesis. The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Tyr also modified the drainage structure dysgenesis in mice with a mutant Foxc1 gene, which is also involved in PCG. These experiments raise the possibility that a tyrosinase/l-dopa pathway modifies human PCG, which could open new therapeutic avenues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Libby, Richard T -- Smith, Richard S -- Savinova, Olga V -- Zabaleta, Adriana -- Martin, Janice E -- Gonzalez, Frank J -- John, Simon W M -- CA34196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624268" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism, Ocular/genetics/pathology ; Animals ; Anterior Eye Segment/*abnormalities ; Aryl Hydrocarbon Hydroxylases/deficiency/genetics ; Cornea/abnormalities ; Cytochrome P-450 CYP1B1 ; *DNA-Binding Proteins ; Disease Models, Animal ; Female ; Forkhead Transcription Factors ; Glaucoma/*congenital/enzymology/*genetics/pathology ; Intraocular Pressure ; Iris/abnormalities ; Levodopa/administration & dosage/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Monophenol Monooxygenase/deficiency/*genetics/metabolism ; Mutation ; Phenotype ; Pregnancy ; Trabecular Meshwork/abnormalities ; Transcription Factors/genetics
    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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    Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, Masahiro -- Sato, Shintaro -- Hemmi, Hiroaki -- Hoshino, Katsuaki -- Kaisho, Tsuneyasu -- Sanjo, Hideki -- Takeuchi, Osamu -- Sugiyama, Masanaka -- Okabe, Masaru -- Takeda, Kiyoshi -- Akira, Shizuo -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):640-3. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855817" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/genetics/*physiology ; Animals ; Antigens, Differentiation/*physiology ; Cells, Cultured ; Cytokines/biosynthesis ; DNA-Binding Proteins/metabolism ; Dimerization ; Embryo, Mammalian ; Fibroblasts/metabolism ; Gene Expression Regulation ; Gene Targeting ; Interferon Regulatory Factor-3 ; Interferon-beta/genetics/*metabolism ; JNK Mitogen-Activated Protein Kinases ; Ligands ; Lipopolysaccharides/immunology/pharmacology ; Macrophages, Peritoneal/immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Poly I-C/pharmacology ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/*physiology ; *Signal Transduction ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Transcription Factors/metabolism
    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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  • 3
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    Generation of viable cholesterol-free mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wechsler, A -- Brafman, A -- Shafir, M -- Heverin, M -- Gottlieb, H -- Damari, G -- Gozlan-Kelner, S -- Spivak, I -- Moshkin, O -- Fridman, E -- Becker, Y -- Skaliter, R -- Einat, P -- Faerman, A -- Bjorkhem, I -- Feinstein, E -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Quark Biotech, Inc., 10265 Carnegie Avenue, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684813" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Bile Acids and Salts/biosynthesis ; Cholesterol/blood/*deficiency/metabolism/*physiology ; Desmosterol/*metabolism ; Female ; Gene Targeting ; Growth ; Humans ; Infertility ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Nerve Tissue Proteins/*genetics/metabolism ; Oxidoreductases Acting on CH-CH Group Donors/*genetics/metabolism ; Phenotype ; Sex Characteristics ; Testis/pathology
    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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  • 4
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    Role of EphA4 and EphrinB3 in local neuronal circuits that control walking (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: Local circuits in the spinal cord that generate locomotion are termed central pattern generators (CPGs). These provide coordinated bilateral control over the normal limb alternation that underlies walking. The molecules that organize the mammalian CPG are unknown. Isolated spinal cords from mice lacking either the EphA4 receptor or its ligand ephrinB3 have lost left-right limb alternation and instead exhibit synchrony. We identified EphA4-positive neurons as an excitatory component of the locomotor CPG. Our study shows that dramatic locomotor changes can occur as a consequence of local genetic rewiring and identifies genes required for the development of normal locomotor behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kullander, Klas -- Butt, Simon J B -- Lebret, James M -- Lundfald, Line -- Restrepo, Carlos E -- Rydstrom, Anna -- Klein, Rudiger -- Kiehn, Ole -- New York, N.Y. -- Science. 2003 Mar 21;299(5614):1889-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, Gothenburg University, Medicinaregatan 9 A, 405 30 Gothenburg, Sweden. klas.kullander@medkem.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Bicuculline/pharmacology ; Carrier Proteins/genetics/metabolism ; Electrophysiology ; Ephrin-B3/genetics/*physiology ; Gait ; In Vitro Techniques ; Interneurons/physiology ; *Membrane Transport Proteins ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/*physiology ; Nipecotic Acids/pharmacology ; Receptor, EphA4/genetics/*physiology ; Sarcosine/pharmacology ; Signal Transduction ; Spinal Cord/*physiology ; Spinal Nerve Roots/physiology ; Strychnine/pharmacology ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2 ; *Vesicular Transport Proteins ; *Walking
    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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    CB1 cannabinoid receptors and on-demand defense against excitotoxicity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsicano, Giovanni -- Goodenough, Sharon -- Monory, Krisztina -- Hermann, Heike -- Eder, Matthias -- Cannich, Astrid -- Azad, Shahnaz C -- Cascio, Maria Grazia -- Gutierrez, Silvia Ortega -- van der Stelt, Mario -- Lopez-Rodriguez, Maria Luz -- Casanova, Emilio -- Schutz, Gunther -- Zieglgansberger, Walter -- Di Marzo, Vincenzo -- Behl, Christian -- Lutz, Beat -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):84-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Behaviour, Max-Planck-Institute of Psychiatry, Kraepelinstrabetae 2-10, 80804 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526074" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/*metabolism/pharmacology ; Brain/drug effects/*metabolism ; Brain-Derived Neurotrophic Factor/genetics/metabolism ; Cannabinoids/*metabolism ; Endocannabinoids ; Epilepsy/*metabolism/physiopathology ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Postsynaptic Potentials ; Furans/pharmacology ; Gene Expression Regulation/drug effects ; Genes, Immediate-Early ; Glutamic Acid/metabolism ; Glycerides/metabolism ; Hippocampus/drug effects/metabolism ; In Vitro Techniques ; Kainic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Neurons/drug effects/*metabolism/physiology ; Neuroprotective Agents/metabolism ; Piperidines/pharmacology ; Polyunsaturated Alkamides ; Prosencephalon/drug effects/metabolism ; Pyrazoles/pharmacology ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Amygdalar and hippocampal theta rhythm synchronization during fear memory retrieval (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: The amygdalohippocampal circuit plays a pivotal role in Pavlovian fear memory. We simultaneously recorded electrical activity in the lateral amygdala (LA) and the CA1 area of the hippocampus in freely behaving fear-conditioned mice. Patterns of activity were related to fear behavior evoked by conditioned and indifferent sensory stimuli and contexts. Rhythmically synchronized activity at theta frequencies increased between the LA and the CA1 after fear conditioning and became significant during confrontation with conditioned fear stimuli and expression of freezing behavior. Synchronization of theta activities in the amygdalohippocampal network represents a neuronal correlate of conditioned fear, apt to improve neuronal communication during memory retrieval.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seidenbecher, Thomas -- Laxmi, T Rao -- Stork, Oliver -- Pape, Hans-Christian -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):846-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Physiologie, Otto-von-Guericke-Universitat, Leipziger Strasse 44, Magdeburg D-39120, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907806" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiology ; Animals ; Behavior, Animal ; Conditioning (Psychology) ; Cues ; Electrophysiology ; Electroshock ; *Fear ; Hippocampus/*physiology ; Male ; *Memory ; Mice ; Mice, Inbred C57BL ; Motor Activity ; *Theta Rhythm
    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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