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  • 11
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    Dopamine neuron agenesis in Nurr1-deficient mice (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: Dopamine neurons of the substantia nigra and ventral tegmental area regulate movement and affective behavior and degenerate in Parkinson's disease. The orphan nuclear receptor Nurr1 was shown to be expressed in developing dopamine neurons before the appearance of known phenotypic markers for these cells. Mice lacking Nurr1 failed to generate midbrain dopaminergic neurons, were hypoactive, and died soon after birth. Nurr1 expression continued into adulthood, and brains of heterozygous animals, otherwise apparently healthy, contained reduced dopamine levels. These results suggest that putative Nurr1 ligands may be useful for treatment of Parkinson's disease and other disorders of midbrain dopamine circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zetterstrom, R H -- Solomin, L -- Jansson, L -- Hoffer, B J -- Olson, L -- Perlmann, T -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):248-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092472" target="_blank"〉PubMed〈/a〉
    Keywords: 3,4-Dihydroxyphenylacetic Acid/metabolism ; Animals ; Cell Differentiation ; Chromatography, High Pressure Liquid ; Corpus Striatum/metabolism ; *DNA-Binding Proteins ; Dopamine/biosynthesis/*metabolism ; Gene Targeting ; Heterozygote ; Ligands ; Mesencephalon/abnormalities/*cytology/growth & development/metabolism ; Mice ; Nerve Tissue Proteins/genetics/*metabolism ; Neurons/*cytology/*metabolism ; Nuclear Receptor Subfamily 4, Group A, Member 2 ; RNA, Messenger/genetics/metabolism ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 12
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    Bloodstream- versus tick-associated variants of a relapsing fever bacterium (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-25
    Description: The relapsing fever spirochete, Borrelia hermsii, alternates infections between a mammal and a tick vector. Whether the spirochete changes phenotypically in the different hosts was examined by allowing the tick vector Ornithodoros hermsi to feed on mice infected with serotype 7 or serotype 8 of B. hermsii. Upon infection of ticks, the spirochetal serotype-specific variable major proteins (Vmps) 7 and 8 became undetectable and were replaced by Vmp33. This switch from a bloodstream- to tick-associated phenotype could be induced in culture by a decrease in temperature. After tick-bite transmission back to mice, the process was reversed and the spirochetes resumed expression of the same Vmp present in the previous infectious blood meal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwan, T G -- Hinnebusch, B J -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1938-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. tom_schwn@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9632392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigenic Variation ; Antigens, Bacterial/analysis/*genetics/immunology ; Antigens, Surface/analysis/genetics/immunology ; Arachnid Vectors/microbiology ; Bacteremia/microbiology ; Bacterial Outer Membrane Proteins/analysis/*genetics/immunology ; Borrelia/classification/*genetics/immunology ; Fluorescent Antibody Technique, Indirect ; Gene Expression ; Genes, Bacterial ; Mice ; Mice, Inbred BALB C ; Relapsing Fever/*microbiology/transmission ; Salivary Glands/microbiology ; Serotyping ; Ticks/*microbiology
    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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  • 13
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    A p53-dependent mouse spindle checkpoint (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-03
    Description: Cell cycle checkpoints enhance genetic fidelity by causing arrest at specific stages of the cell cycle when previous events have not been completed. The tumor suppressor p53 has been implicated in a G1 checkpoint. To investigate whether p53 also participates in a mitotic checkpoint, cultured fibroblasts from p53-deficient mouse embryos were exposed to spindle inhibitors. The fibroblasts underwent multiple rounds of DNA synthesis without completing chromosome segregation, thus forming tetraploid and octaploid cells. Deficiency of p53 was also associated with the development of tetraploidy in vivo. These results suggest that murine p53 is a component of a spindle checkpoint that ensures the maintenance of diploidy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cross, S M -- Sanchez, C A -- Morgan, C A -- Schimke, M K -- Ramel, S -- Idzerda, R L -- Raskind, W H -- Reid, B J -- R01CA55814/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; DNA/biosynthesis ; Demecolcine/pharmacology ; Diploidy ; Female ; Genes, p53 ; Male ; Mice ; *Mitosis ; Nocodazole/pharmacology ; Ploidies ; Spindle Apparatus/*physiology ; Tumor Suppressor Protein p53/*physiology
    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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  • 14
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    Evidence for developmentally programmed transdifferentiation in mouse esophageal muscle (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-12-15
    Description: Transdifferentiation is a relatively rare phenomenon in which cells of one differentiated type and function switch to a second discrete identity. In vertebrate embryos, smooth muscle and skeletal muscle are distinct tissues that arise from separate compartments of the mesoderm. The musculature of the mouse esophagus was found to undergo a conversion from smooth muscle in the fetus to skeletal muscle during early postnatal development. The switch from smooth to skeletal muscle features the transitory appearance of individual cells expressing a mixed phenotype, which suggests that this conversion is a result of programmed transdifferentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patapoutian, A -- Wold, B J -- Wagner, R A -- AR40708/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Dec 15;270(5243):1818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8525375" target="_blank"〉PubMed〈/a〉
    Keywords: Actinin/metabolism ; Animals ; Animals, Newborn ; Apoptosis ; Cell Differentiation/*genetics ; Embryonic and Fetal Development ; Esophagus/cytology/*embryology ; Mice ; Muscle Development ; Muscle, Skeletal/cytology/*embryology/growth & development/metabolism ; Muscle, Smooth/cytology/*embryology/metabolism ; Myogenic Regulatory Factors/metabolism ; Myosin Heavy Chains/metabolism ; Myosin Light Chains/metabolism ; Phenotype
    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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  • 15
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    Potentiated necrosis of cultured cortical neurons by neurotrophins (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-28
    Description: The effects of neurotrophins on several forms of neuronal degeneration in murine cortical cell cultures were examined. Consistent with other studies, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 all attenuated the apoptotic death induced by serum deprivation or exposure to the calcium channel antagonist nimodipine. Unexpectedly, however, 24-hour pretreatment with these same neurotrophins markedly potentiated the necrotic death induced by exposure to oxygen-glucose deprivation or N-methyl-D-aspartate. Thus, certain neurotrophins may have opposing effects on different types of death in the same neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Gwag, B J -- Lobner, D -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Brain-Derived Neurotrophic Factor ; Calcium/metabolism ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; Dizocilpine Maleate/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Necrosis ; Nerve Degeneration/*drug effects ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/pharmacology ; Neurons/*cytology/drug effects/pathology ; Neurotrophin 3 ; Quinoxalines/pharmacology ; Receptors, AMPA/antagonists & inhibitors
    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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