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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
TAG-1 is a neural recognition molecule in the immunoglobulin superfamily that is predominantly expressed in the developing brain. Several lines of evidence suggest that TAG-1 is involved in the outgrowth, guidance, and fasciculation of neurites. To directly assess the function of TAG-1 in vivo, we have generated mice with a deletion in the gene encoding TAG-1 using homologous recombination in embryonic stem cells. Gross morphological analysis of the cerebellum, the spinal cord, and the hippocampus appeared normal in TAG-1-deficient mice. However, TAG-1 (-/-) mice showed the upregulation of the adenosine A1 receptors determined by [(3)H]cyclopentyl-1,3-dipropylxanthine in the hippocampus, and their greater sensitivity to convulsant stimuli than that in TAG-1 (+/+) mice. We suspect that the subtle changes in neural plasticity induced by TAG-1 deficiency during development cause the selective vulnerability of specific brain regions and the epileptogenicity in TAG-1 (-/-) mice.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0006-291X
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pubmed:author |
pubmed-author:AiharaOO,
pubmed-author:AkasakaKK,
pubmed-author:AsanoMM,
pubmed-author:FukamauchiFF,
pubmed-author:HorieMM,
pubmed-author:IwakuraYY,
pubmed-author:KawanoHH,
pubmed-author:SudoKK,
pubmed-author:TakedaYY,
pubmed-author:WangY JYJ,
pubmed-author:WatanabeKK
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pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
281
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
220-6
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11178983-Animals,
pubmed-meshheading:11178983-Antibodies,
pubmed-meshheading:11178983-Blotting, Southern,
pubmed-meshheading:11178983-Blotting, Western,
pubmed-meshheading:11178983-Cell Adhesion,
pubmed-meshheading:11178983-Cell Adhesion Molecules, Neuronal,
pubmed-meshheading:11178983-Cerebellum,
pubmed-meshheading:11178983-Contactin 2,
pubmed-meshheading:11178983-Embryo, Mammalian,
pubmed-meshheading:11178983-Gene Deletion,
pubmed-meshheading:11178983-Hippocampus,
pubmed-meshheading:11178983-Immunohistochemistry,
pubmed-meshheading:11178983-Membrane Glycoproteins,
pubmed-meshheading:11178983-Mice,
pubmed-meshheading:11178983-Mice, Knockout,
pubmed-meshheading:11178983-Models, Genetic,
pubmed-meshheading:11178983-Mutagenesis, Site-Directed,
pubmed-meshheading:11178983-Rabbits,
pubmed-meshheading:11178983-Receptors, Purinergic P1,
pubmed-meshheading:11178983-Recombination, Genetic,
pubmed-meshheading:11178983-Seizures,
pubmed-meshheading:11178983-Spinal Cord,
pubmed-meshheading:11178983-Stem Cells,
pubmed-meshheading:11178983-Up-Regulation
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pubmed:year |
2001
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pubmed:articleTitle |
TAG-1-deficient mice have marked elevation of adenosine A1 receptors in the hippocampus.
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pubmed:affiliation |
Department of Molecular Medical Science, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10, Kandasurugadai, Chiyoda-ku, Tokyo, 101-0062, Japan. ff.epi@mri.tmd.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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