pubmed-article:11178983 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11178983 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:11178983 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
pubmed-article:11178983 | lifeskim:mentions | umls-concept:C0001451 | lld:lifeskim |
pubmed-article:11178983 | lifeskim:mentions | umls-concept:C0702240 | lld:lifeskim |
pubmed-article:11178983 | lifeskim:mentions | umls-concept:C1706089 | lld:lifeskim |
pubmed-article:11178983 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11178983 | pubmed:dateCreated | 2001-2-22 | lld:pubmed |
pubmed-article:11178983 | 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. | lld:pubmed |
pubmed-article:11178983 | pubmed:language | eng | lld:pubmed |
pubmed-article:11178983 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11178983 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11178983 | pubmed:month | Feb | lld:pubmed |
pubmed-article:11178983 | pubmed:issn | 0006-291X | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:WatanabeKK | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:WangY JYJ | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:AkasakaKK | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:SudoKK | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:TakedaYY | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:AsanoMM | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:HorieMM | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:KawanoHH | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:IwakuraYY | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:FukamauchiFF | lld:pubmed |
pubmed-article:11178983 | pubmed:author | pubmed-author:AiharaOO | lld:pubmed |
pubmed-article:11178983 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11178983 | pubmed:day | 16 | lld:pubmed |
pubmed-article:11178983 | pubmed:volume | 281 | lld:pubmed |
pubmed-article:11178983 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11178983 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11178983 | pubmed:pagination | 220-6 | lld:pubmed |
pubmed-article:11178983 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:11178983 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11178983 | pubmed:articleTitle | TAG-1-deficient mice have marked elevation of adenosine A1 receptors in the hippocampus. | lld:pubmed |
pubmed-article:11178983 | 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 | lld:pubmed |
pubmed-article:11178983 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11178983 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:21367 | entrezgene:pubmed | pubmed-article:11178983 | lld:entrezgene |
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