| pubmed-article:9949198 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0035934 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0055817 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0439858 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0443177 | lld:lifeskim |
| pubmed-article:9949198 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:9949198 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9949198 | pubmed:dateCreated | 1999-5-3 | lld:pubmed |
| pubmed-article:9949198 | pubmed:abstractText | A mouse model of Rubinstein-Taybi syndrome (RTS) was generated by an insertional mutation into the cyclic AMP response element-binding protein (CREB)-binding protein (CBP) gene. Heterozygous CBP-deficient mice, which had truncated CBP protein (residues 1-1084) containing the CREB-binding domain (residues 462-661), showed clinical features of RTS, such as growth retardation (100%), retarded osseous maturation (100%), hypoplastic maxilla with narrow palate (100%), cardiac anomalies (15%) and skeletal abnormalities (7%). Truncated CBP is considered to have been acting during development as a dominant-negative inhibitor to lead to the phenotypes of RTS in mice. Our studies with step-through-type passive avoidance tests and with fear conditioning test showed that mice were deficient in long-term memory (LTM). In contrast, short-term memory (STM) appeared to be normal. These results implicate a crucial role for CBP in mammalian LTM. Our CBP +/- mice would be an excellent model for the study of the role of CBP in development and memory storage mechanisms. | lld:pubmed |
| pubmed-article:9949198 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9949198 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9949198 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9949198 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9949198 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9949198 | pubmed:issn | 0964-6906 | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:SuzukiMM | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:NodaYY | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:MamiyaTT | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:YasueHH | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:ArakiKK | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:YamamuraKK | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:NabeshimaTT | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:OikeYY | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:HataAA | lld:pubmed |
| pubmed-article:9949198 | pubmed:author | pubmed-author:KanameTT | lld:pubmed |
| pubmed-article:9949198 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9949198 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:9949198 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9949198 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9949198 | pubmed:pagination | 387-96 | lld:pubmed |
| pubmed-article:9949198 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9949198 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:9949198 | pubmed:articleTitle | Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism. | lld:pubmed |
| pubmed-article:9949198 | pubmed:affiliation | Department of Developmental Genetics, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Kuhonji 4-24-1, Kumamoto 862-0976, Japan. | lld:pubmed |
| pubmed-article:9949198 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9949198 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:12914 | entrezgene:pubmed | pubmed-article:9949198 | lld:entrezgene |
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