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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1999-5-3
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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.
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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 |
Mar
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pubmed:issn |
0964-6906
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
387-96
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9949198-Animals,
pubmed-meshheading:9949198-Base Sequence,
pubmed-meshheading:9949198-Behavior, Animal,
pubmed-meshheading:9949198-CREB-Binding Protein,
pubmed-meshheading:9949198-DNA Primers,
pubmed-meshheading:9949198-Disease Models, Animal,
pubmed-meshheading:9949198-Female,
pubmed-meshheading:9949198-Genes, Dominant,
pubmed-meshheading:9949198-Heterozygote,
pubmed-meshheading:9949198-Humans,
pubmed-meshheading:9949198-Male,
pubmed-meshheading:9949198-Memory,
pubmed-meshheading:9949198-Mice,
pubmed-meshheading:9949198-Mice, Mutant Strains,
pubmed-meshheading:9949198-Motor Activity,
pubmed-meshheading:9949198-Mutagenesis, Insertional,
pubmed-meshheading:9949198-Nuclear Proteins,
pubmed-meshheading:9949198-Phenotype,
pubmed-meshheading:9949198-Pregnancy,
pubmed-meshheading:9949198-Rubinstein-Taybi Syndrome,
pubmed-meshheading:9949198-Sequence Deletion,
pubmed-meshheading:9949198-Trans-Activators
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pubmed:year |
1999
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pubmed:articleTitle |
Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism.
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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.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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