| pubmed-article:8700893 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8700893 | lifeskim:mentions | umls-concept:C0027794 | lld:lifeskim |
| pubmed-article:8700893 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8700893 | lifeskim:mentions | umls-concept:C0205161 | lld:lifeskim |
| pubmed-article:8700893 | lifeskim:mentions | umls-concept:C1160340 | lld:lifeskim |
| pubmed-article:8700893 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:8700893 | pubmed:dateCreated | 1996-9-5 | lld:pubmed |
| pubmed-article:8700893 | pubmed:abstractText | F52 is a myristoylated, alanine-rich substrate for protein kinase C. We have generated F52-deficient mice by the gene targeting technique. These mutant mice manifest severe neural tube defects that are not associated with other complex malformations, a phenotype reminiscent of common human neural tube defects. The neural tube defects observed include both exencephaly and spina bifida, and the phenotype exhibits partial penetrance with about 60% of homozygous embryos developing neural tube defects. Exencephaly is the prominent type of defect and leads to high prenatal lethality. Neural tube defects are observed in a smaller percentage of heterozygous embryos (about 10%). Abnormal brain development and tail formation occur in homozygous mutants and are likely to be secondary to the neural tube defects. Disruption of F52 in mice therefore identifies a gene whose mutation results in isolated neural tube defects and may provide an animal model for common human neural tube defects. | lld:pubmed |
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| pubmed-article:8700893 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8700893 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8700893 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8700893 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8700893 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8700893 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8700893 | pubmed:author | pubmed-author:RayW BWB | lld:pubmed |
| pubmed-article:8700893 | pubmed:author | pubmed-author:TonegawaSS | lld:pubmed |
| pubmed-article:8700893 | pubmed:author | pubmed-author:SasaokaTT | lld:pubmed |
| pubmed-article:8700893 | pubmed:author | pubmed-author:ChenD FDF | lld:pubmed |
| pubmed-article:8700893 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8700893 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:8700893 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8700893 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8700893 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8700893 | pubmed:pagination | 2110-5 | lld:pubmed |
| pubmed-article:8700893 | pubmed:dateRevised | 2010-9-13 | lld:pubmed |
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| pubmed-article:8700893 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8700893 | pubmed:articleTitle | Neural tube defects and abnormal brain development in F52-deficient mice. | lld:pubmed |
| pubmed-article:8700893 | pubmed:affiliation | Howard Hughes Medical Institute, Center for Learning and Memory, Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. | lld:pubmed |
| pubmed-article:8700893 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8700893 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8700893 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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