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rdf:type |
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lifeskim:mentions |
umls-concept:C0003969,
umls-concept:C0016663,
umls-concept:C0017337,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0062003,
umls-concept:C0242417,
umls-concept:C0596988,
umls-concept:C0678227,
umls-concept:C1314792,
umls-concept:C1442161
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pubmed:issue |
9
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pubmed:dateCreated |
2005-8-1
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pubmed:abstractText |
Using a mouse mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation, reduced bone formation, and development of spontaneous fractures.
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pubmed:grant |
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pubmed:commentsCorrections |
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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 |
Sep
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pubmed:issn |
0884-0431
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pubmed:author |
pubmed-author:BaylinkDavid JDJ,
pubmed-author:ChadwickRobert BRB,
pubmed-author:ChungYoon-SokYS,
pubmed-author:ChungYoon-SukYS,
pubmed-author:CrawfordGrace CGC,
pubmed-author:DonahueLeah RaeLR,
pubmed-author:KapoorAnilA,
pubmed-author:MohanSubburamanS,
pubmed-author:RosenCliffordC,
pubmed-author:SinggihAnnyA,
pubmed-author:TaylorTimT,
pubmed-author:WergedalJonJ,
pubmed-author:XXX,
pubmed-author:YuHongrunH
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pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1597-610
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16059632-Animals,
pubmed-meshheading:16059632-Ascorbic Acid,
pubmed-meshheading:16059632-Ascorbic Acid Deficiency,
pubmed-meshheading:16059632-Bone Marrow Cells,
pubmed-meshheading:16059632-Bone and Bones,
pubmed-meshheading:16059632-Cell Differentiation,
pubmed-meshheading:16059632-Chromosome Mapping,
pubmed-meshheading:16059632-DNA, Complementary,
pubmed-meshheading:16059632-DNA Primers,
pubmed-meshheading:16059632-Densitometry,
pubmed-meshheading:16059632-Femur,
pubmed-meshheading:16059632-Fracture Healing,
pubmed-meshheading:16059632-Fractures, Bone,
pubmed-meshheading:16059632-Gene Deletion,
pubmed-meshheading:16059632-Genome,
pubmed-meshheading:16059632-Genotype,
pubmed-meshheading:16059632-L-Gulonolactone Oxidase,
pubmed-meshheading:16059632-Mice,
pubmed-meshheading:16059632-Mice, Inbred BALB C,
pubmed-meshheading:16059632-Models, Genetic,
pubmed-meshheading:16059632-Mutation,
pubmed-meshheading:16059632-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:16059632-Osteoblasts,
pubmed-meshheading:16059632-Osteoporosis,
pubmed-meshheading:16059632-Phenotype,
pubmed-meshheading:16059632-RNA,
pubmed-meshheading:16059632-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16059632-Stromal Cells,
pubmed-meshheading:16059632-Tibia,
pubmed-meshheading:16059632-X-Rays
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pubmed:year |
2005
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pubmed:articleTitle |
Spontaneous fractures in the mouse mutant sfx are caused by deletion of the gulonolactone oxidase gene, causing vitamin C deficiency.
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pubmed:affiliation |
Molecular Genetics Division, Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, California, USA. Subburaman.Mohan@med.va.gov
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, N.I.H., Extramural
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