Evaluation of gene expression profiling in a mouse model of L-gulonolactone oxidase gene deficiency.
Document Type
Article
Publication Date
2007
First Page
322
Last Page
329
JAX Location
see Reprint Collection (a pdf is available)
JAX Source
Genet Mol Biol 2007 30(2):322-29.
Abstract
Humans and guinea pigs are species which are unable to synthesize ascorbic acid (vitamin C) because, unlike rodents, they lack the enzyme L-gulonolactone oxidase (Gulo). Although the phenotype of lacking vitamin C in humans, named scurvy, has long been well known, information on the impact of lacking Gulo on the gene expression profiles of different tissues is still missing. This knowledge could improve our understanding of molecular pathways in which Gulo may be involved. Recently, we discovered a deletion that includes all 12 exons in the gene for Gulo in the sfx mouse, characterized by spontaneous bone fractures. We report here the initial analysis of the impact of the Gulo gene deletion on the murine gene expression profiles in the liver, femur and kidney.
Recommended Citation
Yan J,
Jiao Y,
Li X,
Jiao F,
Beamer WG,
Rosen CJ,
Gu W.
Evaluation of gene expression profiling in a mouse model of L-gulonolactone oxidase gene deficiency. Genet Mol Biol 2007 30(2):322-29.