Evaluation of gene expression profiling in a mouse model of L-gulonolactone oxidase gene deficiency

Genetics and Molecular Biology

Jian Yan²  Yan Jiao¹  Xinmin Li¹  Feng Jiao¹  Wesley G. Beamer¹  Cliff J. Rosen¹  Weikuan Gu¹ 

[1] ,University of Memphis Department of Biology Memphis TN ,USA

关键词: spontaneous fracture;    bone;    gene expression;    L-gulonolactone oxidase;    vitamin C;   

DOI  :  10.1590/S1415-47572007000300004

来源: SciELO

【 摘 要 】

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.

【 授权许可】

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