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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Animal models reveal pathophysiologies of tyrosinemias.

The activity of the enzyme 4-hydroxyphenylpyruvic acid dioxygenase (HPD) is regulated by transcription factors. Mutations in the HPD locus are related to two known distinct diseases: hereditary tyrosinemia type 3 and hawkinsinuria. HPD-deficient mice are a good model with which to examine the biological effects of 4-hydroxyphenylpyruvic acid, which is a keto acid that causes no apparent visceral damage. In contrast, hereditary tyrosinemia type 1, a genetic disease caused by a deficiency of fumarylacetoacetate hydrolase (FAH), induces severe visceral injuries. Mice with FAH deficiency are lethal after birth; thus, efforts to elucidate the mechanisms of the disease process have been impeded. The use of Fah(-/-) Hpd(-/-) double-mutant mice has enabled studies on tyrosinemias, and essential features of visceral injury have been reveale.[1]


  1. Animal models reveal pathophysiologies of tyrosinemias. Endo, F., Tanaka, Y., Tomoeda, K., Tanoue, A., Tsujimoto, G., Nakamura, K. J. Nutr. (2003) [Pubmed]
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