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

A mouse model of galactose-induced cataracts.

Galactokinase (GK; EC is the first enzyme in the metabolism of galactose. In humans, GK deficiency results in congenital cataracts due to an accumulation of galactitol within the lens. In an attempt to make a galactosemic animal model, we cloned the mouse GK gene (Glk1) and disrupted it by gene targeting. As expected, galactose was very poorly metabolized in GK-deficient mice. In addition, both galactose and galactitol accumulated in tissues of GK-deficient mice. Surprisingly, the GK-deficient animals did not form cataracts even when fed a high galactose diet. However, the introduction of a human aldose reductase transgene into a GK-deficient background resulted in cataract formation within the first postnatal day. This mouse represents the first mouse model for congenital galactosemic cataract.[1]


  1. A mouse model of galactose-induced cataracts. Ai, Y., Zheng, Z., O'Brien-Jenkins, A., Bernard, D.J., Wynshaw-Boris, T., Ning, C., Reynolds, R., Segal, S., Huang, K., Stambolian, D. Hum. Mol. Genet. (2000) [Pubmed]
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