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This is usually enough to begin a candidate gene approach toward identifying the gene which when mutated gives rise to the phenotype of interest. So far, we have identified the causative mutation for four phenotypically deviant mouse lines. A mutation in the Lcat (lecithin cholesterol acyltransferase) newspaper gene leads to very low levels of HDL cholesterol in plasma. Gck (glucokinase) mutations lead to diabetes newspaper due to inadequate secretion of insulin for a given glucose load. In humans, Gck mutations lead to a newspaper form of diabetes called MODY2 (maturity onset diabetes of the young 2). Nephrogenic diabetes insipidus in humans can be caused by mutations in the Aqp2 (aquaporin 2) gene. We now have the first mouse model of this rare human disease. Finally, a point mutation in PC1 (prohormone convertase 1) leads to obesity in mice, as it does in humans.
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