[Gene engineering studies on sleep].
Recent advancements in molecular engineering techniques have enabled us to study sleep of animals lacking or overproducing any protein molecule we are interested in. Abnormalities in sleep have already been observe in knockout mice lacking the gene for prion protein, 55 kD-receptor of tumor necrosis factor, etc. We also started a project to examine the effect of the loss or the overproduction of prostaglandin D synthase in sleep. The enzyme is responsible for biosynthesis of prostaglandin D2, the most potent endogenous substance to promote sleep reported so far. We generated both knockout and transgenic mice of prostaglandin D synthase. We are currently analysing the sleep of these mutant mice.
Urade
Y
Y
Osaka Bioscience Institute, Department of Molecular Behavioral Biology.
D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000235:genetics / Q000378:metabolism; D054834:Lipocalins; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009154:Mutation; D011328:Prions / Q000235:genetics; D015230:Prostaglandin D2 / Q000096:biosynthesis; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics; D047888:Receptors, Tumor Necrosis Factor, Type I; D012893:Sleep Wake Disorders / Q000235:genetics*
D015703:Antigens, CD; D054834:Lipocalins; D011328:Prions; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D019746:Intramolecular Oxidoreductases; C022466:prostaglandin R2 D-isomerase; D015230:Prostaglandin D2