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dc.contributor.authorMcDonald, J. David
dc.contributor.authorCotton, R.G.
dc.contributor.authorJennings, I.
dc.contributor.authorLedley, F.D.
dc.contributor.authorWoo, S.L.
dc.contributor.authorBode, Vernon C.
dc.date.accessioned2013-04-18T17:07:59Z
dc.date.available2013-04-18T17:07:59Z
dc.date.issued1988-02
dc.identifier.citationMcDonald, J. David; Cotton, R. G.; Jennings, I.; Ledley, F. D.; Woo, S. L.; Bode, V. C. 1988. Biochemical defect of the hph-1 mouse mutant is a deficiency in GTP-cyclohydrolase activity. Journal of Neurochemistry, v.50 no.2 pp.655-657en_US
dc.identifier.otherPMID: 3335865
dc.identifier.urihttp://hdl.handle.net/10057/5639
dc.descriptionClick on the link to access the article (may not be free).en_US
dc.description.abstractA hyperphenylalaninemic mouse mutant, hph-1, has been identified in the progeny of mice treated with the mutagen ethylnitrosourea. Phenylalanine hydroxylase activity levels in mutant liver lysates are reduced relative to normal, but correction for the amount of enzyme protein present demonstrates that the specific activity of this enzyme is normal in mutant mice. Quinonoid-dihydropteridine reductase activity is also normal. GTP-cyclohydrolase activity levels are essentially absent early in life and greatly diminished later in life. This finding has significant implications for the study of catecholamine neurotransmitter synthesis because GTP-cyclohydrolase catalyzes an important step in the de novo synthesis of tetrahydrobiopterin, an enzyme cofactor required for the synthesis of 3,4-dihydroxyphenylalanine (DOPA) and serotonin.en_US
dc.language.isoen_USen_US
dc.publisherPubMeden_US
dc.relation.ispartofseriesJournal of Neurochemistry;v.50 no.2
dc.titleBiochemical defect of the hph-1 mouse mutant is a deficiency in GTP-cyclohydrolase activityen_US
dc.typeArticleen_US


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