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Publication : Congenital copper deficiency: copper therapy and dopamine-beta-hydroxylase activity in the mottled (brindled) mouse.

First Author  Wenk G Year  1983
Journal  J Neurochem Volume  41
Issue  6 Pages  1648-52
PubMed ID  6644305 Mgi Jnum  J:7251
Mgi Id  MGI:55722 Doi  10.1111/j.1471-4159.1983.tb00876.x
Citation  Wenk G, et al. (1983) Congenital copper deficiency: copper therapy and dopamine-beta-hydroxylase activity in the mottled (brindled) mouse. J Neurochem 41(6):1648-52
abstractText  The mottled (Mo) mouse is an animal model of the human congenital copper (Cu) deficiency disorder, Menkes' kinky hair syndrome. Intraperitoneal Cu chloride injections have been shown to produce clinical and morphological improvements in this mutant mouse. Cu injections (10 micrograms/g) on postnatal days 7 and 10 are shown to increase endogenous activity of the Cu-dependent enzyme dopamine-beta-hydroxylase in the brains of Mo mice. The present study provides insight into the long-term neurochemical changes resulting from a possible treatment regimen for Menkes' kinky hair syndrome.
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