Tyrosine aminotransferase deficiency in mink (Mustela vision): A model for human tyrosinemia II
- 1 August 1981
- journal article
- research article
- Published by Springer Nature in Biochemical Genetics
- Vol. 19 (7-8) , 687-693
- https://doi.org/10.1007/bf00484001
Abstract
Mink pseudodistemper, a recessive disease associated with high blood tyrosinelevels, is an animal analogue of the human inborn error of metabolism, tyrosinemia II. Affected mink and man have eye and skin lesions. Affected mink have no hepatic tyrosine aminotransferase (TAT) activity, as measured immunologically and biochemically. Hepatic mitochondrial aspartate aminotransferase is increased to 188% of control. This new genetic animal model of TAT deficiency should allow new studies of tyrosine metabolism.This publication has 16 references indexed in Scilit:
- Regulation of the tyrosine oxidizing system in fetal rat liverArchives of Biochemistry and Biophysics, 1980
- Hepatic Enzymes of Tyrosine Metabolism in Tyrosinemia IIJournal of Investigative Dermatology, 1979
- A syndrome of hereditary tyrosinemia in mink (Mustela vison Schreb.).1979
- Tyrosine aminotransferase isoenzyme deficiencyThe Journal of Pediatrics, 1979
- Properties of tyrosine aminotransferase from rat liverAnalytical Biochemistry, 1979
- Molecular Biology and Molecular Pathology of a Newly Described Molecular Disease – Tyrosinemia II (The Richner-Hanhart Syndrome)Pathobiology, 1978
- Soluble and mitochondrial forms of tyrosine aminotransferase. Relation to human tyrosinemiaBiochemistry, 1969
- The Molecular Weight and other Properties of Aspartate Aminotransferase from Pig Heart MuscleEuropean Journal of Biochemistry, 1968
- Assay of tyrosine transaminase activity by conversion of p-hydroxyphenylpyruvate to p-hydroxybenzaldehydeAnalytical Biochemistry, 1966
- PROTEIN MEASUREMENT WITH THE FOLIN PHENOL REAGENTJournal of Biological Chemistry, 1951