Determination of functional effects of mutations in the steroid 21-hydroxylase gene (CYP21) using recombinant vaccinia virus


Por: Tusie-Luna M.-T., Traktman P., White P.C.

Publicada: 1 ene 1990
Resumen:
Steroid 21-hydroxylase (P450c21) is absent or defective in more than 90% of patients with congenital adrenal hyperplasia. This disorder of cortisol biosynthesis occurs in a wide spectrum of clinical severity; specific mutations in the 21-hydroxylase gene (CYP21) have been found in association with particular clinical phenotypes. To determine the functional effects of mutations causing amino acid substitutions, normal P450c21 and three mutagenized P450c21 enzymes were expressed at high levels in cultured COS-1 cells using recombinant vaccinia virus. A single amino acid substitution (Val281 ? Leu) present in patients with mild "nonclassical" 21-hydroxylase deficiency resulted in an enzyme with 20-50% of normal activity. A mutation (Ile172 ? Asn) identified in patients with the "simple virilizing" form (poor cortisol synthesis but adequate aldosterone synthesis) resulted in an enzyme with less than 2% of normal activity. Finally, a cluster mutation (Ile-Val-Glu-Met234,238 ? Asn-Glu-Glu-Lys) found in a patient with severe "salt wasting" 21-hydroxylase deficiency (inadequate aldosterone synthesis) results in an enzyme with no detectable activity. These data indicate that the severity of 21-hydroxylase deficiency correlates with the degree of enzymatic compromise.

Filiaciones:
Tusie-Luna M.-T.:
 Division of Pediatric, Endocrinology, Cornell Univ. Medical College, New York, NY 10021, United States

Traktman P.:
 Division of Pediatric, Endocrinology, Cornell Univ. Medical College, New York, NY 10021, United States

White P.C.:
 Division of Pediatric, Endocrinology, Cornell Univ. Medical College, New York, NY 10021, United States
ISSN: 00219258
Editorial
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 265 Número: 34
Páginas: 20916-20922
WOS Id: A1990EL02000033
ID de PubMed: 2249999

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