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1 impaired activity of 17alpha-hydroxylase and 21-hydroxylase.
2 each followed by an intact gene for steroid 21-hydroxylase.
3 lase, whereas 2C5 is a low K(m) progesterone 21-hydroxylase.
6 conclude that human CYP17A1 has progesterone 21-hydroxylase activity and human CYP21A2 has progestero
7 I114A, F297G, and V363L showed 5-15% of the 21-hydroxylase activity of 2C5, whereas F206V showed hig
9 chrome P450 (P450) 21A2 is the major steroid 21-hydroxylase, and deficiency of this enzyme is involve
10 droxylase/17,20-lyase) and CYP21A2 (P450c21, 21-hydroxylase) catalyze progesterone hydroxylation at o
11 )21A2 gene, which encodes the enzyme steroid 21-hydroxylase, cause the majority of cases in congenita
12 e P450 (P450, CYP) 21A2 is the major steroid 21-hydroxylase, converting progesterone to 11-deoxycorti
13 threonine nuclear protein kinase RP, steroid 21-hydroxylase (CYP21), and tenascin (TNX), which togeth
16 n with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25 children with the salt-was
17 of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency (CAH) and have performed 8,290
18 ng the CYP21B and TNX genes, that results in 21-hydroxylase deficiency and a connective-tissue disord
19 ss numbers of affected newborns with classic 21-hydroxylase deficiency by contributing to the early d
20 7.5 million newborns have been screened for 21-hydroxylase deficiency congenital adrenal hyperplasia
22 rplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of
27 d out on plasma samples from 117 adults with 21-hydroxylase deficiency receiving their usual glucocor
29 multiple members affected with nonclassical 21-hydroxylase deficiency together with the results of q
30 mens obtained from three other patients with 21-hydroxylase deficiency who had undergone bilateral ad
31 diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) with testicular adrenal rest
32 imates of the gene frequency of nonclassical 21-hydroxylase deficiency, also called attenuated, late-
34 esterone concentrations for classic (severe) 21-hydroxylase deficiency, the most common type of conge
35 be a far more common disorder than classical 21-hydroxylase deficiency, which occurs in 1/8,000 birth
40 renal hyperplasia (CAH) due to deficiency of 21-hydroxylase is a disorder of the adrenal cortex chara
41 , which encodes P450c21, the adrenal steroid 21-hydroxylase needed for glucocorticoid synthesis, lies
42 e data indicate that strong CTL responses to 21-hydroxylase often occur in vivo, and that reactive CT
43 ed by a large gene that overlaps the steroid 21-hydroxylase (P450c21) gene in the HLA locus on chromo
44 CD8(+) T cells showed their ability to lyse 21-hydroxylase-positive target cells, consistent with a
45 HLA class I tetramer-guided isolation of 21-hydroxylase-specific CD8(+) T cells showed their abil
46 this article, we demonstrate highly frequent 21-hydroxylase-specific T cells detectable in 20 patient
47 ge proportion of patients, CD8(+) and CD4(+) 21-hydroxylase-specific T cells were very abundant and d
48 l cells (PCAs), tissue transglutaminase, and 21-hydroxylase was tested using a linear mixed-model reg
49 g 18-aa peptides spanning the full length of 21-hydroxylase, we identified immunodominant CD8(+) and
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