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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.
4          The enzymes most often affected are 21-hydroxylase, 11 beta-hydroxylase, and 3 beta-hydroxys
5 ld-containing B1, tryptophan hydroxlase, and 21-hydroxylase (21-OH), and the homozygous c.967_979del1
6 structed that showed 60% of 2C5 progesterone 21-hydroxylase activity and 57% regioselectivity.
7 conclude that human CYP17A1 has progesterone 21-hydroxylase activity and human CYP21A2 has progestero
8  I114A, F297G, and V363L showed 5-15% of the 21-hydroxylase activity of 2C5, whereas F206V showed hig
9               Autoantibodies against steroid 21-hydroxylase, an intracellular key enzyme of the adren
10 chrome P450 (P450) 21A2 is the major steroid 21-hydroxylase, and deficiency of this enzyme is involve
11 droxylase/17,20-lyase) and CYP21A2 (P450c21, 21-hydroxylase) catalyze progesterone hydroxylation at o
12 )21A2 gene, which encodes the enzyme steroid 21-hydroxylase, cause the majority of cases in congenita
13 e P450 (P450, CYP) 21A2 is the major steroid 21-hydroxylase, converting progesterone to 11-deoxycorti
14 threonine nuclear protein kinase RP, steroid 21-hydroxylase (CYP21), and tenascin (TNX), which togeth
15                                      Steroid 21-hydroxylase (cytochrome P450 21A2, CYP21A2) deficienc
16              The majority of cases is due to 21-hydroxylase deficiency (21-OHD).
17 n with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25 children with the salt-was
18  of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency (CAH) and have performed 8,290
19 ng the CYP21B and TNX genes, that results in 21-hydroxylase deficiency and a connective-tissue disord
20 ss numbers of affected newborns with classic 21-hydroxylase deficiency by contributing to the early d
21  7.5 million newborns have been screened for 21-hydroxylase deficiency congenital adrenal hyperplasia
22 renal insufficiency in patients with classic 21-hydroxylase deficiency congenital adrenal hyperplasia
23               The penetrance of nonclassical 21-hydroxylase deficiency gene in the HLA-B14 containing
24 rplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of
25                         Nonclassical steroid 21-hydroxylase deficiency is an autosomal recessive diso
26                    The gene for nonclassical 21-hydroxylase deficiency is in genetic linkage disequil
27                           Thus, nonclassical 21-hydroxylase deficiency is probably the most frequent
28                                              21-Hydroxylase deficiency is responsible for more than 9
29 d out on plasma samples from 117 adults with 21-hydroxylase deficiency receiving their usual glucocor
30  congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency require treatment with glucoco
31                        We found nonclassical 21-hydroxylase deficiency to be a far more common disord
32  multiple members affected with nonclassical 21-hydroxylase deficiency together with the results of q
33 mens obtained from three other patients with 21-hydroxylase deficiency who had undergone bilateral ad
34 diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) with testicular adrenal rest
35 imates of the gene frequency of nonclassical 21-hydroxylase deficiency, also called attenuated, late-
36                         Unlike CAH caused by 21-hydroxylase deficiency, the disease is far more commo
37 n the management and treatment of CAH due to 21-hydroxylase deficiency, the most common type of CAH.
38 esterone concentrations for classic (severe) 21-hydroxylase deficiency, the most common type of conge
39 be a far more common disorder than classical 21-hydroxylase deficiency, which occurs in 1/8,000 birth
40 urs in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
41 alomas may be homozygous or heterozygous for 21-hydroxylase deficiency.
42 ria that distinguishes it from the classical 21-hydroxylase deficiency.
43                                          The 21-hydroxylase-deficient mouse has provided a useful mod
44 renal hyperplasia (CAH) due to deficiency of 21-hydroxylase is a disorder of the adrenal cortex chara
45 , which encodes P450c21, the adrenal steroid 21-hydroxylase needed for glucocorticoid synthesis, lies
46 e data indicate that strong CTL responses to 21-hydroxylase often occur in vivo, and that reactive CT
47 ed by a large gene that overlaps the steroid 21-hydroxylase (P450c21) gene in the HLA locus on chromo
48  CD8(+) T cells showed their ability to lyse 21-hydroxylase-positive target cells, consistent with a
49     HLA class I tetramer-guided isolation of 21-hydroxylase-specific CD8(+) T cells showed their abil
50 this article, we demonstrate highly frequent 21-hydroxylase-specific T cells detectable in 20 patient
51 ge proportion of patients, CD8(+) and CD4(+) 21-hydroxylase-specific T cells were very abundant and d
52 l cells (PCAs), tissue transglutaminase, and 21-hydroxylase was tested using a linear mixed-model reg
53 g 18-aa peptides spanning the full length of 21-hydroxylase, we identified immunodominant CD8(+) and