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Information on EC 1.14.15.5 - corticosterone 18-monooxygenase for references in articles please use BRENDA:EC1.14.15.5Word Map on EC 1.14.15.5
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The enzyme appears in viruses and cellular organisms
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corticosterone 18-monooxygenase
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corticosterone + 2 reduced adrenodoxin + O2 + 2 H+ = 18-hydroxycorticosterone + 2 oxidized adrenodoxin + H2O
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mineralocorticoid biosynthesis
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Steroid hormone biosynthesis
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corticosterone,reduced-adrenal-ferredoxin:oxygen oxidoreductase (18-hydroxylating)
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corticosterone 18-hydroxylase
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corticosterone methyl oxidase
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oxygenase, corticosterone 18-mono-
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catalyzes a hydroxylation at position C11 of the steroid intermediate deoxycorticosterone yielding corticosterone, reaction of EC 1.14.15.4, followed by a hydroxylation at position C18, reaction of EC 1.14.15.5
UniProt
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
additional information
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reduced enzyme activity occurs in hyponatremia and hyperkalemia due to an isolated aldosterone biosynthesis defect, the phenotype can be rescued by a fludrocortisone replacement therapy, overview
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
additional information
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reduced enzyme activity occurs in hyponatremia and hyperkalemia due to an isolated aldosterone biosynthesis defect, the phenotype can be rescued by a fludrocortisone replacement therapy, overview
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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corticosterone + reduced adrenal ferredoxin + O2
18-hydroxycorticosterone + oxidized adrenal ferredoxin + H2O
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reaction in the biosynthesis of aldosterone
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reduced adrenal ferredoxin
NADPH
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activation, no activation by NADH, FAD, FMN, cytochrome c, GSH, dehydroascorbate, in vitro best stimulation by NADPH-regenerating system instead of exogenous NADPH
NADPH
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activation, no activation by NADH, FAD, FMN, cytochrome c, GSH, dehydroascorbate, in vitro best stimulation by NADPH-regenerating system instead of exogenous NADPH
NADPH
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activation, no activation by NADH, FAD, FMN, cytochrome c, GSH, dehydroascorbate, in vitro best stimulation by NADPH-regenerating system instead of exogenous NADPH
reduced adrenal ferredoxin
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reduced adrenal ferredoxin
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reduced adrenal ferredoxin
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Ca2+
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increase of activity, Na+, K+ alone or together are ineffective
Ca2+
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increase of activity, Na+, K+ alone or together are ineffective
Ca2+
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increase of activity, Na+, K+ alone or together are ineffective
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1,2-Bis(3-pyridyl)-2-methyl-1-propanone
3-(1,2, 3,4-Tetrahydr-1-oxo-2-naphthyl)pyridine
1,2-Bis(3-pyridyl)-2-methyl-1-propanone
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SU 4885
1,2-Bis(3-pyridyl)-2-methyl-1-propanone
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SU 4885
1,2-Bis(3-pyridyl)-2-methyl-1-propanone
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SU 4885
18-hydroxycorticosterone
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product inhibition
18-hydroxycorticosterone
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product inhibition
18-hydroxycorticosterone
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product inhibition
3-(1,2, 3,4-Tetrahydr-1-oxo-2-naphthyl)pyridine
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SU 9055
3-(1,2, 3,4-Tetrahydr-1-oxo-2-naphthyl)pyridine
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SU 9055
3-(1,2, 3,4-Tetrahydr-1-oxo-2-naphthyl)pyridine
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SU 9055
Co2+
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Cu2+
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diethyldithiocarbamate
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diethyldithiocarbamate
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diethyldithiocarbamate
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Fe3+
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Formamidine acetate
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Hg2+
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Mn2+
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NEM
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higher concentrations
NEM
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higher concentrations
NEM
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higher concentrations
p-chloromercuribenzoate
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p-chloromercuribenzoate
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p-chloromercuribenzoate
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SU 10603
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less effective
SU 10603
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less effective
SU 10603
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less effective
Zn2+
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7.3
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assay at
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assay at
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lyophilization, mitochondria lose 90% activity
lyophilization, mitochondria lose 90% activity
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lyophilization, mitochondria lose 90% activity
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lyophilization, mitochondria lose 90% activity
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expression in COS7 cells
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expression in Escherichia coli
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V386A
the combination of the V386A mutation with the variant CYP11B2 173Arg only slightly reduces the 18-hydroxylase and 18-oxidase activity, whereas the V386A mutation with the CYP11B2 173Lys variant almost abolishes the 18-hydroxylation and 18-oxidation. In both cases the 11-hydroxylase activity is not affected
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C11B2_HUMAN
503
57560
Swiss-Prot
C11B2_MESAU
500
57332
Swiss-Prot
C11B2_MOUSE
500
57373
Swiss-Prot
C11B2_RAT
510
58241
Swiss-Prot
C11B3_RAT
500
57122
Swiss-Prot
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Adrenogenital Syndrome
CYP17- and CYP11B-dependent steroid hydroxylases as drug development targets.
cholinesterase deficiency
Genetic screening in the Persian Jewish community: A pilot study.
corticosterone 18-monooxygenase deficiency
Biochemical diagnosis and management of corticosterone methyl oxidase type II deficiency.
corticosterone 18-monooxygenase deficiency
Computational analysis of functional single nucleotide polymorphisms associated with the CYP11B2 gene.
corticosterone 18-monooxygenase deficiency
Congenital hypoaldosteronism: the Visser-Cost syndrome revisited.
corticosterone 18-monooxygenase deficiency
Corticosterone Methyl Oxidase Deficiency Type 1 with Normokalemia in an Infant.
corticosterone 18-monooxygenase deficiency
Hereditary defect in biosynthesis of aldosterone: aldosterone synthase deficiency 1964-1997.
corticosterone 18-monooxygenase deficiency
Homozygosity for a mutation in the CYP11B2 gene in an infant with congenital corticosterone methyl oxidase deficiency type II.
corticosterone 18-monooxygenase deficiency
Multisteroid analysis in children with terminal aldosterone biosynthesis defects.
corticosterone 18-monooxygenase deficiency
Mutation THR-185 ILE is associated with corticosterone methyl oxidase deficiency type II.
corticosterone 18-monooxygenase deficiency
The effect of ACTH stimulation on plasma steroids in two patients with congenital hypoaldosteronism and in their relatives.
Dehydration
Corticosterone methyl oxidase type II deficiency: a cause of failure to thrive and recurrent dehydration in early infancy.
Diabetes Mellitus
Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism.
Disorders of Sex Development
CYP17- and CYP11B-dependent steroid hydroxylases as drug development targets.
Herpes Zoster
18-Hydroxy-11-deoxycortisol: a new steroid isolated from incubations of the adrenal with 11-deoxycortisol.
Herpes Zoster
Reversible hyporeninemic hypoaldosteronism in a patient with tetraplegia.
Hyperaldosteronism
Computational analysis of functional single nucleotide polymorphisms associated with the CYP11B2 gene.
Hypoaldosteronism
Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism.
Hypoaldosteronism
Severe hypoaldosteronism due to corticosterone methyl oxidase type II deficiency in two boys: metabolic and gas chromatography-mass spectrometry studies.
Hypoaldosteronism
[Primary hypoaldosteronism and secondary pseudo-hypoaldosteronism]
Muscular Diseases
Genetic screening in the Persian Jewish community: A pilot study.
steroid 11beta-monooxygenase deficiency
Corticosterone Methyl Oxidase Deficiency Type 1 with Normokalemia in an Infant.
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Raman, P.B.; Sharma, D.C.; Dorfman, R.I.
Studies on aldosterone biosynthesis in vitro
Biochemistry
5
1795-1804
1966
Bos taurus, Cavia porcellus, Ovis aries
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Nomoto, S.; Massa, G.; Mitani, F.; Ishimura, Y.; Miyahara, K.; Toda, K.; Nagano, I; Yamashiro, T.; Ogoshi, S.; Fukata, J.I.; Onishi, S.; Hashimoto, K.; Doi, Y.; Imura, H.; Shizuta, Y.
CMO I deficiency caused by a point mutation in exon 8 of the human CYP11B2 gene encoding steroid 18-hydroxylase (P450C18)
Biochem. Biophys. Res. Commun.
234
382-385
1997
Homo sapiens
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Sethupathi, V.; Vijayakumar, M.; Janakiraman, L.; Nammalwar, B.R.
Congenital hypoaldosteronism
Indian Pediatr.
45
695-697
2008
Homo sapiens
brenda
Neunzig, J.; Khatri, Y.; Bernhardt, R.
The impact of the clinical CYP11B2 mutation V386A strongly depends on the enzymes genetic background
Endocr. J.
64
457-461
2017
Homo sapiens (P19099)
brenda
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