1.3.1.21: 7-dehydrocholesterol reductase
This is an abbreviated version!
For detailed information about 7-dehydrocholesterol reductase, go to the full flat file.
Word Map on EC 1.3.1.21
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1.3.1.21
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smith-lemli-opitz
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malformation
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cyp2r1
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anomaly
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25-hydroxyvitamin
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syndactyly
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d-related
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desmosterol
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8-dehydrocholesterol
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dhcr24
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genitalia
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oxysterols
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holoprosencephaly
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rsh
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ecdysteroids
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cholesterogenic
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medicine
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diagnostics
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25-hydroxylase
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trazodone
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aripiprazole
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ebp
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hmgcs1
- 1.3.1.21
-
smith-lemli-opitz
- malformation
- cyp2r1
- anomaly
-
25-hydroxyvitamin
-
syndactyly
-
d-related
- desmosterol
- 8-dehydrocholesterol
- dhcr24
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genitalia
- oxysterols
- holoprosencephaly
- rsh
- ecdysteroids
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cholesterogenic
- medicine
- diagnostics
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25-hydroxylase
- trazodone
- aripiprazole
- ebp
- hmgcs1
Reaction
Synonyms
3-hydroxysterol DELTA7-reductase, 3beta-hydroxysterol DELTA7-reductase, 3beta-hydroxysterol-DELTA7-reductase, 7-dehydrocholesterol DELTA7 reductase, 7-dehydrocholesterol DELTA7-reductase, 7-DHC reductase, 7-DHCR, Csa7G447780, DAF-36, DELTA5,7-sterol DELTA7-reductase, Des7, Dhcr7, Dhcr7-AS-1, Dhcr7-AS-2, Dhcr7-AS-4, Dwarf5 protein, DWF5, Neverland, Nvd, reductase, 7-dehydrocholesterol, Sterol delta-7-reductase, sterol DELTA7 reductase, sterol DELTA7-reductase
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Natural Substrates Products
Natural Substrates Products on EC 1.3.1.21 - 7-dehydrocholesterol reductase
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REACTION DIAGRAM
cholesterol + O2 + NAD(P)H + H+
cholesta-5,7-dien-3beta-ol + NAD(P)+ + 2 H2O
first committed step in biosynthesis of Caenorhabditis elegans bile acid-like steroids called dafachronic acids
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desmosterol + NADP+
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terminal step in desmosterol de novo biosynthesis, pathway and physiological role, overview
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
highly regiospecific for DELTA7-bond reduction, but wide substrate specificity
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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defect in cholesterol biosynthesis cause multiple congenital, developmental and morphogenic anomalies, e.g. the Smith-Lemli-Opitz syndrome due to a gene mutation, overview
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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defect in cholesterol biosynthesis cause multiple congenital, developmental and morphogenic anomalies, e.g. the Smith-Lemli-Opitz syndrome due to a gene mutation, overview
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol biosynthesis
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol biosynthesis
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol formation outside myelin sheath
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol biosynthesis
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol biosynthesis
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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cholesterol biosynthesis
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cholesta-5,7-dien-3-beta-ol + NADPH
cholesterol + NADP+
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reversibility of the reaction in vivo could not be proven
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cholesterol + NADP+
enzyme catalyzes the terminal step in cholesterol biosynthesis by reducing 7-dehydrocholesterol
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
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final step in cholesterol biosynthesis
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
last step in cholesterol biosynthesis
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
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terminal step in cholesterol de novo biosynthesis, pathway and physiological role, overview
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
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terminal step in cholesterol de novo biosynthesis, physiological role, overview
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
enzyme catalyzes the terminal step in cholesterol biosynthesis by reducing 7-dehydrocholesterol
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cholesta-5,7-dien-3beta-ol + NADPH
cholesterol + NADP+
enzyme catalyzes the terminal step in cholesterol biosynthesis by reducing 7-dehydrocholesterol
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cholesta-5,7-dien-3beta-ol + NADPH + H+
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ergosta-5-ene-3beta-ol + NADP+
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ergosta-5,7-diene-3beta-ol + NADPH
ergosta-5-ene-3beta-ol + NADP+
also ergosta-5,24(28)-, ergosta-5,22,24(28)-eneols and cholesta-5,24- or cholesta-5,22,24-eneols can be formed in vivo in the mutants of Saccharomyces cerevisiae
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a mutational enzyme defect causes the Smith-Lemli-Opitz syndrome, a severe developmental disorder associated with multiple congenital anomalies, with low cholesterol and high precurosor 7-hydrocholesterol contents in plasma and tissues, clinical symptoms, overview
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additional information
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over 92% reduced enzyme activity, due to autosomal recessive mutational disorder, leads to the Smith-Lemli-Opitz syndrome in multiple cell types
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additional information
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reduced enzyme activity due to mutation leads to holoprosencephaly in vivo, phenotype
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additional information
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reduced enzyme activity due to mutation leads to holoprosencephaly in vivo, phenotype
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additional information
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several enzyme mutational defects cause the Smith-Lemli-Opitz syndrome, a severe developmental disorder associated with multiple congenital malformations and mental retardation, or desmosterolosis and lathosterolosis, rare autosomal recessive disorders, defect cholesterol synthesis, clinical symptoms, overview
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additional information
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enzyme is regulated through tissue-specific transcription and differential alternative splicing
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additional information
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enzyme is regulated through tissue-specific transcription and differential alternative splicing
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additional information
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enzyme is essential for steroidogenesis, enzyme is not regulated by the luteinizing hormone LH
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additional information
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enzyme is regulated through tissue-specific transcription and differential alternative splicing, enzyme is induced when sterols are depleted both in vivo and in vitro
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additional information
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enzyme is regulated through tissue-specific transcription and differential alternative splicing, enzyme is induced when sterols are depleted both in vivo and in vitro
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