1.14.99.24: steroid 9alpha-monooxygenase
This is an abbreviated version!
For detailed information about steroid 9alpha-monooxygenase, go to the full flat file.
Word Map on EC 1.14.99.24
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1.14.99.24
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synthesis
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4-androstene-3,17-dione
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3-ketosteroids
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medicine
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rhodococcus
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two-component
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oxygenases
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1,4-androstadiene-3,17-dione
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flavin
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unmarked
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iron-sulfur
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erythropolis
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tuberculosis
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smegmatis
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cholesterol
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delta1-dehydrogenase
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sterol
- 1.14.99.24
- synthesis
- 4-androstene-3,17-dione
- 3-ketosteroids
- medicine
- rhodococcus
-
two-component
- oxygenases
- 1,4-androstadiene-3,17-dione
- flavin
-
unmarked
-
iron-sulfur
- erythropolis
- tuberculosis
- smegmatis
- cholesterol
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delta1-dehydrogenase
- sterol
Reaction
Synonyms
3-ketosteroid 9alpha-hydroxylase, KSH, steroid 9alpha-hydroxylase
ECTree
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General Information
General Information on EC 1.14.99.24 - steroid 9alpha-monooxygenase
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metabolism
physiological function
additional information
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3-ketosteroid 9alpha-hydroxylase is a critical pathogenicity factor of strainH37Rv involved in steroid and cholesterol catabolism
metabolism
key enzyme in steroid degradation. The two key enzymes, 3-ketosteroid DELTA1-dehydrogenase, KsdD, and 3-ketosteroid 9alpha-hydroxylase, KSH, are essential for the production and accumulation of 4-androstene-3,17-dione and 1,4-androstadiene-3,17-dione from soy bean, Glycine max
metabolism
Mycolicibacterium neoaurum NwIB-01
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key enzyme in steroid degradation. The two key enzymes, 3-ketosteroid DELTA1-dehydrogenase, KsdD, and 3-ketosteroid 9alpha-hydroxylase, KSH, are essential for the production and accumulation of 4-androstene-3,17-dione and 1,4-androstadiene-3,17-dione from soy bean, Glycine max
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metabolism
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3-ketosteroid 9alpha-hydroxylase is a critical pathogenicity factor of strainH37Rv involved in steroid and cholesterol catabolism
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genes kshA and kshB are essential factors for Mycobacterium tuberculosis pathogenesis
physiological function
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genes kshA and kshB are essential factors for Mycobacterium tuberculosis pathogenesis
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DELTAkshA and DELTAkshB deletion mutants of strain H37Rv are unable to use cholesterol and 4-androstene-3,17-dione as primary carbon and energy sources, and are also unable to metabolize the steroid substrate 5alpha-androstane-3,17-dione in contrast to the wild-type enzyme. The deletion of either of these genes leads to rapid death of the microorganism in murine infection models and in macrophages, showing that kshA and kshB are essential factors for Mycobacterium tuberculosis pathogenesis
additional information
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DELTAkshA and DELTAkshB deletion mutants of strain H37Rv are unable to use cholesterol and 4-androstene-3,17-dione as primary carbon and energy sources, and are also unable to metabolize the steroid substrate 5alpha-androstane-3,17-dione in contrast to the wild-type enzyme. The deletion of either of these genes leads to rapid death of the microorganism in murine infection models and in macrophages, showing that kshA and kshB are essential factors for Mycobacterium tuberculosis pathogenesis
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