Abstract
Investigation of the post-PKS biosynthetic steps to the cholesterol-lowering agent lovastatin (1) using an Aspergillus terreus strain with a disrupted lovC gene, which is essential for formation of 4a,5-dihydromonacolin L (3), shows that 7 and 3 are precursors to 1, and demonstrates that lovastatin diketide synthase (lovF protein) does not require lovC.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Anticholesteremic Agents / metabolism
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Aspergillus / enzymology*
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Aspergillus / genetics
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Aspergillus / metabolism
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Fungal Proteins*
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Hydroxymethylglutaryl-CoA Reductase Inhibitors / metabolism
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Lovastatin / analogs & derivatives*
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Lovastatin / biosynthesis*
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Multienzyme Complexes / genetics*
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Multienzyme Complexes / metabolism
Substances
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Anticholesteremic Agents
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Fungal Proteins
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Multienzyme Complexes
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lovC protein, Aspergillus terreus
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mevastatin
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Lovastatin