The first three control mechanisms are exerted by cholesterol itself. Cholesterol acts as a feed-back inhibitor of pre-existing HMGR as well as inducing rapid degradation of the enzyme. The latter is the result of cholesterol-induced polyubiquitination of HMGR and its degradation in the proteosome (see proteolytic degradation below). This ability of cholesterol is a consequence of the sterol sensing domain, SSD of HMGR. In addition, when cholesterol is in excess the amount of mRNA for HMGR is reduced as a result of decreased expression of the gene. The mechanism by which cholesterol (and other sterols) affect the transcription of the HMGR gene is described below under regulation of sterol content .
Camphor was a scarce and expensive natural product with a worldwide demand. [ when? ] [ according to whom? ] Haller and Blanc synthesized camphor from camphor acid; [ when? ]  however, the precursor, camphoric acid, was of unknown structure. When Finnish chemist Gustav Komppa synthesized camphoric acid from diethyl oxalate and 3,3-dimethylpentanoic acid in 1904, the structure of these precursors allowed chemists at the time to infer the complicated ring structure of camphor. Shortly thereafter, [ when? ] William Perkin published another synthesis of camphor. [ relevant? – discuss ] The work on the total chemical synthesis of camphor allowed Komppa to begin industrial production of this compound, in Tainionkoski, Finland , in 1907.
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