TAILIEUCHUNG - A RECEPTOR-MEDIATED PATHWAY FOR CHOLESTEROL HOMEOSTASIS

Some countries wish to control the wildlife trade at the national as well as the international level, and impose domestic measures. This provides a secondary level of control if medicines and raw materials have entered a country evading import controls. The following gives examples of some countries that have imposed national laws and regulations to control domestic trade in addition to the implementation of CITES. In May 1993, in response to international conservation concern about the threat to rhinoceroses and tigers posed by the commercial trade, the State Council of the People’s Republic of China issued a ban on trade in rhinoceros horn, tiger bone and their. | A RECEPTOR-MEDIATED PATHWAY FOR CHOLESTEROL HOMEOSTASIS Nobel lecture 9 December 1985 by MICHAEL S. BROWN AND JOSEPH L. GOLDSTEIN Department of Molecular Genetics University of Texas Health Science Center Southwestern Medical School 5323 Harry Hines Blvd. Dallas Texas . In 1901 a physician Archibald Garrod observed a patient with black urine. He used this simple observation to demonstrate that a single mutant gene can produce a discrete block in a biochemical pathway which he called an inborn error of metabolism . Garrod s brilliant insight anticipated by 40 years the one gene-one enzyme concept of Beadle and Tatum. In similar fashion the chemist Linus Pauling and the biochemist Vernon Ingram through study of patients with sickle cell anemia showed that mutant genes alter the amino acid sequences of proteins. Clearly many fundamental advances in biology were spawned by perceptive studies of human genetic diseases 1 . We began our work in 1972 in an attempt to understand a human genetic disease familial hypercholesterolemia or FH. In these patients the concentration of cholesterol in blood is elevated many fold above normal and heart attacks occur early in life. We postulated that this dominantly inherited disease results from a failure of end-product repression of cholesterol synthesis. The possibility fascinated us because genetic defects in feedback regulation had not been observed previously in humans or animals and we hoped that study of this disease might throw light on fundamental regulatory mechanisms. Our approach was to apply the techniques of cell culture to unravel the postulated regulatory defect in FH. These studies led to the discovery of a cell surface receptor for a plasma cholesterol transport protein called low density lipoprotein LDL and to the elucidation of the mechanism by which this receptor mediates feedback control of cholesterol synthesis 2 3 . FH was shown to be caused by inherited defects in the gene encoding the LDL receptor which

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