By Simon M. Jackson, Johan Ericsson, Peter A. Edwards (auth.), Robert Bittman (eds.)
Experts examine the biochemical and biomedical facets of ldl cholesterol, addressing its metabolism in common and ailment states. They talk about a large diversity of issues, together with key steps within the ldl cholesterol biosynthetic pathway, and the position of ldl cholesterol in melanoma, atherosclerosis, and illnesses of the fearful process. The book's finished assurance additionally contains the pathological effects and strength cures for numerous sickness states, and the advance of latest anti-atherogenic drugs.
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Extra resources for Cholesterol: Its Functions and Metabolism in Biology and Medicine
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117:11-13. , 1995, Digging into caveolae, Science 269:1398-1399. , 1994, Inhibition of isoprenoid biosynthesis induces apoptosis in human promyelocytic HL-60 cells, Biochem. Biophys. Res. Commun. 199:1209-1215. Pfiffer, S. R, Dirac-Svejstrup, A. , 1995, Rab GDP dissociation inhibitor: putting Rab GTPases in the right place. 1. Bioi. 270:17057-17059. Porter, J. , and Spurgeon, S. , 1981, Biosynthesis of Isoprenoid Compounds, pp. 1-534, Wiley, New York. Rilling, H. , 1985, The mechanism of the condensation reactions of cholesterol biosynthesis, Biochem.
In summary, the transcription of a number of important genes is regulated by the nuclear localization of the mature 68-kDa SREBP. The release of this unique transcription factor from the endoplasmic reticulum is under the control of a sterol-regulated proteolytic cleavage of the precursor 125-kDa SREBP. The mechanism by which sterols regulate this cleavage event is likely to add one more interesting twist to the picture of cellular cholesterol homeostasis that has developed over the last 30 years.
Low levels of cellular sterols and farnesol would result in increased stability of HMG-CoA reductase and, hence, increased synthesis of sterols. Interestingly, a microsomal phosphatase specific for farnesyl diphosphate has recently been described (Bansal and Vaidya, 1994). It is not known if this phosphatase is also regulated by the sterol status of the cell, thus regulating the production offarnesol. Farnesol has always been considered to be a dead-end product whose fate was excretion from the cell or body.