By Alessandra Pani

This quantity is dedicated to melanoma and atherosclerosis, of crucial proliferative pathologies on the planet this day. This ebook presents an invaluable aspect of reference at the mechanisms that hyperlink ldl cholesterol esters to phone proliferation, summarizing the most recent advances either in simple technological know-how and medical research.This ebook could be of undoubted worth to biomedical scholars and academics, in addition to these actively engaged in examine on ldl cholesterol metabolism, melanoma, and atherosclerosis.

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Extra resources for Cell Growth and Cholesterol Esters

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23 These studies supported the idea that low HDL-C levels might represent a specific response to cell proliferation as a consequence of the greater utilization and storage of cholesterol esters by growing tissues. 33 Since during proliferative processes cholesterol esters accumulate in proliferating tissues, it is possible that the observed decrease in HDL may reflect a reduced release of cholesterol from proliferating cells to HDL. 6,37 Furthermore, Oram et al38 demonstrated that Apo AI-HDL binds to cell surface receptors and promotes selective removal of excess cholesterol from intracellular pool.

Gibbs JB, Graham SL, Hartman GD et al. Farnesyltransferase inhibitors versus Ras inhibitors. Curr Opin Chem Biol 1997; 1:197-203. 34. Reuther GW, Der CJ. The Ras branch of small GTPase: Ras family members don’t fall far from the tree. Curr Opin Chem Biol 2000; 12:157-165. 35. Sinensky M. Recent advances in the study of prenylated proteins. Biochim Biophys Acta 2000; 1494(2-3):93-106. 36. Fielding CJ, Fielding PE. Cholesterol and caveolae: structural and functional relationships. Biochem Biophys Acta 2000; 1529:210-222.

6,37 Furthermore, Oram et al38 demonstrated that Apo AI-HDL binds to cell surface receptors and promotes selective removal of excess cholesterol from intracellular pool. The activity of these receptors is regulated by both the availability of exogenous cholesterol and by the growth state of the cells. 40 32 Cell Growth and Cholesterol Esters Fig. 3. Cholesterol metabolism during cell proliferation. • A supply of cholesterol required by proliferating cells is achieved both endogenously (de novo synthesis) and exogenously (LDL uptake).

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