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Transparency declarations. Low-density lipoprotein and ritonavir: an interaction between antiretrovirals and lipids mediated by P-glycoprotein Massimo Tempestilli. Oxford Academic. Google Scholar. Federica Elisei. Eleonora Cimini. Antonio D'Avolio. Germana Grassi. Emanuele Nicastri. Pasquale Narciso.

Lipids, Lipoproteins, and Drugs | David Kritchevky | Springer

Federico Martini. Tonino Alonzi. Leopoldo Paolo Pucillo. Cite Citation. Permissions Icon Permissions. Open in new tab Download slide. Since exposure of P-gp on the plasma membrane surface could be due to either cellular redistribution or new synthesis, we measured MDR1 gene expression upon LDL stimulation at different timepoints. To investigate whether treatment with LDL can influence P-gp activity, we measured the efflux of Rho. Search ADS. Low-level viremia persists for at least 7 years in patients on suppressive antiretroviral therapy.

Lipid profiles in HIV-infected patients receiving combination antiretroviral therapy: are different antiretroviral drugs associated with different lipid profiles? Combination antiretroviral therapy and the risk of myocardial infarction. P-glycoprotein in human immunodeficiency virus type 1 infection and therapy. Inhibition of P-glycoprotein and multidrug resistance-associated proteins modulates the intracellular concentration of lopinavir in cultured CD4 T cells and primary human lymphocytes. Determination of P-glycoprotein surface expression and functional ability after in vitro treatment with darunavir or raltegravir in lymphocytes of healthy donors.

Up-regulation of caveolae and caveolar constituents in multidrug-resistant cancer cells. Interaction of the P-glycoprotein multidrug efflux pump with cholesterol: effects on ATPase activity, drug binding and transport. The multidrug transporter, P-glycoprotein, actively mediates cholesterol redistribution in the cell membrane. Cholesterol modulates P-glycoprotein activity in human peripheral blood mononuclear cells.

Transport of lipids by ABC proteins: interactions and implications for cellular toxicity, viability and function. THP-1 cells form foam cells in response to coculture with lipoproteins but not platelets. A comparison of rhodamine accumulation and efflux in cells with P-glycoprotein-mediated and MRP-associated multidrug resistance phenotypes.

Studies on the biological properties of polyene antibiotics.

Synthetic Nano-Low Density Lipoprotein As a Targeted Drug Delivery Vehicle IB-1931

Evidence for the direct interaction of filipin with cholesterol. Determination of P-gp and MRP1 expression and function in peripheral blood mononuclear cells in vivo.

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Intracellular and plasma pharmacokinetics of efavirenz in HIV-infected individuals. An HPLC-PDA method for the simultaneous quantification of the HIV integrase inhibitor raltegravir, the new nonnucleoside reverse transcriptase inhibitor etravirine, and 11 other antiretroviral agents in the plasma of HIV-infected patients.

Association of serum lipid levels with HIV serostatus, specific antiretroviral agents, and treatment regimens. In vivo emergence of HIV-1 variants resistant to multiple protease inhibitors. Modulation of cellular cholesterol alters P-glycoprotein activity in multidrug-resistant cells. Membrane fluidization by ether, other anesthetics, and certain agents abolishes P-glycoprotein ATPase activity and modulates efflux from multidrug-resistant cells.

The importance of cholesterol in maintenance of P-glycoprotein activity and its membrane perturbing influence. Authors contributing to RSC publications journal articles, books or book chapters do not need to formally request permission to reproduce material contained in this article provided that the correct acknowledgement is given with the reproduced material. If the material has been adapted instead of reproduced from the original RSC publication "Reproduced from" can be substituted with "Adapted from".

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All Journals. New Titles. Pick and Choose. Literature Updates. For Members. There are some therapies in development for treatment of lipoprotein lipase deficiency and apolipoprotein CII deficiency. In familial hypercholesterolemia, the total cholesterol level is high. People may have inherited one abnormal gene or they may have inherited two abnormal genes, one from each parent.

People who have two abnormal genes homozygotes are more severely affected than people who have only one abnormal gene heterozygotes. About 1 in people are heterozygotes, and 1 in , to 1 in 1 million people are homozygotes. Affected people may have fatty deposits xanthomas in the tendons at the heels, knees, elbows, and fingers. Rarely, xanthomas appear by age Familial hypercholesterolemia can result in rapidly progressive atherosclerosis and early death due to coronary artery disease.

Children with two abnormal genes may have a heart attack or angina by age 20, and men with one abnormal gene often develop coronary artery disease between ages 30 and Women with one abnormal gene are also at increased risk, but the risk usually starts about 10 years later than in men. People who smoke or have high blood pressure, diabetes, or obesity may develop atherosclerosis even earlier.

Treatment of familial hypercholesterolemia begins with following a diet that is low in saturated fats and cholesterol.