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This Concept Map, created with IHMC CmapTools, has information related to: Tangier edited by EE, HDL normally loads Apo C II and Apo E onto VLDL, plasma cholesterol levels decreased levels seen in Heterozygous patient for ABCA1 mutation, Apo C II lack of these on VLDL prevents CETP and LPL activity, leading to inability to deliver TAG to tissues, resulting in increased plasma TAG level, SR-B1 allows uptake of cholesterol from HDL to Liver, arterial macrophages accumulation of cholesterol which was contained in oxidized LDL/VLDL causes transformation to foam cells, plasma HDL level decreases from faliure to assemble functional HDL particles, which leads to rapid renal filtration and catabolism of Apo A1, cholesterol transferred from HDL to LDL, VLDL requires for CETP exchange, LPL activity Apo C II, LDL is converted to oxidized LDL, Tangier's Disease is expressed biochemically as Autsomal CoDominant trait, LDL low levels due to lack of HDL leads to cholesterol build up in other areas, causing decreased plasma cholesterol levels, LCAT converts cholesterol to cholesterol ester in HDL, tunica intima formation of plaque leads to greater risk of Coronary Artery Disease compared to homozygotes, TAG loss of TAG from VLDL mediated by CETP, Nascent HDL contains Apo E, LPL and hepatic lipase by removing TAGs, converts VLDL into IDL, Homozygous patient for ABCA1 mutation has mutation in both alleles for ABCA1 gene, plasma TAG level accumulates in schwann cells, cholesterol transferred from HDL to VLDL, oxidized LDL engulfed by and accumulates in arterial macrophages