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This Concept Map, created with IHMC CmapTools, has information related to: Tangier Disease - final, ABCA1 protein mutation causes decreased plasma HDL level, cholesterol ester converted from cholesterol by LCAT, Tangier's Disease is expressed clincally as Autosomal Recessive trait, Apo E lack of these on VLDL prevents CETP and LPL activity, leading to inability to deliver TAG to tissues, resulting in increased plasma TAG level, LPL and hepatic lipase by removing TAGs, converts VLDL into IDL, VLDL engulfed by and accumulates in arterial macrophages, Nascent HDL through the addition of cholesterol, is converted to HDL, Autsomal CoDominant trait will have complete expression of biochemical phenotype in a Homozygous patient for ABCA1 gene mutation, enlarged tonsils in Homozygous patient for ABCA1 gene mutation, SR-B1 allows uptake of cholesterol from HDL to Liver, phospholipids together forms nascent HDL through lipidation by ABCA1 protein, schwann cells lipid accumulation leads to axonal degeneration, foam cells accumulate in and causes enlarged tonsils, Nascent HDL contains phospholipids, cholesterol can be converted to cholesterol ester, de novo cholesterol in liver source of cholesterol transported to VLDL, circulating macrophages pick up cholesterol throughout body, migrate to and deposit cholesterol in Tonsils, IDL contains Apo B-100, LDL low levels due to lack of HDL leads to cholesterol build up in other areas, causing decreased plasma cholesterol levels, HDL normally loads Apo C II and Apo E onto VLDL