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Synthesis of receptors in the cell is regulated by the level of free intracellular cholesterol; if it is in excess for the needs of the cell then the transcription of the receptor gene will be inhibited. [28] LDL receptors are translated by ribosomes on the endoplasmic reticulum and are modified by the Golgi apparatus before travelling in ...
In humans, excess cholesterol in the blood is captured by low-density lipoprotein (LDL) and removed by the liver via endocytosis of the LDL receptor. [4] Recent evidence indicates that the members of the LDL receptor gene family are active in the cell signalling pathways between specialized cells in many, if not all, multicellular organisms. [5 ...
Basic amino acids important for LDL receptor binding are clustered into a surface patch on one long helix. [9] Apolipoprotein F (apoF) is one of the minor apolipoprotein in blood plasma and it is a lipid transfer inhibit protein to inhibit cholesteryl ester transfer protein-mediated transfers of cholesteryl esters and triglycerides. [10] [11]
In FH, LDL receptor function is reduced or absent, [9] and LDL circulates for an average duration of 4.5 days, resulting in significantly increased level of LDL cholesterol in the blood with normal levels of other lipoproteins. [6] In mutations of ApoB, reduced binding of LDL particles to the receptor causes the increased level of LDL cholesterol.
The uptake of LDL-C alone does not cause foam cell formation; however, the co-internalization of LDL-C with modified LDL in macrophages can result in foam cell development. Modified LDL affects the intracellular trafficking and metabolism of native LDL, such that not all LDL need to be modified for foam cell formation when LDL levels are high.
Level of the good cholesterol HDL is also increased. Fibrates may decrease LDL, though generally to a lesser degree than statins. Similar to statins, the risk of muscle damage exists. Nicotinic acid, like fibrates, is also well suited for lowering triglycerides by 20–50%. It may also lower LDL by 5–25% and increase HDL by 15–35%.
Oxidized low-density lipoprotein receptor 1 (Ox-LDL receptor 1) also known as lectin-type oxidized LDL receptor 1 (LOX-1) is a protein that in humans is encoded by the OLR1 gene. [ 5 ] [ 6 ] LOX-1 is the main receptor for oxidized LDL on endothelial cells , macrophages , smooth muscle cells , [ 7 ] and other cell types. [ 8 ]
There is a high level of conservation within the LDL receptor family. In particular, there is 50% overall sequence homology between VLDLR and ApoER2, another lipoprotein receptor of this family. [6] Comparing LDLR and VLDLR, it was found that their primary structures are 55% identical within their ligand-binding regions. The modular structures ...