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APOB — LCAT

Text-mined interactions from Literome

McCall et al., Arterioscler Thromb Vasc Biol 2001 : In this study, we investigated the effects of HOCl modified LDL on the activity of lecithin-cholesterol acyltransferase ( LCAT ), an enzyme essential for high density lipoprotein maturation and the antiatherogenic reverse cholesterol transport pathway
Crook et al., Baillieres Clin Endocrinol Metab 1990 : LDL levels are controlled by the activity of B100, E receptors and, to a lesser extent, changes in LCAT activity
Subbaiah et al., J Lipid Res 1990 (Abetalipoproteinemia) : The LCAT activity of a normal d greater than 1.063 g/ml fraction also was stimulated by the normal VLDL or LDL , but there was no alteration in the species of CE formed ... These results suggest that while the VLDL and LDL are required for the maximal activity of LCAT , the species of CE formed are primarily determined by the molecular species composition of phosphatidylcholine in the plasma
Banerji et al., J Lipid Res 1989 (Abetalipoproteinemia) : In order to study the role of very low density lipoproteins ( VLDL ) and low density lipoproteins (LDL) in determining the molecular species composition of phosphatidylcholine ( PC ) and the specificity of lecithin:cholesterol acyltransferase ( LCAT ) in human plasma, we studied the PC species composition in plasma from abetalipoproteinemic (ABL) and control subjects before and after incubation at 37 degrees C
Klimov et al., Biokhimiia 1989 : The role of high density lipoproteins ( HDL ), their subfractions ( HDL2 and HDL3 ) and lecithin: cholesterol acyltransferase ( LCAT ) on peroxidative modification of low density lipoproteins (LDL) in vitro was studied
Rifai et al., Arch Pathol Lab Med 1986 (Coronary Disease) : Apolipoprotein AI activates the lecithin cholesterol acyltransferase , apolipoprotein CII and CIII regulate the lipoprotein lipase, and apolipoprotein B-100 , B-48, and E control the cholesterol uptake into hepatic and extrahepatic cells
Kodama et al., Biochim Biophys Acta 1983 (Hypolipoproteinemias...) : Although several lipoprotein abnormalities were similar to those in classical familial lecithin:cholesterol acyltransferase deficiency, remaining lecithin:cholesterol acyltransferase activity may, however, cause a lack of reduction of apolipoprotein B level, a low level of large sized LDL and also a low level of discoidal HDL
Reuter et al., ZFA 1982 (Cardiovascular Diseases...) : Incorporation of cholesterol into HDL enables cholesterol to be eliminated from the vessels and catabolized in the liver through various mechanism ( LCAT substrate, cholesterol esterification and transport, and competitive LDL inhibition )
Huang et al., Arterioscler Thromb 1993 : This demonstrated that LDL is the major source of UC to the LCAT reaction and that the transfer of UC from LDL to HDL is LCAT dependent
Liu et al., Biochim Biophys Acta 1993 : The lysolecithin acyltransferase (LAT) activity of lecithin-cholesterol acyltransferase ( LCAT ) converts lysophosphatidylcholine ( lyso PC ) to PC, and requires low-density lipoproteins (LDL)
Bielicki et al., J Lipid Res 1996 : To determine whether LCAT was directly affected by oxidized LDL , independent of crosslinking of apoA-I, we used an exogenous, [ 14C ] cholesterol labeled proteoliposome substrate to measure plasma LCAT activity