The binding of animal low-density lipoproteins to human apolipoprotein(a).
The binding of animal low-density lipoproteins to human apolipoprotein(a).
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动物低密度脂蛋白与人载脂蛋白（a）的结合。
DOI：
10.1042/bj3090899
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
McConathy,WJ
中科院分区：
文献类型：
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作者：
Trieu,VN;McConathy,WJ
脂蛋白(a) [Lp(a)]是冠心病的危险因素。它由脂质和载脂蛋白(a) [apo(a)]组成，通过载脂蛋白(a) kringle 36的Cys-4057和apoB的Cys-3734之间的二硫键连接到载脂蛋白B （apoB）。我们称之为共价apo(a): apoB-Lp相互作用，以区别于非共价apo(a)/Lp(a): apoB-Lp相互作用，后者可能是由apo(a)的kringle 33和apoB的3304-3317残基介导的。非共价相互作用可能是在共价连锁和Lp(a)形成之前将载脂蛋白(a)和载脂蛋白ob结合在一起的初始相互作用。apoB上的非共价apo(a)/Lp(a)结合位点在进化上比apoB上的共价apo(a)结合位点更古老。人类和非人类低密度脂蛋白（ldl）与人类载脂蛋白(a)/脂蛋白(a)非共价结合；然而，只有兔和人ldl与人载脂蛋白(a)共价结合。小鼠LDL与人载脂蛋白(a)/脂蛋白(a)之间的非共价相互作用的Kd为（1.7 +/- 1.33）× 10(-7) M （n = 3）。这解释了人类载脂蛋白(a)和小鼠载脂蛋白ob在人类载脂蛋白(a)转基因小鼠的动脉粥样硬化病变中的共定位，并支持了我们的假设，即非共价相互作用是导致载脂蛋白(a)动脉粥样硬化的一个因素。
Lipoprotein(a) [Lp(a)] is a risk factor for coronary artery disease. It is composed of lipids and apolipoprotein(a) [apo(a)] linked to apolipoprotein B (apoB) by a disulphide bond between Cys-4057 of apo(a)'s kringle 36 and possibly Cys-3734 of apoB. We call this the covalent apo(a): apoB-Lp interaction, to distinguish it from the non-covalent apo(a)/Lp(a): apoB-Lp interaction, which is probably mediated by apo(a)'s kringle 33 and residues 3304-3317 of apoB. The non-covalent interaction could be the initial interaction which brings apo(a) and apoB together prior to covalent linkage and Lp(a) formation. The non-covalent apo(a)/Lp(a)-binding site on apoB is evolutionarily more ancient than the covalent apo(a)-binding site on apoB. Both human and non-human low-density lipoproteins (LDLs) bind non-covalently to human apo(a)/Lp(a); however, only rabbit and human LDLs bind covalently to human apo(a). The non-covalent interaction between mouse LDL and human apo(a)/Lp(a) has a Kd of (1.7 +/- 1.33) x 10(-7) M (n = 3). This explains the co-localization of human apo(a) and mouse apoB in the atherosclerotic lesions of human apo(a) transgenic mice and supports our hypothesis that the non-covalent interaction is a contributing factor to apo(a) atherogenicity.