Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
Trends Cardiovasc Med. 1994 Sep-Oct;4(5):231-5. doi: 10.1016/1050-1738(94)90039-6.
Apolipoprotein B (apo B) circulates in two distinct isomorphic forms, each the product of a single gene. The larger form, referred to as apo B-100, is the major protein of plasma low-density lipoproteins (LDLs) and is synthesized by the human liver. The smaller form, referred to as apo B-48, is produced in the small intestine as a result of a site-specific cytidine deamination, which alters a CAA codon, encoding glutamine in the unedited (apo B-100) mRNA to UAA, which specifies an in-frame stop codon. Apo B-48 lacks the domains involved in LDL receptor interaction and in complex formation with apolipoprotein(a). DNA sequence analysis of the gene that mediates this site-specific cytidine deamination suggests that apo B mRNA editing is an evolutionary adaptation to limit the atherogenic potential of intestinal lipoproteins.
载脂蛋白 B（apo B）以两种不同的同型异构体循环，每种异构体都是单个基因的产物。较大的形式，称为 apo B-100，是血浆低密度脂蛋白（LDL）的主要蛋白质，由人类肝脏合成。较小的形式，称为 apo B-48，是在小肠中产生的，由于特定的胞嘧啶脱氨酶，改变了一个 CAA 密码子，该密码子在未经编辑的（apo B-100）mRNA 中编码谷氨酰胺，变成 UAA，指定一个框架内的终止密码子。apo B-48 缺乏与 LDL 受体相互作用和与载脂蛋白(a)形成复合物的域。介导这种特定胞嘧啶脱氨酶的基因的 DNA 序列分析表明，apo B mRNA 编辑是一种进化适应，旨在限制肠脂蛋白的动脉粥样硬化潜力。
