Seetharam Bellur, Yammani Raghunatha R
Division of Gastroenterology and Hepatology, Department of Medicine, Medical College of Wisconsin and Clement Zablocki Veterans Medical Center, Milwaukee, WI 53295, USA.
Expert Rev Mol Med. 2003 Jun 13;5(18):1-18. doi: 10.1017/S1462399403006422.
The primary function of cobalamin (Cbl; vitamin B12) is the formation of red blood cells and the maintenance of a healthy nervous system. Before cells can utilise dietary Cbl, the vitamin must undergo cellular transport using two distinct receptor-mediated events. First, dietary Cbl bound to gastric intrinsic factor (IF) is taken up from the apical pole of ileal epithelial cells via a 460 kDa receptor, cubilin, and is transported across the cell bound to another Cbl-binding protein, transcobalamin II (TC II). Second, plasma TC II-Cbl is taken up by cells that need Cbl via the TC II receptor (TC II-R), a 62 kDa protein that is expressed as a functional dimer in cellular plasma membranes. Human Cbl deficiency can develop as a result of acquired or inherited dysfunction in either of these two transmembrane transport events. This review focuses on the biochemical, cellular and molecular aspects of IF and TC II and their cell-surface receptors.
钴胺素（Cbl；维生素B12）的主要功能是红细胞的形成和维持健康的神经系统。在细胞能够利用膳食中的Cbl之前，该维生素必须通过两个不同的受体介导事件进行细胞转运。首先，与胃内因子（IF）结合的膳食Cbl通过一种460 kDa的受体——cubilin，从回肠上皮细胞的顶端极被摄取，并与另一种Cbl结合蛋白——转钴胺素II（TC II）结合转运穿过细胞。其次，血浆中的TC II-Cbl被需要Cbl的细胞通过TC II受体（TC II-R）摄取，TC II-R是一种62 kDa的蛋白质，在细胞质膜中以功能性二聚体形式表达。人类Cbl缺乏症可能由于这两种跨膜转运事件中任何一种的获得性或遗传性功能障碍而发生。本综述重点关注IF和TC II及其细胞表面受体的生化、细胞和分子方面。
