Bryant David M, Stow Jennifer L
Institute for Molecular Bioscience and School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland 4072, Australia.
Trends Cell Biol. 2004 Aug;14(8):427-34. doi: 10.1016/j.tcb.2004.07.007.
One way of controlling the activity of E-cadherin--a protein that is, simultaneously, a major cell-adhesion molecule, a powerful tumour suppressor, a determinant of cell polarity and a partner to the potent catenin signalling molecules--is to keep it on the move. During the past two decades, many insights into the fundamental role of E-cadherin in these processes have been garnered. Studies during the past five years have begun to reveal the importance of intracellular trafficking as a means of regulating the functions of E-cadherin. E-cadherin is trafficked to and from the cell surface by exocytic and multiple endocytic pathways. In this article, we survey the vesicle-trafficking machinery that is responsible for the sorting, transport, actin association and vesicle targeting of E-cadherin to regulate its movement and function during growth and development and, possibly, in cancer.
控制E-钙黏蛋白活性的一种方法是使其保持移动状态。E-钙黏蛋白是一种蛋白质,它同时也是一种主要的细胞黏附分子、一种强大的肿瘤抑制因子、细胞极性的决定因素以及强效连环蛋白信号分子的伙伴。在过去二十年里,人们对E-钙黏蛋白在这些过程中的基本作用有了许多深入了解。过去五年的研究开始揭示细胞内运输作为调节E-钙黏蛋白功能的一种方式的重要性。E-钙黏蛋白通过外排和多种内吞途径在细胞表面往返运输。在本文中,我们综述了负责E-钙黏蛋白的分选、运输、肌动蛋白结合和囊泡靶向的囊泡运输机制,以调节其在生长发育过程中以及可能在癌症中的移动和功能。