Sanes J R, Apel E D, Burgess R W, Emerson R B, Feng G, Gautam M, Glass D, Grady R M, Krejci E, Lichtman J W, Lu J T, Massoulié J, Miner J H, Moscoso L M, Nguyen Q, Nichol M, Noakes P G, Patton B L, Son Y J, Yancopoulos G D, Zhou H
Department of Anatomy, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Physiol Paris. 1998 Jun-Aug;92(3-4):167-72. doi: 10.1016/s0928-4257(98)80004-1.
Formation of the skeletal neuromuscular junction is a multi-step process that requires communication between the nerve and muscle. Studies in many laboratories have led to identification of factors that seem likely to mediate these interactions. 'Knock-out' mice have now been generated with mutations in several genes that encode candidate transsynaptic messengers and components of their effector mechanisms. Using these mice, it is possible to test hypotheses about the control of synaptogenesis. Here, we review our studies on neuromuscular development in mutant mice lacking agrin alpha CGRP, rapsyn, MuSK, dystrophin, dystrobrevin, utrophin, laminin alpha 5, laminin beta 2, collagen alpha 3 (IV), the acetylcholine receptor epsilon subunit, the collagenous tail of acetylcholinesterase, fibroblast growth factor-5, the neural cell adhesion molecule, and tenascin-C.
骨骼神经肌肉接头的形成是一个多步骤过程,需要神经和肌肉之间进行通讯。许多实验室的研究已鉴定出似乎可能介导这些相互作用的因子。现已培育出几种基因发生突变的“基因敲除”小鼠,这些基因编码候选跨突触信使及其效应机制的组成部分。利用这些小鼠,可以检验关于突触发生控制的假说。在此,我们综述了对缺乏聚集蛋白α、降钙素基因相关肽、rapsyn、肌肉特异性激酶、抗肌萎缩蛋白、肌萎缩蛋白结合蛋白、类肌萎缩蛋白、层粘连蛋白α5、层粘连蛋白β2、胶原蛋白α3(IV)、乙酰胆碱受体ε亚基、乙酰胆碱酯酶的胶原尾部、成纤维细胞生长因子-5、神经细胞黏附分子和肌腱蛋白-C的突变小鼠神经肌肉发育的研究。