Marazzi G, Bard F, Klymkowsky M W, Rubin L L
Laboratory of Neurobiology, Rockefeller University, New York 10021.
J Cell Biol. 1989 Nov;109(5):2337-44. doi: 10.1083/jcb.109.5.2337.
We have shown previously that chick muscle cells transformed with Rous sarcoma virus are unable to form clusters of acetylcholine receptors (AChRs) (Anthony, D. T., S. M. Schuetze, and L. L. Rubin. 1984. Proc. Natl. Acad. Sci. USA. 81:2265-2269) and are missing a 37-KD tropomyosin-like protein (TM-2) (Anthony, D. T., R. J. Jacobs-Cohen, G. Marazzi, and L. L. Rubin. 1988. J. Cell Biol. 106:1713-1721). In an attempt to clarify the role of TM-2 in the formation and/or maintenance of AChR clusters, we have microinjected a monoclonal antibody specific for TM-2 (D3-16) into normal chick muscle cells in culture. D3-16 injection blocks the formation of new clusters but does not affect the preexisting ones. In addition, TM-2 is concentrated at rat neuromuscular junctions. These data suggest that TM-2 may play an important role in promoting the formation of AChR clusters.
我们先前已表明,用劳斯肉瘤病毒转化的鸡肌肉细胞无法形成乙酰胆碱受体(AChRs)簇(安东尼,D.T.,S.M.舒茨和L.L.鲁宾。1984年。美国国家科学院院刊。81:2265 - 2269),并且缺少一种37千道尔顿的原肌球蛋白样蛋白(TM - 2)(安东尼,D.T.,R.J.雅各布斯 - 科恩,G.马拉齐和L.L.鲁宾。1988年。细胞生物学杂志。106:1713 - 1721)。为了阐明TM - 2在AChR簇形成和/或维持中的作用,我们已将一种对TM - 2特异的单克隆抗体(D3 - 16)显微注射到培养的正常鸡肌肉细胞中。注射D3 - 16会阻断新簇的形成,但不影响已有的簇。此外,TM - 2集中在大鼠神经肌肉接头处。这些数据表明TM - 2可能在促进AChR簇的形成中起重要作用。