Internalization of the M2 muscarinic acetylcholine receptor proceeds through an atypical pathway in HEK293 cells that is independent of clathrin and caveolae.
Internalization of the M2 muscarinic acetylcholine receptor proceeds through an atypical pathway in HEK293 cells that is independent of clathrin and caveolae.
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发表时间：
2001-02
影响因子：
4
通讯作者：
A. G. Roseberry;M. Hosey
中科院分区：
文献类型：
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作者：
A. G. Roseberry;M. Hosey
M2毒蕈碱型乙酰胆碱受体是一种G蛋白偶联受体，其通过一种未鉴定的途径经历激动剂诱导的内化，该途径在HEK293细胞中表现出对发动蛋白功能的非典型依赖性。在这份报告中，我们利用几个独立的方法来揭示，M2毒蕈碱乙酰胆碱受体的内化不利用网格蛋白涂层的坑或小窝。然而，我们确实观察到用高渗蔗糖治疗完全抑制了M2毒蕈碱乙酰胆碱受体的内化，高渗蔗糖被广泛报道为通过网格蛋白包被的小凹特异性抑制内吞作用。因此，介导M2毒蕈碱乙酰胆碱受体内化的途径似乎是非典型的，因为它表现出对发动蛋白的不寻常的敏感性，并被高渗蔗糖抑制，但缺乏网格蛋白和小窝的参与。
The M2 muscarinic acetylcholine receptor is a G-protein coupled receptor that undergoes agonist-induced internalization through an unidentified pathway that exhibits an atypical dependence on dynamin function in HEK293 cells. In this report we utilized several independent approaches to reveal that the internalization of the M2 muscarinic acetylcholine receptor did not utilize clathrin-coated pits or caveolae. However, we did observe that treatment with hypertonic sucrose, which is widely reported to specifically inhibit endocytosis through clathrin-coated pits, completely inhibited internalization of the M2 muscarinic acetylcholine receptor. Thus, the pathway that mediates the internalization of the M2 muscarinic acetylcholine receptor appears to be atypical in that it exhibits an unusual sensitivity to dynamin and is inhibited by hypertonic sucrose but lacks the involvement of clathrin and caveolae.