摘要
在真核细胞的房间，受体 endocytosis 是调整发信号的 transduction 的一个关键事件。Adiponectin 受体属于从 G-protein-coupled 受体是不同的并且在糖尿病和新陈代谢的症候群的致病有关键角色的一个新受体家庭。这里，我们分析了 adiponectin 和 adiponectin 受体的 endocytosis 1 (AdipoR1 ) 并且发现他们两个都被使内在化进跟随类似的交通线路的 transferrin 积极的分隔空间。由表示 Eps15 异种或弄空的 K+ 堵住调停 clathrin 的 endocytosis 在血浆膜套住 AdipoR1，并且 K+ 弄空废除了 adiponectin 成为主观，显示 AdipoR1 和 adiponectin 的 endocytosis 是 clathrin 依赖的。K+ 的弄空和异种提高的 Eps15 的 overexpression 刺激 adiponectin 的激活安培的蛋白质 kinase phosphorylation，建议 AdipoR1 力量 downregulate adiponectin 发信号的 endocytosis。另外，有小 GTPase Rab5 的 AdipoR1 colocalizes，和主导的否定 Rab5 废除 AdipoR1 endocytosis。这些数据显示 AdipoR1 通过一条 clathrin 依赖、 Rab5 依赖的小径被使内在化并且 endocytosis 可以在 adiponectin 发信号的规定起一个作用。
In eukaryotic cells, receptor endocytosis is a key event regulating signaling transduction. Adiponectin receptors belong to a new receptor family that is distinct from G-protein-coupled receptors and has critical roles in the pathogenesis of diabetes and metabolic syndrome. Here, we analyzed the endocytosis of adiponectin and adiponectin receptor 1 （AdipoR1） and found that they are both internalized into transferrin-positive compartments that follow similar traffic routes. Blocking clathrin-mediated endocytosis by expressing Eps15 mutants or depleting K^＋ trapped AdipoR1 at the plasma membrane, and K^＋ depletion abolished adiponectin internalization, indicating that the endocytosis of AdipoR1 and adiponectin is clathrin-dependent. Depletion of K^＋ and overexpression of Eps15 mutants enhance adiponectin- stimulated AMP-activated protein kinase phosphorylation, suggesting that the endocytosis of AdipoR1 might down-regulate adiponectin signaling. In addition, AdipoR1 colocalizes with the small GTPase Rab5, and a dominant negative Rab5 abrogates AdipoR1 endocytosis. These data indicate that AdipoR1 is internalized through a clathrin- and Rab5- dependent pathway and that endocytosis may play a role in the regulation of adiponectin signaling.
