Turu Gábor, Szidonya László, Gáborik Zsuzsanna, Buday László, Spät András, Clark Adrian J L, Hunyady László
Department of Physiology, Semmelweis University, Faculty of Medicine, H-1444 Budapest, P.O. Box 259, Budapest, Hungary.
FEBS Lett. 2006 Jan 9;580(1):41-5. doi: 10.1016/j.febslet.2005.11.044. Epub 2005 Dec 6.
Agonist stimulation of G protein-coupled receptors causes receptor activation, phosphorylation, beta-arrestin binding and receptor internalization. Angiotensin II (AngII) causes rapid internalization of the AT1 receptors, whereas AngII-bound AT2 receptors do not internalize. Although the activation of the rat AT1A receptor with AngII causes translocation of beta-arrestin2 to the receptor, no association of this molecule with the AT2 receptor can be detected after AngII treatment with confocal microscopy or bioluminescence resonance energy transfer. These data demonstrate that the two subtypes of angiotensin receptors have different mechanisms of regulation.
G蛋白偶联受体的激动剂刺激会导致受体激活、磷酸化、β-抑制蛋白结合以及受体内化。血管紧张素II（AngII）会导致AT1受体快速内化，而结合了AngII的AT2受体不会内化。尽管用AngII激活大鼠AT1A受体会导致β-抑制蛋白2转位至该受体，但在用共聚焦显微镜或生物发光共振能量转移技术进行AngII处理后，未检测到该分子与AT2受体有任何关联。这些数据表明，血管紧张素受体的两种亚型具有不同的调控机制。
