Lodowski David T, Pitcher Julie A, Capel W Darrell, Lefkowitz Robert J, Tesmer John J G
Institute for Cellular and Molecular Biology, Department of Chemistry and Biochemistry, University of Texas at Austin, Austin, TX 78712, USA.
Science. 2003 May 23;300(5623):1256-62. doi: 10.1126/science.1082348.
The phosphorylation of heptahelical receptors by heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor kinases (GRKs) is a universal regulatory mechanism that leads to desensitization of G protein signaling and to the activation of alternative signaling pathways. We determined the crystallographic structure of bovine GRK2 in complex with G protein beta1gamma2 subunits. Our results show how the three domains of GRK2-the RGS (regulator of G protein signaling) homology, protein kinase, and pleckstrin homology domains-integrate their respective activities and recruit the enzyme to the cell membrane in an orientation that not only facilitates receptor phosphorylation, but also allows for the simultaneous inhibition of signaling by Galpha and Gbetagamma subunits.
异源三聚体鸟嘌呤核苷酸结合蛋白(G蛋白)偶联受体激酶(GRK)对七螺旋受体的磷酸化作用是一种普遍的调节机制,可导致G蛋白信号脱敏并激活替代信号通路。我们确定了牛GRK2与G蛋白β1γ2亚基复合物的晶体结构。我们的结果表明,GRK2的三个结构域——RGS(G蛋白信号调节剂)同源结构域、蛋白激酶结构域和普列克底物蛋白同源结构域——如何整合各自的活性,并以一种不仅有助于受体磷酸化,还能同时抑制Gα和Gβγ亚基信号传导的方向将该酶募集到细胞膜上。