Hwang J I, Heo K, Shin K J, Kim E, Yun C, Ryu S H, Shin H S, Suh P G
Department of Life Science, National Creative Research Initiative Center for Calcium and Learning, Division of Molecular and Life Science and School of Environmental Engineering, Pohang University of Science and Technology, Pohang 790-784, South Korea.
J Biol Chem. 2000 Jun 2;275(22):16632-7. doi: 10.1074/jbc.M001410200.
Among the phospholipase C that catalyzes the hydrolysis of phosphatidylinositol 4,5-bisphosphate, four mammalian phospholipase C-beta (PLC-beta) isotypes (isotypes 1-4) are activated through G protein-coupled receptors (GPCRs). Although the regulation of the PLC-betas by GPCRs and heterotrimeric G proteins has been extensively studied, little is known about the molecular determinants that regulate their activity. The PLC-beta isozymes carry a putative PSD-95/Dlg/ZO-1 (PDZ) binding motif (X(S/T)X(V/L)COOH) at their carboxyl terminus, which is implicated in specific interactions with anchor proteins. Using the yeast two-hybrid system, we identified Na(+)/H(+) exchanger regulatory factor 2 (NHERF2) as a protein that interacted with a C-terminal heptapeptide of PLC-beta3. Immunoprecipitation studies revealed that NHERF2 interacts specifically with PLC-beta3, but not with other PLC-beta isotypes. Furthermore, PLC-beta3 interacted with NHERF2 rather than with other PDZ-containing proteins. This interaction required the COOH-terminal NTQL sequence of PLC-beta3 and the second PDZ domain of NHERF2. Interestingly, NHERF2 potentiated the PLC-beta activation by carbachol in COS7 and HeLa cells, while mutant NHERF2, lacking the second PDZ domain, had no such effect. Taken together, the data suggest that NHERF2 may act as a modulator underlying the process of PLC-beta3-mediated signaling.
在催化磷脂酰肌醇4,5 - 二磷酸水解的磷脂酶C中,四种哺乳动物磷脂酶C - β(PLC - β)亚型(亚型1 - 4)通过G蛋白偶联受体(GPCR)被激活。尽管GPCR和异源三聚体G蛋白对PLC - β的调节已得到广泛研究,但关于调节其活性的分子决定因素却知之甚少。PLC - β同工酶在其羧基末端带有一个假定的PSD - 95/Dlg/ZO - 1(PDZ)结合基序(X(S/T)X(V/L)COOH),这与与锚定蛋白的特异性相互作用有关。利用酵母双杂交系统,我们鉴定出钠/氢交换调节因子2(NHERF2)是一种与PLC - β3的C末端七肽相互作用的蛋白质。免疫沉淀研究表明,NHERF2与PLC - β3特异性相互作用,但不与其他PLC - β亚型相互作用。此外,PLC - β3与NHERF2相互作用,而不是与其他含PDZ的蛋白质相互作用。这种相互作用需要PLC - β3的COOH末端NTQL序列和NHERF2的第二个PDZ结构域。有趣的是,NHERF2增强了卡巴胆碱在COS7和HeLa细胞中对PLC - β的激活作用,而缺乏第二个PDZ结构域的突变型NHERF2则没有这种作用。综上所述,数据表明NHERF2可能作为PLC - β3介导的信号传导过程的一种调节因子发挥作用。