Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, AZ 85259, USA.
Am J Physiol Cell Physiol. 2012 Apr 15;302(8):C1202-12. doi: 10.1152/ajpcell.00273.2011. Epub 2012 Jan 25.
The secretin receptor is a prototypic class B G protein-coupled receptor that is activated by binding of its natural peptide ligand. The signaling effects of this receptor are mediated by coupling with Gs, which activates cAMP production, and Gq, which activates intracellular calcium mobilization. We have explored the molecular basis for the coupling of each of these G proteins to this receptor using systematic site-directed mutagenesis of key residues within each of the intracellular loop regions, and studying ligand binding and secretin-stimulated cAMP and calcium responses. Mutation of a conserved histidine in the first intracellular loop (H157A and H157R) markedly reduced cell surface expression, resulting in marked reduction in cAMP and elimination of measurable calcium responses. Mutation of an arginine (R153A) in the first intracellular loop reduced calcium, but not cAMP responses. Mutation of a dibasic motif in the second intracellular loop (R231A/K232A) had no significant effects on any measured responses. Mutations in the third intracellular loop involving adjacent lysine and leucine residues (K302A/L303A) or two arginine residues separated by a leucine and an alanine (R318A/R321A) significantly reduced cAMP responses, while the latter also reduced calcium responses. Additive effects were elicited by combining the effective mutations, while combining all the effective mutations resulted in a construct that continued to bind secretin normally, but that elicited no significant cAMP or calcium responses. These data suggest that, while some receptor determinants are clearly shared, there are also distinct determinants for coupling with each of these G proteins.
缩胆囊素受体是一种典型的 B 类 G 蛋白偶联受体,其天然肽配体的结合可激活该受体。该受体的信号转导作用通过与 Gs 偶联来介导,Gs 激活 cAMP 的产生,而 Gq 则激活细胞内钙动员。我们使用系统的定点突变技术探索了每个细胞内环区域中的关键残基,研究了配体结合和缩胆囊素刺激的 cAMP 和钙反应,从而探讨了每种 G 蛋白与该受体偶联的分子基础。突变第一个细胞内环中的保守组氨酸(H157A 和 H157R)会明显降低细胞表面表达,导致 cAMP 显著减少,并消除可测量的钙反应。突变第一个细胞内环中的精氨酸(R153A)会降低钙,但不会降低 cAMP 反应。突变第二个细胞内环中的双碱性基序(R231A/K232A)对任何测量的反应均无明显影响。第三个细胞内环中的突变涉及相邻的赖氨酸和亮氨酸残基(K302A/L303A)或两个由亮氨酸和丙氨酸隔开的精氨酸残基(R318A/R321A),显著降低了 cAMP 反应,而后者也降低了钙反应。有效的突变组合会产生累加效应,而将所有有效的突变组合在一起,则会导致一种构建体继续正常结合缩胆囊素,但不会引起明显的 cAMP 或钙反应。这些数据表明,虽然一些受体决定因素显然是共享的,但与每种 G 蛋白偶联也存在明显不同的决定因素。