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Regulation of G protein signaling by RKTG via sequestrating Gbetagamma subunit to Golgi apparatus
Yuhui Jiang, Xiaoduo Xie, Yixuan Zhang, Xiaolin Luo, Xiao Wang, Fengjuan Fan, Dawei Zheng, Zhenzhen Wang, and Yan Chen*
Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
Upon ligand binding, G protein coupled receptors (GPCRs) impart the signal to heterotrimeric G proteins composed of , and subunits, leading to dissociation of G subunit from G subunit. While the G subunit is imperative for downstream signaling, the G subunit, in its own right, mediates a variety of cellular responses such as GPCR desensitization via recruiting GRK to plasma membrane and AKT stimulation. Here we report a mode of spatial regulation of G subunit through alteration in subcellular compartmentation. RKTG (Raf Kinase Trapping to Golgi) is a newly characterized membrane protein specifically localized at the Golgi apparatus. The N-terminus of RKTG interacts with Gand tethers G to the Golgi. Overexpression of RKTG impedes the interaction of G with GRK2, abrogates the ligand-induced change of subcellular distribution of GRK2, reduces isoproterenol-stimulated phosphorylation of 2-adrenergic receptor (2AR), and alters 2AR desensitization. In addition, RKTG inhibits G- and ligand-mediated AKT that is enhanced in cells with downregulation of RKTG. Silencing of RKTG also enhances GRK2 internalization and compromises ligand-induced G translocation to the Golgi apparatus. Taken together, our results reveal that RKTG can modulate GPCR signaling through sequestering G to the Golgi apparatus and whereby attenuating the functions of G.
