作者: Longyan Yang , Junfang Zheng , Ying Xiong , Ran Meng , Qian Ma
DOI: 10.1007/S00726-015-1965-6
关键词:
摘要: The beta-2 adrenergic receptor (β2AR), a member of GPCR, can activate multiple signaling pathways and is an important treatment target for cardiac failure. However, the molecular mechanism about β2AR regulation not fully understood. In this study, we found that cystic fibrosis transmembrane conductance regulator-associated ligand (CAL) overexpression reduced β2AR-mediated extracellular signal-regulated kinase-1/2 (ERK1/2) activation. Further study identified CAL as novel binding partner β2AR. associated with mainly via third intracellular loop (ICL3) coiled-coil domains CAL, which distinct from CAL/β1AR interaction mediated by carboxyl terminal (CT) β1AR PDZ domain CAL. retarded expression in Golgi apparatus plasma membrane.