Endosomal signaling via cAMP in parathyroid hormone (PTH) type 1 receptor biology

被引:3
|
作者
Pena, Karina A. [1 ]
Savransky, Sofya [1 ,2 ]
Lewis, Breanna [1 ,3 ]
机构
[1] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Lab GPCR Biol, Pittsburgh, PA 15260 USA
[2] Univ Pittsburgh, Sch Med, Grad Program Mol Pharmacol, Pittsburgh, PA 15261 USA
[3] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA
关键词
BONE-MINERAL DENSITY; ALLOSTERIC MODULATION; POSTMENOPAUSAL WOMEN; ADENYLATE-CYCLASE; PROTEIN; PEPTIDE; BINDING; ABALOPARATIDE; RETROMER; MUTATION;
D O I
10.1016/j.mce.2023.112107
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Compartmentalization of GPCR signaling is an emerging topic that highlights the physiological relevance of spatial bias in signaling. The parathyroid hormone (PTH) type 1 receptor (PTH1R) was the first GPCR described to signal via heterotrimeric G-protein and cAMP from endosomes after beta-arrestin mediated internalization, challenging the canonical GPCR signaling model which established that signaling is terminated by receptor internalization. More than a decade later, many other GPCRs have been shown to signal from endosomes via cAMP, and recent studies have proposed that location of cAMP generation impacts physiological outcomes of GPCR signaling. Here, we review the extensive literature regarding PTH1R endosomal signaling via cAMP, the mechanisms that regulate endosomal generation of cAMP, and the implications of spatial bias in PTH1R physiological functions.
引用
收藏
页数:9
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