Inhibition of adenylyl cyclase by GTPase-deficient Gα_i is mechanistically different from that mediated by receptor-activated Gα_i.

ABSTRACT: Signal transduction through G protein-coupled receptors (GPCRs) has been a major focus in cell biology for decades. Numerous disorders are associated with GPCRs that utilize G_i proteins to inhibit adenylyl cyclase (AC) as well as regulate other effectors. Several early studies have successfully defined the AC-interacting domains of several members of Gα_i by measuring the loss of activity upon homologous replacements of putative regions of constitutive active Gα_i mutants. However, whether such findings can indeed be translated into the context of a receptor-activated Gα_i have not been rigorously verified. To address this issue, an array of known and new chimeric mutations was introduced into GTPase-deficient Q204L (QL) and R178C (RC) mutants of Gα

SUBMITTER: Chung YK 

PROVIDER: S-EPMC10996109 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature