Exploring the inhibition mechanism of adenylyl cyclase type 5 by n-terminal myristoylated Gαi1.

ABSTRACT: Adenylyl cyclase (AC) is an important messenger involved in G-protein-coupled-receptor signal transduction pathways, which is a well-known target for drug development. AC is regulated by activated stimulatory (Gαs) and inhibitory (Gαi) G proteins in the cytosol. Although experimental studies have shown that these Gα subunits can stimulate or inhibit AC's function in a non-competitive way, it is not well understood what the difference is in their mode of action as both Gα subunits appear structurally very similar in a non-lipidated state. However, a significant difference between Gαs and Gαi is that while Gαs does not require any lipidation in order to stimulate AC, N-terminal myristoylation is crucial for Gαi's inhibitory function as AC is not inhibited by non-myristoylated Gαi. At present

SUBMITTER: van Keulen SC 

PROVIDER: S-EPMC5608429 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature