G protein coupled-receptor signaling and reversible lysine acetylation

Emerging data suggest that interaction with reversible protein acetylation is an important mediator of GPCR-initiated changes in transcription and other processes. Alteration of acetylation downstream of GPCR activation occurs through a variety of mechanisms, including kinase-dependent and -independent regulation of histone deacetylases (HDACs) and histone acetyltransferases (HATs). The prominence of both GPCR and acetylation in pathology and drug development efforts highlights the importance of understanding cross-talk between these two signaling mechanisms.