title: G protein coupled-receptor signaling and reversible lysine acetylation.
abstract: 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.
authors.affiliation: Department of Chemistry and Biochemistry, Rider University , New Jersey , USA.
authors.forename: Bryan D
authors.initials: BD
authors.lastname: Spiegelberg
mesh_terms: D000107:Acetylation; D019393:Arrestin / Q000378:metabolism; D004734:Energy Metabolism / Q000235:genetics*; D051548:Histone Acetyltransferases / Q000235:genetics / Q000378:metabolism*; D006655:Histone Deacetylases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D010084:Oxidation-Reduction; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics
chemical_list: D019393:Arrestin; D043562:Receptors, G-Protein-Coupled; D051548:Histone Acetyltransferases; D006655:Histone Deacetylases