02260nam 2200433z- 450 991055722200332120231214132850.0(CKB)5400000000041724(oapen)https://directory.doabooks.org/handle/20.500.12854/73699(EXLCZ)99540000000004172420202111d2020 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierG Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease RegulatorsFrontiers Media SA20201 electronic resource (182 p.)2-88963-547-3 G protein-coupled receptor kinases (GRKs) and arrestins were initially identified as a pivotal player in the process of desensitization of agonist-activated G protein-coupled receptors (GPCRs). However, growing evidence suggests GRKs and arrestins fulfill a vital role in regulating a variety of cellular proteins involved in signal transduction independently of GPCRs. Thus, GRKs and arrestins can interact with non-GPCRs. GRKs and arrestins may directly affect functioning of non-GPCRs or indirectly regulate non-GPCR signaling. In addition, emerging evidence supports that changes in function and/or expression of GRKs and arrestins may be important in cardiovascular, inflammatory, metabolic, or cancer pathologies. A better understanding of the pathological roles of GRKs and arrestins would provide a basis for new therapeutic targets in different human diseases.G Protein-Coupled Receptor Kinases Science: general issuesbicsscPharmacologybicsscGRKbeta-arrestinscardiovascularinflammationcancerScience: general issuesPharmacologyHattori Yuichiedt1302137Michel Martin CedtHattori YuichiothMichel Martin CothBOOK9910557222003321G Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease Regulators3026157UNINA