LEADER 02260nam 2200433z- 450 001 9910557222003321 005 20231214132850.0 035 $a(CKB)5400000000041724 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/73699 035 $a(EXLCZ)995400000000041724 100 $a20202111d2020 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aG Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease Regulators 210 $cFrontiers Media SA$d2020 215 $a1 electronic resource (182 p.) 311 $a2-88963-547-3 330 $aG 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. 517 $aG Protein-Coupled Receptor Kinases 606 $aScience: general issues$2bicssc 606 $aPharmacology$2bicssc 610 $aGRK 610 $abeta-arrestins 610 $acardiovascular 610 $ainflammation 610 $acancer 615 7$aScience: general issues 615 7$aPharmacology 700 $aHattori$b Yuichi$4edt$01302137 702 $aMichel$b Martin C$4edt 702 $aHattori$b Yuichi$4oth 702 $aMichel$b Martin C$4oth 906 $aBOOK 912 $a9910557222003321 996 $aG Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease Regulators$93026157 997 $aUNINA