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. 2017 Oct 21;174(Suppl Suppl 1):S17–S129. doi: 10.1111/bph.13878
Nomenclature GPR19 GPR20 GPR21 GPR22 GPR25 GPR26 GPR27
HGNC, UniProt GPR19, Q15760 GPR20, Q99678 GPR21, Q99679 GPR22, Q99680 GPR25, O00155 GPR26, Q8NDV2 GPR27, Q9NS67
Comments Reported to inhibit adenylyl cyclase constitutively through Gi/o [743]. GPR20 deficient mice exhibit hyperactivity characterised by increased total distance travelled in an open field test [213]. Gpr21 knockout mice were resistant to diet‐induced obesity, exhibiting an increase in glucose tolerance and insulin sensitivity, as well as a modest lean phenotype [1516]. Gene disruption results in increased severity of functional decompensation following aortic banding [10]. Identified as a susceptibility locus for osteoarthritis [520, 975, 2011]. Has been reported to activate adenylyl cyclase constitutively through Gs [923]. Gpr26 knockout mice show increased levels of anxiety and depression‐like behaviours [2209]. Knockdown of Gpr27 reduces endogenous mouse insulin promotor activity and glucose‐stimulated insulin secretion [1059].