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It has also been shown that RvD1 could accelerate the airway mucous metaplasia in the resolution of established allergic airway responses. Recently, two GPCRs of RvD1 have been identified and validated using a GPCR/arrestin-coupled system, namely, Orphan GPR32 and ALX. Extracellular signals interact with GPCRs to activate adenylate cyclase/guanylyl cyclase and stimulate formation of the second messenger cyclic adenosine monophosphate/cyclic guanosine monophosphate (cAMP/cGMP), which activates protein kinase A/protein kinase C.
In addition, research has shown, for the first time, that human platelets express the SPM receptors G-protein-coupled receptor 32 (GPR32) and ALX, and maresin 1 regulates platelet hemostatic function by enhancing platelet aggregation and spreading, while suppressing the release of proinflammatory and prothrombotic mediators, indicating maresin 1 could be a novel class of antiplatelet agents that play an important role in the resolution of inflammation in cardiovascular diseases .
RvD1 exerts its biological functions through interaction with G-protein-coupled receptor 32 (GPR32) or lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2).
Individual S23 showed evidence of deletion of all of KLK3, along with a long region upstream of KLK3 that included KLK15, KLK1, ACPT (acid phosphatase, testicular), and GPR32 (G protein-coupled receptor 32).
So far, two receptors of RvD1 have been identified: ALX and GPR32. ALX could also be the receptor of lipoxins, while GPR32 being an orphan.
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