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- W2921819986 abstract "Platelet activation is tightly regulated by inhibitory mechanisms that limit platelet accumulation at sites of vascular injury. This chapter covers the most well-established platelet inhibitory receptors and their associated signaling pathways, including: the Gs-coupled prostacyclin (prostaglandin [PG] I2) receptor, which signals via cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA); the nitric oxide (NO) receptor soluble guanylate cyclase, which signals via cyclic GMP (cGMP) and protein kinase G (PKG); and the immunoreceptor tyrosine-based inhibition motif (ITIM)-containing receptors platelet endothelial cell adhesion molecule 1 (PECAM-1) and G6b-B, which signal via the Src Homology 2 (SH2) domain-containing tyrosine phosphatases Shp1 and Shp2. A central concept underpinning how all of these receptors function is the phosphorylation and dephosphorylation of key targets modulating platelet activation. The emphasis in this chapter is on the latter two ITIM-containing receptors, classically recognized as inhibitors of immunoreceptor tyrosine-based activation motif (ITAM)-containing receptors, but also implicated in regulating integrin and G protein-coupled receptor (GPCR) signaling. Congenital macrothrombocytopenia and myelofibrosis observed in G6b-B-deficient mice and humans is also discussed, illustrating the central role of G6b-B in regulating platelet homeostasis." @default.
- W2921819986 created "2019-03-22" @default.
- W2921819986 creator A5003349503 @default.
- W2921819986 creator A5083653940 @default.
- W2921819986 date "2019-01-01" @default.
- W2921819986 modified "2023-10-14" @default.
- W2921819986 title "Platelet Inhibitory Receptors" @default.
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