Figure 3 Potential mechanisms of PAR activation by thrombin and aPC

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Figure 3 Potential mechanisms of PAR activation by thrombin and aPC Figure 3 | Potential mechanisms of PAR activation by thrombin and aPC. An example scheme of protease activated receptors (PARs) and the N-terminal sequences of human PAR1 and PAR3 depicting distinct cleavage sites for thrombin and activated protein C (aPC; arrows). The qualitatively distinct signalling mechanisms of thrombin and aPC can be attributed to the distinct proteolytic activation mechanisms of the G protein-coupled receptor (GPCR) N-terminus, resulting in protease-specific tethered ligands (shown in red for thrombin and blue for aPC) or induction of distinct protease-specific signalling complexes. PAR3 is not considered to be signalling competent and the function of the tethered ligands remains incompletely resolved. Activation of PARs might elicit protease-specific classical GPCR signalling by activation of individual PAR receptors (that is protomers) or ligand-specific PAR–PAR heterodimers. In addition, coagulation-protease-dependent signalling might engage non-PAR receptors, enabling biased signalling and thus leading to signalling diversity. Other proteases can cleave PARs at different sites, for example matrix metalloproteinase-1 cleaves PAR1 at Asp39 and neutrophil elastase cleaves PAR-1 at Leu45. Kerlin, B. A. & Isermann, B. et al. (2015) The emerging role of coagulation proteases in kidney disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.177