凝血酶激活蛋白酶激活的受体（PARS），其通过G12 / 13和GQ系列的异趾蛋白，从而连接到一系列细胞内信号传导途径。凝血酶通过切割N-末端肽来激活解析，然后与受体的主体结合以实现跨膜信号传导。通过另一个分子分子的分子间连接可以发生但比自我结扎效率较低。序列SFLLN的合成肽，当凝血酶裂解PAR1时产生的新N-末端的前六个氨基酸，可以与蛋白酶和受体裂解无关的PAR1。Pars是血小板激活的关键。已经鉴定了四个判定方法，其中1,3和4是凝血酶的基质。在人体参照图1是主要凝血酶受体，然后是PAR4，其对凝血酶不太响应。PAR 3对人类血小板反应的重要性虽然这不是鼠标的情况。PAR2在血小板中没有表达。在小鼠血小板中，GQ对于蛋白质触发形状变化的血小板分泌和聚集是必需的。 G13 appears to contribute to platelet aggregation as well as shape change in response to low concentrations of thrombin but to be unnecessary at higher agonist concentrations; G12 appears to be dispensable for thrombin signaling in platelets. G alpha (q) activates phospholipase C beta thereby triggering phosphoinositide hydrolysis, calcium mobilization and protein kinase C activation. This provides a path to calcium-regulated kinases and phosphatases, GEFs, MAP kinase cassettes and other proteins that mediate cellular responses ranging from granule secretion, integrin activation, and aggregation in platelets. Gbeta:gamma subunits can activate phosphoinositide-3 kinase and other lipid modifying enzymes, protein kinases, and channels. PAR1 activation indirectly leads to activation of cell surface 'sheddases' that liberate ligands for receptor tyrosine kinases, providing a link between thrombin and receptor tyrosine kinases involved in cell growth and differentiation. The pleiotrophic effects of PAR activation are consistent with many of thrombin's diverse actions on cells.