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首页> 外文期刊>Journal of thrombosis and haemostasis: JTH >Akt and mitogen-activated protein kinase enhance C-type lectin-like receptor2-mediated platelet activation by inhibition of glycogen synthase kinase 3 alpha/beta
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Akt and mitogen-activated protein kinase enhance C-type lectin-like receptor2-mediated platelet activation by inhibition of glycogen synthase kinase 3 alpha/beta

机译:Akt和丝裂原激活的蛋白激酶通过抑制糖原合酶激酶3 alpha / beta增强C型凝集素样受体2介导的血小板活化

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摘要

BackgroundThe C-type lectin-like receptor2 (CLEC-2) and the collagen receptor glycoprotein (GP)VI activate platelets through Src and Syk tyrosine kinases, and phospholipaseC2. The initial events in the two signaling cascades, however, are distinct, and there are quantitative differences in the roles of proteins downstream of Syk activation. The activation of Akt and mitogen-activated protein kinases (MAPKs) has been shown to enhance platelet activation by GPVI, but their role in CLEC-2 signaling is not known.
机译:背景C型凝集素样受体2(CLEC-2)和胶原受体糖蛋白(GP)VI通过Src和Syk酪氨酸激酶和磷脂酶C2激活血小板。但是,两个信号级联反应中的初始事件是截然不同的,并且在Syk激活下游的蛋白质作用中存在定量差异。 Akt和有丝分裂原激活的蛋白激酶(MAPKs)的激活已显示可通过GPVI增强血小板激活,但它们在CLEC-2信号传导中的作用尚不清楚。

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