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The adaptor protein BIN2 was recently identified as part of the platelet activation machinery [64]. Megakaryocyte/platelet-specific deletion of BIN2 only affected hemostasis in a TxA2-dependent fashion, since tail bleeding time in these mice was only impaired in the presence of aspirin, confirming that the functional defect in (hem)ITAM-signaling can be compensated by TxA2 in vivo [64]. More importantly, the time to vessel occlusion in a mechanical injury model of the abdominal aorta was significantly prolonged in BIN2-deficient mice when compared with wild-type animals [64]. In line with this observation, lack of BIN2 resulted in highly reduced infarct volumes and decreased occluded vessels in the ipsilateral hemisphere in a tMCAO mouse model of ischemic stroke [64]. Together, these results clearly pinpoint BIN2 as an important player in arterial GPVI-dependent thrombosis and ischemic stroke with subsequent brain infarction and tissue damage. 2b1af7f3a8