Defective platelet activation in G alpha q deficient mice

摘要: Platelets are small disc-shaped cell fragments which undergo a rapid transformation when they encounter vascular damage. They become more spherical and extrude pseudopodia, their fibrinogen receptors activated, causing them to aggregate, release granule contents, eventually form plug is responsible for primary haemostasis. Activation of platelets also implicated in the pathogenesis unstable angina, myocardial infarction stroke. Here we show that from mice deficient α-subunit heterotrimeric guanine-nucleotide-binding protein Gq unresponsive variety physiological platelet activators. As result, G α_q-deficient have increased bleeding times protected collagen adrenaline-induced thromboembolism. We conclude α_q essential signalling processes used by different activators it cannot be replaced α_i or βγ subunits proteins. may thus new target drugs designed block activation platelets.