首页> 外文期刊>Thrombosis and Haemostasis: Journal of the International Society on Thrombosis and Haemostasis >Normal filopodia extension in VASP-deficient platelets upon activation by adhesive matrices or soluble agonists.
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Normal filopodia extension in VASP-deficient platelets upon activation by adhesive matrices or soluble agonists.

机译:粘附基质或可溶性激动剂激活后,VASP缺陷型血小板中正常的丝足扩张。

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摘要

Shape change is one of the earliest visible responses after platelet activation with a soluble agonist or following contact with an adhesive substratum (1). Platelet shape change is a composite of several distinct morphological changes. Early observations reported that ADP-activated platelets undergo transformation from a smooth discoid shape, to discs extending a few short pseudopodia, and progressively to spheres with numerous long filopodial extensions (1). The same types of transformations have since been observed also in response to adhesive matrices such as von Willebrand factor (VWF) (2) and fibrinogen (3). On these matrices progressive growth of lamellipodia finally results in extensive platelet spreading. Whereas filopodia and lamellipodia are membrane protrusions driven by actin polymerisation, sphering of the platelet body has been linked to a distinct process powered by an actomyosin-driven contraction, tubulin depoly-merisation, and cortical actin cytoskeleton severing.
机译:形状变化是在使用可溶性激动剂活化血小板后或与粘附性基质接触后最早出现的可见反应之一(1)。血小板形状变化是几种不同形态变化的综合。早期的观察报道,ADP激活的血小板经历了从平滑的盘状形状转变为延伸了几个短假足的盘状,并逐渐转变为具有许多长丝状延伸的球体(1)。此后,还观察到了对粘附基质(如冯·威布兰德因子(VWF)(2)和纤维蛋白原(3))的相同类型的转化。在这些基质上,lamellipodia的进行性生长最终导致广泛的血小板扩散。丝状伪足和片状脂质体是由肌动蛋白聚合作用驱动的膜突出物,而血小板体的球化与由肌动球蛋白驱动的收缩,微管蛋白解聚和皮质肌动蛋白细胞骨架切断驱动的独特过程有关。

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