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Modulation of platelet adhesion based on the surface-exposed beta-switch loop of platelet glycoprotein IB-alpha

机译:基于血小板糖蛋白IB-alpha暴露于表面的β-开关环来调节血小板粘附

摘要

The invention relates to the adhesion of platelet GpIbα to strand β3 of domain A1 of von Willebrand factor (vWF), the strand β3 comprising amino acid residues at amino acid position 560-566 and/or a functional part or equivalent thereof, the platelet GpIbα, the GpIbα region comprising an amino acid sequence corresponding to a beta-switch loop of platelet GpIbα, comprising amino acid residues at amino acid position 227-242 and/or a functional part or equivalent thereof. The invention provides a method of interfering with adhesion of blood platelets to vWF that includes modulating adhesion. The invention further provides proteinaceous compounds, antibodies, medicaments and pharmaceutical compositions to that end. The invention also provides means and methods to increase platelet adhesion by topical application of a compound increasing platelet adhesion.
机译:本发明涉及血小板GpIbα对von Willebrand因子(vWF)的结构域A1的链β3的粘附,链β3在氨基酸位置560-566和/或其功能部分或等同物包含氨基酸残基,所述血小板GpIbα ,GpIbα区域包含对应于血小板GpIbα的β-开关环的氨基酸序列,其在氨基酸位置227-242和/或其功能部分或等同物包含氨基酸残基。本发明提供了一种干扰血小板对vWF的粘附的方法,该方法包括调节粘附。为此,本发明进一步提供了蛋白质化合物,抗体,药物和药物组合物。本发明还提供了通过局部施用增加血小板粘附力的化合物来增加血小板粘附力的手段和方法。

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