Research around β2-glycoprotein I:: A major target for antiphospholipid antibodies
Research around β2-glycoprotein I:: A major target for antiphospholipid antibodies
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DOI：
10.1080/08916930500124312
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发表时间：
2005-08-01
期刊：
影响因子：
3.5
通讯作者：
Koike, T
中科院分区：
文献类型：
--
作者：
Atsumi, T;Amengual, O;Koike, T
beta 2-糖蛋白 I (beta 2GPI) 是一种磷脂结合蛋白，是抗磷脂综合征 (APS) 患者中发现的抗磷脂抗体 (aPL) 的主要靶抗原之一。 APS 患者的血栓形成性疾病与 aPL 密切相关，其致病特性取决于 β2GPI 的存在。 aPL 通过 β2GPI 刺激促凝血细胞是 APS 中最可能的血栓形成机制之一，p38 丝裂原激活蛋白激酶 (MAPK) 途径在这种激活中发挥着至关重要的作用。 β 2GPI 在结构域 V 中被激活的 X 因子或纤溶酶进行蛋白水解切割，导致产生切口形式的 β 2GPI。最近，越来越多的注意力集中在 nicked-beta 2GPI 作为外源性纤溶途径调节剂的作用上。
beta 2-Glycoprotein I (beta 2GPI), a phospholipid-binding protein, is one of the major target antigens for antiphospholipid antibodies (aPL) found in patients with antiphospholipid syndrome (APS). Thrombophilic disorders in APS patients are strongly associated with aPL, and their pathogenic properties depend on the presence of beta 2GPI. Procoagulant cell stimulation by aPL, via beta 2GPI, is one of the most plausible mechanisms of thrombosis in APS, and p38 mitogen activated protein kinase (MAPK) pathway plays a crucial role in such activation. beta 2GPI is proteolytically cleaved in domain V by activated factor X or plasmin, leading to the generation of the nicked form of beta 2GPI. Recently, increasing attention is focused on the role of nicked-beta 2GPI as a regulator of extrinsic fibrinolysis pathway.