Aggregin: a platelet ADP receptor that mediates activation.
Aggregin: a platelet ADP receptor that mediates activation.
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聚集蛋白：介导激活的血小板 ADP 受体。
DOI：
10.1096/fasebj.4.5.2407587
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Colman,RW
中科院分区：
文献类型：
--
作者：
Colman,RW
已知ADP可诱导血小板形状改变、聚集和暴露纤维蛋白原结合部位，并抑制受刺激的腺苷环化酶。血小板的独特之处在于，它的嘌呤能受体更喜欢ADP，而不是作为竞争性拮抗剂的ATP。亲和试剂5‘-对氟磺酰基苯甲酰腺苷(FSBA)被用来共价标记单个膜蛋白聚集素，其分子质量为100 kDa。伴随着FSBA的掺入，ADP诱导的形状改变、聚集和纤维蛋白原结合被抑制。FSBA在短时间和高浓度下也是一种弱激动剂，这表明先前的非共价结合发生在共价修饰之前。Aggregin与血小板膜糖蛋白IIIa的物理和免疫化学性质不同。Aggregin不同于与腺苷环化酶偶联的受体。以FSBA为探针，血栓素A2类似物和胶原诱导的血小板聚集依赖于ADP，但不依赖于这些激动剂引起的形状变化。肾上腺素诱导的聚集需要与聚集素结合。反过来，肾上腺素增加了ADP对其受体的亲和力。浓度大于2 NM(0.2单位/毫升)的凝血酶刺激不依赖ADP的血小板聚集，但通过增加胞浆钙离子激活血小板钙蛋白酶，进而裂解聚集素。因此，聚集素除了作为与形状变化和聚集相关的ADP受体外，还在纤维蛋白原受体潜伏期中发挥作用，该潜伏期可通过ADP与聚集素的结合或聚集素的蛋白分解而完全解除。-Colman，R.W.Aggregin：A PLATET ADP Receptor介导性激活。FASE B J.4：1425-1435；1990。
ADP is known to induce platelet shape change, aggregation, and exposure of fibrinogen binding sites as well as inhibit stimulated adenylate cyclase. The platelet is unique in that its purinergic receptor prefers ADP over ATP, which functions as a competitive antagonist. The affinity reagent, 5'‐p‐fluorosulfonylbenzoyl adenosine (FSBA), has been used to covalently label a single membrane protein, aggregin, on the external platelet surface with mol wt of 100 kDa. Concomitant with incorporation of FSBA, ADP‐induced shape change, aggregation, and fibrinogen binding is inhibited. FSBA is also a weak agonist at short times and high concentration, which suggests that prior noncovalent binding to aggregin takes place before covalent modification. Aggregin differs from platelet glycoprotein IIIa in its physical and immunochemical properties. Aggregin is distinct from the receptor coupled to adenylate cyclase. Using FSBA as a probe, platelet aggregation by thromboxane A2analogs and collagen was shown to be dependent on ADP but not the shape change induced by these agonists. Binding to aggregin is required for epinephrine‐induced aggregation. In turn, epinephrine increases the affinity of ADP for its receptor. Thrombin at concentrations greater than 2 nM (0.2 units/ml) stimulates platelet aggregation independent of ADP, but by raising cytoplasmic Ca2+it activates platelet calpain, which in turn cleaves aggregin. Thus aggregin, in addition to serving as the ADP receptor linked to shape change and aggregation, plays a role in fibrinogen receptor latency that is relieved entirely by ADP binding to or proteolysis of aggregin.— Colman, R. W. Aggregin: a platelet ADP receptor mediating activation.FASEB J.4: 1425‐1435; 1990.