Properdin: binding to C3b and stabilization of the C3b-dependent C3 convertase.
Properdin: binding to C3b and stabilization of the C3b-dependent C3 convertase.
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DOI：
10.1084/jem.142.4.856
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发表时间：
1975-10-01
期刊：
影响因子：
--
通讯作者：
Austen KF
中科院分区：
文献类型：
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作者：
Fearon DT;Austen KF
P在替代补体途径中的一个作用是以剂量依赖的方式延长EAC43B上溶血位点的一级衰变。由于初始转换酶位点的数量不变，即使当激活的备解素(P)使t1/2增加10倍或更多时，P也起到稳定而不是揭示额外位点的作用。P与EAC43结合生成EAC43P的反应在15摄氏度时比0摄氏度略快一些，但达到相同的平台，不需要二价阳离子。EAC43P上P的存在不仅稳定了随后在该细胞上形成的转换酶，而且还允许转移到其他细胞上的转换酶位置，而受体中间体的稳定性取决于可用于转移的P。P与C3b结合和稳定C3b的能力与C3b失活剂对这种放大转换酶形成的抑制作用形成对比。
A function of P in the alternative complement pathway is to prolong the first order decay of the hemolytic sites on EAC43B in a dose-dependent manner. As the number of initial convertase sites is not changed, even when activated properdin (P) increases the t1/2 10-fold or more, P acts to stabilize rather than to uncover additional sites. P binds to EAC43 to generate EAC43P in a reaction that proceeds slightly more rapidly at 15 degrees C than at 0 degrees C, but reaches the same plateau and does not require divalent cations. The presence of P on EAC43P not only stabilizes the convertase subsequently formed on that cell, but, alternatively, permits transfer to convertase sites on other cells with the stability of the recipient intermediate being dependent on the P available for transfer. The capacity of P to bind to C3b and stabilize C3B contrasts with the inhibitory effect of the C3b inactivator on formation of this amplification convertase.