Nicholson-Weller A, Wang C E
Charles A. Dana Research Institute, Harvard-Thorndike Laboratories, Boston, MA.
J Lab Clin Med. 1994 Apr;123(4):485-91.
Studies of decay-accelerating factor (DAF) function and structure are reviewed. DAF was first recognized as a species restricting factor operating at the level of C3/C5 activation. Cloning of the gene indicates that DAF has four short consensus repeats of the type characteristic of the regulators of complement activation gene cluster family. The third short consensus repeat is responsible for DAF's complement regulatory activity and signaling. DAF, like other glycophosphatidylinositol (GPI) anchored proteins, is associated with tyrosine kinases, and these kinases are probably the signaling devices. The details of how DAF's GPI anchor in the outer leaflet of plasma membrane connects with the tyrosine kinases on the inner leaflet are not known. Although DAF does not have an essential role in controlling hemolysis of erythrocytes, it does have important role in regulating the deposition of C3 on nucleated cells. The therapeutic potential of DAF is discussed.
本文综述了衰变加速因子（DAF）的功能和结构研究。DAF最初被认为是一种在C3/C5激活水平起作用的种属限制因子。该基因的克隆表明，DAF具有补体激活调节基因簇家族特征类型的四个短共有重复序列。第三个短共有重复序列负责DAF的补体调节活性和信号传导。与其他糖基磷脂酰肌醇（GPI）锚定蛋白一样，DAF与酪氨酸激酶相关，这些激酶可能是信号传导装置。目前尚不清楚质膜外小叶中的DAF的GPI锚如何与内小叶上的酪氨酸激酶相连。虽然DAF在控制红细胞溶血方面没有至关重要的作用，但它在调节有核细胞上C3的沉积方面具有重要作用。本文还讨论了DAF的治疗潜力。
