Hong K, Kinoshita T, Miyazaki W, Izawa T, Inoue K
J Immunol. 1979 Jun;122(6):2418-23.
A monocarboxylic acid derivative (K-76 COOH) of K-76, purified from the culture filtrate of Stachybotrys complement I nov. sp. K-76, inhibits complement (C) activity. Its inhibitory action is mainly on C5 step. It strongly inhibits the generation of EAC1,4b,2a,3b,5b from C5 and EAC1,4b,2a,3b, and accelerates the decay of EAC1,4b,2a,3b,5b. It also causes some inhibition of the reactions of the reactions of C2,C3,C6,C7 and C9 with their respective preceding intermediate cells. It has no effect on the generation of EAC1,4b from C4 and EAC1, or of EAC-8 from C8 and EAC-7, and apparently increases the generation of EAC1,4b from C1 and EAC4b probably by inhibiting transfer or turnover of C1. It does not affect the rate of decay of EAC1,4b,2a or the T max of generation of EAC1,4b,2a, and it inhibits immune adherence only at high concentration. K-76 COOH also strongly inhibits hemolysis through the alternative pathway of C activation by cobra venom factor, but it does not seem to inhibit the early steps of the alternative pathway, because it has little affect on the consumption of C3 or the conversion of beta 1C to beta 1A on treatment of C serum with zymosan. K-76 COOH probably combines with C5 molecules, forming the inactive complexes, or it causes the structural alteration of C5.
从新的链格孢属K - 76菌株培养滤液中纯化得到的K - 76的单羧酸衍生物（K - 76 COOH）可抑制补体（C）活性。其抑制作用主要作用于C5步骤。它强烈抑制由C5和EAC1,4b,2a,3b生成EAC1,4b,2a,3b,5b，并加速EAC1,4b,2a,3b,5b的衰变。它还对C2、C3、C6、C7和C9与其各自先前的中间细胞的反应产生一定抑制作用。它对由C4和EAC1生成EAC1,4b或由C8和EAC - 7生成EAC - 8没有影响，并且显然通过抑制C1的转移或周转增加了由C1和EAC4b生成EAC1,4b的量。它不影响EAC1,4b,2a的衰变速率或EAC1,4b,2a生成的Tmax，并且仅在高浓度时抑制免疫黏附。K - 76 COOH还通过眼镜蛇毒因子强烈抑制补体激活的替代途径引起的溶血，但它似乎不抑制替代途径的早期步骤，因为在用酵母聚糖处理C血清时它对C3的消耗或β1C向β1A的转化影响很小。K - 76 COOH可能与C5分子结合，形成无活性复合物，或者它导致C5的结构改变。
