Patston P A, Qi M, Schifferli J A, Schapira M
Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA.
Toxicon. 1995 Jan;33(1):53-61. doi: 10.1016/0041-0101(95)93621-z.
The effect of cleavage of C1-inhibitor at Pro36 by a Crotalus atrox alpha-proteinase fraction on the properties of this serpin was studied. This truncated C1-inhibitor (des 1-36) was fully active as an inhibitor of kallikrein, beta-factor XIIa, and C1s, and modulated the functions of C1 in a normal manner. Also, the half-life of the truncated protein in the circulation of rabbits, both alone and in complex with C1, was not altered. These results show that shock-like symptoms caused by C. atrox envenomation are not attributable to a deficiency in C1-inhibitor caused by the action of the metalloproteinase in the alpha-proteinase fraction.
研究了响尾蛇α-蛋白酶组分在Pro36处切割C1抑制因子对该丝氨酸蛋白酶抑制剂特性的影响。这种截短的C1抑制因子（缺失1-36位氨基酸）作为激肽释放酶、β-因子XIIa和C1s的抑制剂具有完全活性，并以正常方式调节C1的功能。此外，截短蛋白在兔体内单独循环以及与C1形成复合物时的半衰期均未改变。这些结果表明，响尾蛇毒液中毒引起的休克样症状并非归因于α-蛋白酶组分中的金属蛋白酶作用导致的C1抑制因子缺乏。
