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肝脏所合成的凝血酶原最初为无生物活性的前体,后经γ羧化转化为有活性的形式.γ羧化酶需维生素K(V_k)作为辅助因子,亦即在蛋白氨基端特异的谷氨酸(Glu)基团经羧化形成凝血酶原的γ-羧基谷氨酸(Gla)基团.在V_k缺乏或用V_k拮抗剂时,Glu不能转化为Gla,因而肝脏释放一种无凝血活性的凝血酶原前体.这种异常凝血酶原被称为“V_k缺乏或V_k拮抗剂Ⅱ诱发的蛋白质”(protein induced by vitamin K absence or antagonist-Ⅱ)或“未羧化的凝血酶原”.作者用单克隆抗体酶标法(ELISA)测定血浆
The prothrombin synthesized by the liver is initially a non-biologically active precursor that is converted to an active form by gamma-carboxylation.γ-carboxylase requires vitamin K (V_k) as a cofactor, which is specific for the amino terminus of the protein Glutamic acid (GIu) groups are carboxylated to form the prothrombin gamma-carboxyglutamate (Gla) group.Glu can not be converted to Gla in the absence of V_k or with a V_k antagonist, and thus the liver releases a Thromboplastin precursor prothrombin. Such abnormal prothrombin is referred to as “V_k deficiency or V_k antagonist induced protein” (protein induced by vitamin K absence or antagonist-Ⅱ) or “uncarboxylated Of prothrombin. ”The authors measured plasma using monoclonal antibody enzyme-linked immunosorbent assay (ELISA)