Millar D S, Wacey A I, Ribando J, Melissari E, Laursen B, Woods P, Kakkar V V, Cooper D N
Charter Molecular Genetics Laboratory, Thrombosis Resarch Institute, London, UK.
Hum Genet. 1994 Nov;94(5):509-12. doi: 10.1007/BF00211016.
The polymerase chain reaction and direct sequencing were used to determine the nature of the mutations in the antithrombin III (AT3) gene in seven unrelated patients with familial antithrombin III (ATIII) deficiency and recurrent venous thrombosis. Three novel mutations were found, two associated with a type I deficiency state (Pro80-->Thr and His120-->Tyr) manifesting reduced synthesis of ATIII. The other novel lesion (Met251-->Ile) was associated with a dysfunctional ATIII protein (type II ATIII deficiency) and is predicted to interfere either with a heparin-induced conformational change in the ATIII molecule or with docking to thrombin. A novel polymorphism (Tyr158-->Cys) was also found to occur in several individuals of Scandinavian origin.
采用聚合酶链反应和直接测序法,对7例无亲缘关系的家族性抗凝血酶III(AT3)缺乏症且反复发生静脉血栓形成的患者,检测抗凝血酶III(ATIII)基因中的突变性质。发现了3个新突变,其中2个与I型缺乏状态相关(Pro80→Thr和His120→Tyr),表现为ATIII合成减少。另一个新病变(Met251→Ile)与功能失调的ATIII蛋白相关(II型ATIII缺乏症),预计会干扰肝素诱导的ATIII分子构象变化或与凝血酶的结合。还发现一种新的多态性(Tyr158→Cys)出现在几个斯堪的纳维亚血统的个体中。