No association of the-105 promoter polymorphism of the selenoprotein S encoding gene SEPS1 with cerebrovascular disease
No association of the-105 promoter polymorphism of the selenoprotein S encoding gene SEPS1 with cerebrovascular disease
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DOI：
10.1111/j.1468-1331.2007.01898.x
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发表时间：
2007-10-01
影响因子：
5.1
通讯作者：
Grond-Ginsbach, C.
中科院分区：
文献类型：
--
作者：
Hyrenbach, S.;Pezzini, A.;Grond-Ginsbach, C.
在来自意大利和德国的年轻中风患者和健康对照受试者中研究了硒蛋白S编码基因（SEPS 1）的常见促炎启动子变体。在205例自发性颈动脉夹层（CAD）导致的缺血性卒中IS患者中有56例（27.3%）发现了-105A等位基因，在295例50岁以下非CAD导致的IS患者中有69例（23.4%）发现了-105A等位基因。SEPS-105 A启动子变异在393名健康对照受试者中的87名（22.1%）和55名无IS的CAD患者中的11名（20%）中检测到。SEPS 1 - 105 A等位基因频率在疾病组和健康对照组之间无显著性差异，表明SEPS 1 - 105 A等位基因不是脑卒中的主要危险因素。
A common pro-inflammatory promoter variant of the selenoprotein S encoding gene (SEPS1) was studied in young stroke patients from Italy and Germany and in healthy control subjects. The -105A-allele was found in 56 of 205 (27.3%) patients with ischemic stroke IS because of a spontaneous cervical artery dissection (CAD), and in 69 of 295 (23.4%) patients < 50 years with IS of non-CAD origin. The SEPS -105A promoter variant was detected in 87 of 393 healthy control subjects (22.1%) and in 11 of 55 CAD patients without IS (20%). The non-significant differences of SEPS1 allele frequencies between disease groups and healthy controls suggest that the SEPS1 -105A allele is not a major-risk factor for stroke.