Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Biological Faculty, Lomonosov Moscow State University, 119234 Moscow, Russia.
Genes (Basel). 2019 Jan 23;10(2):77. doi: 10.3390/genes10020077.
Genome-wide association studies (GWASes) revealed several single-nucleotide polymorphisms (SNPs) in the human 17q12-21 locus associated with autoimmune diseases. However, follow-up studies are still needed to identify causative SNPs directly mediating autoimmune risk in the locus. We have chosen six SNPs in high linkage disequilibrium with the GWAS hits that showed the strongest evidence of causality according to association pattern and epigenetic data and assessed their functionality in a local genomic context using luciferase reporter system. We found that rs12946510, rs4795397, rs12709365, and rs8067378 influenced the reporter expression level in leukocytic cell lines. The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.
全基因组关联研究(GWAS)揭示了人类 17q12-21 位与自身免疫性疾病相关的几个单核苷酸多态性(SNP)。然而,仍需要进行后续研究以确定直接介导该位自身免疫风险的因果 SNP。我们选择了六个与 GWAS 命中高度连锁不平衡的 SNP,这些 SNP 根据关联模式和表观遗传数据显示出最强的因果关系证据,并使用荧光素酶报告系统在局部基因组背景下评估了它们的功能。我们发现 rs12946510、rs4795397、rs12709365 和 rs8067378 影响了白细胞系中的报告基因表达水平。在三种不同细胞类型中观察到的最强效应是 rs12946510,该 SNP 预测会改变 MEF2A/C 和 FOXO1 结合位点。