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ICAM-1 molecular mechanism and genome wide SNPs association studies

机译:ICAM-1分子机制与全基因组SNP的关联研究

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摘要

Macrophages transformed foam cell formation occurs as a result of leukocyte accumulation mediated through intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin, secreted by inflamed or damaged endothelium. The key molecule is the ICAM-1, member of the adhesion immunoglobulin super family that maps to chromosome 19 p13.2-p13.3 codes for 505 amino acids have five extracellular domains including circulatory leukocytes binding site (primarily monocytes) for recruiting it at the sites of inflammation and the tight adhesion with vascular endothelium for the above mentioned pathogenesis as an initial step. Hence the objective of the current paper is to review the Genome Wide Association (GWA) studies and summarizes its understanding of functional Single Nucleotide Polymorphism (SNP's) of ICAM-1 clinical association to provide better guidance for the clinicians and researchers of the merits, demerits of the current results and direct them to do research on larger number of population for better prospective.
机译:巨噬细胞转化的泡沫细胞形成是由于白细胞积累而引起的,白细胞积累是通过发炎或受损的内皮细胞分泌的细胞间粘附分子1(ICAM1),血管细胞粘附分子1(VCAM1)和E-选择素介导的。关键分子是ICAM-1,ICAM-1是粘附免疫球蛋白超家族的成员,该家族映射到19号染色体p13.2-p13.3,编码505个氨基酸,具有五个胞外域,包括循环白细胞结合位点(主要是单核细胞),可在此募集它。作为上述发病机理的第一步,是炎症的部位和与血管内皮的紧密粘附。因此,本论文的目的是回顾基因组广泛协会(GWA)的研究,并总结其对ICAM-1临床协会功能性单核苷酸多态性(SNP's)的理解,以便为临床医生和研究人员的优缺点提供更好的指导。评估当前的结果,并指导他们对更大数量的人群进行研究,以获得更好的前瞻性。

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