| http://purl.uniprot.org/citations/26261042 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26261042 | http://www.w3.org/2000/01/rdf-schema#comment | "Th17/IL-23 axis is an important pro-inflammatory pathway in atherosclerosis. IL-23 receptor (IL-23R) pathway has an important role in T-helper cells 17 (Th17) differentiation and survival. We compared normal subjects and patients with atherosclerosis in terms of the R381Q variant of the IL-23R gene as a functional single-nucleotide polymorphism (SNP). This case-control study recruited 200 patients who presented with cardiovascular symptoms to Afshar Hospital, Yazd, Iran. The participants were allocated to five groups based on angiographic results. The severity of the disease was determined according to the numbers of involved vessels. Patients with normal coronary arteries, minimal coronary artery involvement, one involved vessel, two involved vessels and three-vessel disease were allocated to groups I-V, respectively. DNA was extracted from whole blood samples by the salting-out method. Genotyping was performed by polymerase chain reaction followed by restriction fragment length polymorphism assay and multinomial logistic regression for analyses The presence of SNP A>G rs11209026 of IL-23 receptor gene was significantly associated with disease severity (P = 0.008). The frequencies of the heterozygous (AG) genotype in the control group and subjects with minimal involvement, and patients with one-, two-, and three-vessel disease were 22.5%, 12.5%, 10%, 10.24% and 4.8%, respectively. Our results indicated an association between the rs11209026 G>A polymorphism of the IL-23 receptor gene and the risk of atherosclerosis. This genetic variant may in fact cause protection against atherosclerosis progression. However, further studies on gene polymorphism and cell expression are required to clarify the mechanisms involved in the pathogenesis of atherosclerosis."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.org/dc/terms/identifier | "doi:10.1111/iji.12223"xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/author | "Alizadeh A."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/author | "Samadi M."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/author | "Shadman M."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/author | "Kave M."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/name | "Int J Immunogenet"xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/pages | "341-345"xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/title | "Analysis of the association between IL-23R rs11209026 polymorphism and incidence of atherosclerosis."xsd:string |
| http://purl.uniprot.org/citations/26261042 | http://purl.uniprot.org/core/volume | "42"xsd:string |
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