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Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people

BACKGROUND: MLL5, a member of the histone-lysine N-methyltransferase family, has been implicated in the control of the cell cycle progression and survival. The aim of this study was to explore the relationship between the interaction of histone-lysine N-methyltransferase MLL5 gene polymorphism and C...

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Autores principales: Yuan, Qinghua, Xie, Xiang, Fu, Zhenyan, Ma, Xiang, Yang, Yining, Huang, Ding, Liu, Fen, Dai, Chuanfang, Ma, Yitong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287819/
https://www.ncbi.nlm.nih.gov/pubmed/25606435
http://dx.doi.org/10.1016/j.mgene.2014.06.001
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author Yuan, Qinghua
Xie, Xiang
Fu, Zhenyan
Ma, Xiang
Yang, Yining
Huang, Ding
Liu, Fen
Dai, Chuanfang
Ma, Yitong
author_facet Yuan, Qinghua
Xie, Xiang
Fu, Zhenyan
Ma, Xiang
Yang, Yining
Huang, Ding
Liu, Fen
Dai, Chuanfang
Ma, Yitong
author_sort Yuan, Qinghua
collection PubMed
description BACKGROUND: MLL5, a member of the histone-lysine N-methyltransferase family, has been implicated in the control of the cell cycle progression and survival. The aim of this study was to explore the relationship between the interaction of histone-lysine N-methyltransferase MLL5 gene polymorphism and CAD in a Chinese Han population. METHODS: Using a case–control study of Chinese CAD patients (n = 565) and healthy controls (n = 694), we investigated the MLL5 gene polymorphism by the use of polymerase chain reaction fragment length polymorphism (PCR–RFLP) analysis. RESULTS: For total, the distribution of SNP1 (rs12671368) and SNP2 (rs2192932) genotypes showed a significant difference between CAD and control participants (P(1) = 0.03, P(2) = 0.02). For total the distribution of SNP1 (rs12671368) and SNP2 (rs2192932) alleles in the dominant model (GG vs. AA + AG) and the recessive model (AA vs. AG + GG) showed a significant difference between CAD and control participants (for allele: P(1) < 0.01 and P(2) = 0.05, for dominant model: P(1) > 0.05 and P(2) = 0.02, for recessive model: P(1) = 0.03 and P(2) = 0.78, respectively). For total the significant difference of the distribution of SNP1 and SNP2 in the dominant model and recessive model was retained after adjusting for covariates (for dominant model: SNP1 OR: 1.68, 95% confidence interval [CI]: 1.08–2.64, P = 0.02; SNP2 OR: 0.51, 95% CI: 0.36–0.72, P = 0.01; for recessive model: SNP1 OR: 1.84, 95% confidence interval [CI]: 1.28–2.64, P < 0.01; SNP2 OR: 0.65, 95% CI: 0.35–1.22, P = 0.18). CONCLUSIONS: The GG genotype of rs12671368 and the AA genotype of rs2192932 in the MLL5 gene could be protective genetic markers of CAD.
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spelling pubmed-42878192015-01-20 Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people Yuan, Qinghua Xie, Xiang Fu, Zhenyan Ma, Xiang Yang, Yining Huang, Ding Liu, Fen Dai, Chuanfang Ma, Yitong Meta Gene Article BACKGROUND: MLL5, a member of the histone-lysine N-methyltransferase family, has been implicated in the control of the cell cycle progression and survival. The aim of this study was to explore the relationship between the interaction of histone-lysine N-methyltransferase MLL5 gene polymorphism and CAD in a Chinese Han population. METHODS: Using a case–control study of Chinese CAD patients (n = 565) and healthy controls (n = 694), we investigated the MLL5 gene polymorphism by the use of polymerase chain reaction fragment length polymorphism (PCR–RFLP) analysis. RESULTS: For total, the distribution of SNP1 (rs12671368) and SNP2 (rs2192932) genotypes showed a significant difference between CAD and control participants (P(1) = 0.03, P(2) = 0.02). For total the distribution of SNP1 (rs12671368) and SNP2 (rs2192932) alleles in the dominant model (GG vs. AA + AG) and the recessive model (AA vs. AG + GG) showed a significant difference between CAD and control participants (for allele: P(1) < 0.01 and P(2) = 0.05, for dominant model: P(1) > 0.05 and P(2) = 0.02, for recessive model: P(1) = 0.03 and P(2) = 0.78, respectively). For total the significant difference of the distribution of SNP1 and SNP2 in the dominant model and recessive model was retained after adjusting for covariates (for dominant model: SNP1 OR: 1.68, 95% confidence interval [CI]: 1.08–2.64, P = 0.02; SNP2 OR: 0.51, 95% CI: 0.36–0.72, P = 0.01; for recessive model: SNP1 OR: 1.84, 95% confidence interval [CI]: 1.28–2.64, P < 0.01; SNP2 OR: 0.65, 95% CI: 0.35–1.22, P = 0.18). CONCLUSIONS: The GG genotype of rs12671368 and the AA genotype of rs2192932 in the MLL5 gene could be protective genetic markers of CAD. Elsevier 2014-07-31 /pmc/articles/PMC4287819/ /pubmed/25606435 http://dx.doi.org/10.1016/j.mgene.2014.06.001 Text en © 2014 The Authors http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).
spellingShingle Article
Yuan, Qinghua
Xie, Xiang
Fu, Zhenyan
Ma, Xiang
Yang, Yining
Huang, Ding
Liu, Fen
Dai, Chuanfang
Ma, Yitong
Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title_full Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title_fullStr Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title_full_unstemmed Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title_short Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people
title_sort association of the histone-lysine n-methyltransferase mll5 gene with coronary artery disease in chinese han people
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287819/
https://www.ncbi.nlm.nih.gov/pubmed/25606435
http://dx.doi.org/10.1016/j.mgene.2014.06.001
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