ArticleMeta gene2014
Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people.
Article in Meta gene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Association of MLL3 and TGF-β signaling gene polymorphisms with the susceptibility and prognostic outcomes of Stanford type B aortic dissection : MLL3 with TGF-β signal pathway association with Stanford type B AD.BMC cardiovascular disorders · 2023Article
- Case Report: A NovelFrontiers in pediatrics · 2022Article
- Cell‑specific histone modifications in atherosclerosis (Review).Molecular medicine reports · 2018Review
- MLL5 (KMT2E): structure, function, and clinical relevance.Cellular and molecular life sciences : CMLS · 2017Review
- TT genotype of rs2941484 in the human HNF4G gene is associated with hyperuricemia in Chinese Han men.Oncotarget · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMLL5, 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.
methodsUsing 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.
resultsFor total, the distribution of SNP1 (rs12671368) and SNP2 (rs2192932) genotypes showed a significant difference between CAD and control participants (P1 = 0.03, P2 = 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: P1 < 0.01 and P2 = 0.05, for dominant model: P1 > 0.05 and P2 = 0.02, for recessive model: P1 = 0.03 and P2 = 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).
conclusionsThe 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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