ATG5型
生物
DNA损伤
基因
自噬
ATG8型
遗传学
自噬相关蛋白13
DNA修复
等位基因
DNA
细胞凋亡
细胞周期
细胞周期蛋白依赖激酶2
作者
Zhihua Li,Junyi Xin,Weihong Chen,Jia Liu,Meng Zhu,Congwen Zhao,Jing Yuan,Guangfu Jin,Hongxia Ma,Jiangbo Du,Zhibin Hu,Tangchun Wu,Hongbing Shen,Juncheng Dai,Hao Yu
出处
期刊:Gene
[Elsevier]
日期:2017-08-01
卷期号:626: 414-419
标识
DOI:10.1016/j.gene.2017.05.017
摘要
Autophagy associated genes (ATGs) played an important role in the repair process of DNA damage and decreased autophagy may weaken the repair process and aggravate DNA damage. Based on this, we hypothesized that DNA damage levels might be modified by genetic variants in autophagy associated genes. In order to validate our hypothesis, 307 subjects were recruited from three different cities (Zhuhai, Wuhan and Tianjin) in China. Demographic data, individual 24-h PM2.5 exposure and peripheral blood DNA damage levels were also detected. Seven potentially functional polymorphisms in four essential autophagy associated genes (ATG5, ATG7, ATG8 and ATG13) were screened to evaluate the relationship between the polymorphisms of autophagy associated genes and DNA damage levels. This association was assessed by using multivariable linear regression model, age, sex, smoke and PM2.5 exposure levels were adjusted in each city. We found that rs12599322 in ATG8 (A > G, β = 0.263, 95% CI: 0.108–0.419, P = 8.98 × 10− 4) and rs7484002 in ATG13 (A > G, β = 0.396, 95% CI: 0.085–0.708, P = 0.013) were significantly associated with higher DNA damage levels. Furthermore, functional annotations showed that both rs12599322 and rs7484002 located at transcription factor binding sites (TFBS), indicating that they could regulate the expression of related genes through TF regulation. Following allelic trend analysis revealed that the DNA damage levels were significantly aggravated with the increasing number of risk variants in autophagy associated genes (P for trend: 8.09 × 10− 5). Our findings suggested that the polymorphisms in ATGs may influence DNA damage levels in one of the Chinese population.
科研通智能强力驱动
Strongly Powered by AbleSci AI