RETRACTED: A novel polymorphism of the GP78 gene is associated with coronary artery disease in Han population in China (Retracted article. See vol. 14, 78, 2015)

被引:4
作者
Cha, Erdenbat [1 ]
Fu, Zhen-Yan [1 ]
Ma, Yi-Tong [1 ]
Zhu, Qing [1 ]
Xie, Xiang [1 ]
Liu, Fen [2 ]
机构
[1] Xinjiang Med Univ, Affiliated Hosp 1, Dept Cardiol, Urumqi 830054, Xinjiang, Peoples R China
[2] Xinjiang Key Lab Cardiovasc Dis Res, Urumqi 830054, Xinjiang, Peoples R China
基金
中国国家自然科学基金;
关键词
gp78; Single nucleotide polymorphism; Coronary artery disease; Case-control study; Haplotype; HMG-COA REDUCTASE; STEROL-REGULATED UBIQUITINATION; AUTOCRINE MOTILITY FACTOR; HEART-DISEASE; CHOLESTEROL-SYNTHESIS; RISK-FACTORS; DEGRADATION; INSIG-1; PROTEIN; SREBP;
D O I
10.1186/1476-511X-13-147
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: GP78 is a membrane-anchored ubiquitin ligase mediating the degradation of 3-hydroxy-3-methyl-glutaryl-CoA coenzyme A reductase (HMGCR) and Insig-1, which was very essential for the synthesis of cholesterol process. Cholesterol levels have a causal role in the development of cardiovascular disease. The aim of the present study was to assess the association between the human gp78 gene polymorphism and coronary artery disease (CAD) in a Han and Uygur population of China. Methods: We used two independent case-control studies: a Han population (602 CAD patients and 572control subjects) and a Uygur population (374 CAD patients and 376control subjects). All CAD patients and controls were genotyped for the same three single nucleotide polymorphisms (SNPs) (rs731119, rs2617849and rs2440472) of gp78 gene by a Real-time PCR instrument. Results: In the Han population, for total and men, the distribution of SNP3 (rs2440472) alleles and the dominant model (AA vs AG + GG) and recessive model (GG vs AG + AA) showed a significant difference between CAD and control participants (for allele: P = 0.003 and P = 0.002, respectively; for dominant model: P = 0.041 and P = 0.026, respectively; for recessive model: p = 0.004 and p = 0.004, respectively). The significant difference in both the two models was retained after adjustment for covariates (for dominant model OR:0.760, 95% confidence interval [CI]:0.584-0.99, P = 0.042; OR:0.686, 95% CI: 0.498-0.946, P = 0.022, respectively; for recessive model OR: 1.451, 95% CI: 1.067-1.974, P = 0.018; OR: 1.789, 95% CI: 1.219-2.627, P = 0.000). Our data was also assessed via haplotype-based case-control studies. For the Han population, for total, The G-T-G haplotype in CAD was significantly higher than that in the control group (P = 0.02), and the G-C-A haplotype in CAD was significantly lower than that in the control group (P = 0.0443), And for man, the G-T-G haplotype in CAD was significantly higher than that in the control group (P = 0.0048). Conclusions: The GG genotype and G allele of rs2440472 in gp78 gene could be a risk genetic marker of CAD in Han population in China.
引用
收藏
页数:11
相关论文
共 29 条
[1]   A map of human genome variation from population-scale sequencing [J].
Altshuler, David ;
Durbin, Richard M. ;
Abecasis, Goncalo R. ;
Bentley, David R. ;
Chakravarti, Aravinda ;
Clark, Andrew G. ;
Collins, Francis S. ;
De la Vega, Francisco M. ;
Donnelly, Peter ;
Egholm, Michael ;
Flicek, Paul ;
Gabriel, Stacey B. ;
Gibbs, Richard A. ;
Knoppers, Bartha M. ;
Lander, Eric S. ;
Lehrach, Hans ;
Mardis, Elaine R. ;
McVean, Gil A. ;
Nickerson, DebbieA. ;
Peltonen, Leena ;
Schafer, Alan J. ;
Sherry, Stephen T. ;
Wang, Jun ;
Wilson, Richard K. ;
Gibbs, Richard A. ;
Deiros, David ;
Metzker, Mike ;
Muzny, Donna ;
Reid, Jeff ;
Wheeler, David ;
Wang, Jun ;
Li, Jingxiang ;
Jian, Min ;
Li, Guoqing ;
Li, Ruiqiang ;
Liang, Huiqing ;
Tian, Geng ;
Wang, Bo ;
Wang, Jian ;
Wang, Wei ;
Yang, Huanming ;
Zhang, Xiuqing ;
Zheng, Huisong ;
Lander, Eric S. ;
Altshuler, David L. ;
Ambrogio, Lauren ;
Bloom, Toby ;
Cibulskis, Kristian ;
Fennell, Tim J. ;
Gabriel, Stacey B. .
NATURE, 2010, 467 (7319) :1061-1073
[2]  
[Anonymous], 1997, Diabetes Care, V20 Suppl 1, pS1
[3]   Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins [J].
Baigent, C ;
Keech, A ;
Kearney, PM ;
Blackwell, L ;
Buck, G ;
Pollicino, C ;
Kirby, A ;
Sourjina, T ;
Peto, R ;
Collins, R ;
Simes, J .
LANCET, 2005, 366 (9493) :1267-1278
[4]   The SREBP pathway: Regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor [J].
Brown, MS ;
Goldstein, JL .
CELL, 1997, 89 (03) :331-340
[5]   Cholesterol fractions and apolipoproteins as risk factors for heart disease mortality in older men [J].
Clarke, Robert ;
Emberson, Jonathan R. ;
Parish, Sarah ;
Palmer, Alison ;
Shipley, Martin ;
Linksted, Pamela ;
Sherliker, Paul ;
Clark, Sarah ;
Armitage, Jane ;
Fletcher, Astrid ;
Collins, Rory .
ARCHIVES OF INTERNAL MEDICINE, 2007, 167 (13) :1373-1378
[6]   High-resolution haplotype structure in the human genome [J].
Daly, MJ ;
Rioux, JD ;
Schaffner, SE ;
Hudson, TJ ;
Lander, ES .
NATURE GENETICS, 2001, 29 (02) :229-232
[7]   Feedback regulation of cholesterol synthesis: sterol-accelerated ubiquitination and degradation of HMG CoA reductase [J].
DeBose-Boyd, Russell A. .
CELL RESEARCH, 2008, 18 (06) :609-619
[8]   A field guide to ubiquitylation [J].
Fang, S ;
Weissman, AM .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2004, 61 (13) :1546-1561
[9]   The cholesterol absorption inhibitor ezetimibe acts by blocking the sterol-induced internalization of NPC1L1 [J].
Ge, Liang ;
Wang, Jing ;
Qi, Wei ;
Miao, Hong-Hua ;
Cao, Jian ;
Qu, Yu-Xiu ;
Li, Bo-Liang ;
Song, Bao-Liang .
CELL METABOLISM, 2008, 7 (06) :508-519
[10]   MEMBRANE-BOUND DOMAIN OF HMG COA REDUCTASE IS REQUIRED FOR STEROL-ENHANCED DEGRADATION OF THE ENZYME [J].
GIL, G ;
FAUST, JR ;
CHIN, DJ ;
GOLDSTEIN, JL ;
BROWN, MS .
CELL, 1985, 41 (01) :249-258