| 4 | Polymorphisms of MTHFD,plasma homocysteine levels, and risk of gastric cancer in ahigh-risk Chinese population显示文摘Purpose:Accumulative evidence suggests that folate has a protective effect on gastric cancer. The methylenetetrahyd-rofolate dlehydrogenase(MTHFD) plays an important role in folate and homocysteine metabolisms, and polymorphisms of MTHFD may result in disturbance of the folate-mediated homocysteine pathway. The aim of this study is to test the hypothesis that genetic variants of MTHFD and plasma homocysteine levels are associated with risk of gastric cancer and modulated by genotypes of methylenetetrahydrofolate reductase(MTHFR). Experimental Design: We genotyped G1958A and T401C in MTHFD and C677T in MTHFR and detected total plasma homocysteine(tHcy) levels in a case-control study of 589 gastric cancer cases and 635 cancer-free controls in a high-risk Chinese population. Results:The variant genotypes of MTHFD 1958AA and 401CC were associated with a significantly increased risk of gastric canceradjusted odds ratio(OR), 2.05; 95% confidence interval(95% CI),1.34-3.13 for 1958AA; adjusted OR,1.43; 95% CI,1.14-1.80 for 401CC compared with 1958GG/GA and 401TT/TC genotypes, respectively. Both of the effects were more evident in the subjects carrying MTHFR 677CT/TT genotypes. The average tHcy level was significantly higher in gastric cancer cases than in controls(P < 0.01), and the upper quartile of tHcy (> 13.6 mu mol/L) was associated with an 82% significantly increased risk of gastric cancer, compared with the lowest quartile of tHcy(<= 8.0 pmol/L;adjusted OR,1.82; 95% CI,1.20-2.75). Conclusions:The strong associations between MTHFD variants and the plasma tHcy levels and gastric cancer risk suggest, for the first time, a possible gene-environment interaction between genetic variants of folate-metabolizing genes and high tHcy levels in gastric carcinogenesis. | Wang, L. N Ke, Q Chen, W. S Wang, J. M Tan, Y. F Zhou, Y Hua, Z. L Ding, W. L Niu, J. Y Shen, J Zhang, Z. F Wang, X. R Xu, Y. H Shen, H. B Yi Xing | 2007 | 南京医科大学学报(自然科学版)2007，27，7： | 10 |
| 5 | Structural basis of AMPK regulation by adenine nucleotides and glycogen显示文摘激活安培的蛋白质 kinase (AMPK ) 为糖尿病,肥胖,和癌症的治疗是一个中央细胞的精力传感器和精力动态平衡,和一个有希望的药目标的管理者。这里我们人的 α 的现在的低分辨率的水晶结构; 1 β 2 γ 1 holo-AMPK 建筑群跳了到它的 allosteric 调节的人安培和肝糖模仿 cyclodextrin,两个在 phosphorylated (4.05 Å) 并且 non-phosphorylated (4.60 Å) 状态。另外,我们解决了 2.95 Å人的 kinase 领域(KD ) 的结构跳了到邻近的 autoinhibitory 领域(帮助) 并且表现了广泛生物化学并且 mutational 研究。一起,这些研究由安培和肝糖说明 allosteric AMPK 调整的内在的机制,其绑定改变在交替的帮助(安培) 和糖类绑定模块(肝糖) 之间的 equilibria 相互作用。 | Xiaodan Li Lili Wang X Edward Zhou Jiyuan Ke Parker W de Waal Xin Gu M H Eileen Tan Dongye Wang Donghai Wu H Eric Xu Karsten Melcher | 2015 | Cell Research2015，25，1： | 8 |
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