👤 Kaiquan Chen

🔍 Search 📋 Browse 🏷️ Tags ❤️ Favourites ➕ Add 🧪 BiometalDB 🧬 Extraction
2981
Articles
1996
Name variants
Also published as: Wen-Chau Chen, Jingzhao Chen, Dexi Chen, Haifeng Chen, Chung-Jen Chen, Bo-Jun Chen, Gao-Feng Chen, Changyan Chen, Weiwei Chen, Fenghua Chen, Xiaojiang S Chen, Xiu-Juan Chen, Jung-Sheng Chen, Xiao-Ying Chen, Chong Chen, Junyang Chen, YiPing Chen, Xiaohan Chen, Li-Zhen Chen, Jiujiu Chen, Shin-Wen Chen, Guangping Chen, Dapeng Chen, Ximei Chen, Renwei Chen, Jianfei Chen, Yulu Chen, Yu-Chi Chen, Jia-De Chen, Rongfang Chen, She Chen, Zetian Chen, Tianran Chen, Emily Chen, Baoxiang Chen, Ya-Chun Chen, Dongxue Chen, Wei-xian Chen, Danmei Chen, Ceshi Chen, Junling Chen, Xia Chen, Daoyuan Chen, Yongbin Chen, Chi-Yu Chen, Dian Chen, Xiuxiu Chen, Bo-Fang Chen, Fangyuan Chen, Jin-An Chen, Xiaojuan Chen, Zhuohui Chen, Junqi Chen, Lina Chen, Fangfang Chen, Hanwen Chen, Yilei Chen, Po-Han Chen, Xiaoxiang Chen, Jimei Chen, Guochong Chen, Yanyun Chen, Yifei Chen, Cheng-Yu Chen, Zi-Jiang Chen, Jiayuan Chen, Miaoran Chen, Junshi Chen, Yu-Ying Chen, Pengxiang Chen, Hui-Ru Chen, Yupeng Chen, Ida Y-D Chen, Xiaofeng Chen, Qiqi Chen, Shengnan Chen, Mao-Yuan Chen, Lizhu Chen, Weichan Chen, Xiang-Bin Chen, Hanxi Chen, Sulian Chen, Zoe Chen, Minghong Chen, Chi Chen, Yananlan Chen, Yanzhu Chen, Shiyi Chen, Ze-Xu Chen, Zhiheng Chen, Jia-Mei Chen, Shuqin Chen, Yi-Hau Chen, Danni Chen, Donglong Chen, Xiaomeng Chen, Yidong Chen, Keyu Chen, Hao Chen, Junmin Chen, Wenlong Chen, Yufei Chen, Wanbiao Chen, Mo Chen, Youjia Chen, Xin-Jie Chen, Lanlan Chen, Huapu Chen, Shuaiyin Chen, Jing-Hsien Chen, Hengsheng Chen, Bing-Bing Chen, Fa-Xi Chen, Zhiqiang Chen, Ming-Huang Chen, Liangkai Chen, Li-Jhen Chen, Zhi-Hao Chen, Yinzhu Chen, Guanghong Chen, Gaozhi Chen, Jiakang Chen, Yongke Chen, Guangquan Chen, Li-Hsien Chen, Yiduo Chen, Zongnan Chen, Jing Chen, Meilan Chen, Jin-Shuen Chen, Huanxiong Chen, Yann-Jang Chen, Guozhong Chen, Yu-Bing Chen, Xiaobin Chen, Catherine Qing Chen, Youhu Chen, Hui Mei Chen, L F Chen, Haiyang Chen, Ruilin Chen, Peng Chen, Kailang Chen, Chao Chen, Suipeng Chen, Zemin Chen, Jianlin Chen, Shang-Chih Chen, Yen-Hsieh Chen, Jia-Lin Chen, Chaojin Chen, Minglang Chen, Xiatian Chen, Zeyu Chen, Kang Chen, Mei-Chi Chen, Jihai Chen, Pei Chen, Defang Chen, Zhao Chen, Tianrui Chen, Tingtao Chen, Caressa Chen, Jiwei Chen, Xuerong Chen, Yizhi Chen, XueShu Chen, Mingyue Chen, Huichao Chen, Chun-Chi Chen, Xiaomin Chen, Hetian Chen, Yuxing Chen, Jie-Hua Chen, Chuck T Chen, Yuanjia Chen, Hong Chen, Jianxiong Chen, S Chen, D M Chen, Jiao-Jiao Chen, Gongbo Chen, Xufeng Chen, Xiao-Jun Chen, Harn-Shen Chen, Qiu Jing Chen, Tai-Heng Chen, Pei-Lung Chen, Kaifu Chen, Huang-Pin Chen, Tse-Wei Chen, Yanrong Chen, Xianfeng Chen, Chung-Yung Chen, Yuelei Chen, Qili Chen, Guanren Chen, TsungYen Chen, Yu-Si Chen, Junsheng Chen, Min-Jie Chen, Xin-Ming Chen, Jiabing Chen, Sili Chen, Qinying Chen, Yue Chen, Lin Chen, Xiaoli Chen, Zhuo Chen, Aoshuang Chen, Junyu Chen, Chunji Chen, Yian Chen, Shanchun Chen, Shuen-Ei Chen, Canrong Chen, Shih-Jen Chen, Yaowu Chen, Han Chen, Yih-Chieh Chen, Wei-Cong Chen, Yanfen Chen, Tao Chen, Huangtao Chen, Jingyi Chen, Sheng Chen, Jing-Wen Chen, Gao Chen, Lei-Lei Chen, Kecai Chen, Yao-Shen Chen, Haiyu Chen, W Chen, Xiaona Chen, Cheng-Sheng Chen, X R Chen, Shuangfeng Chen, Jingyuan Chen, Xinyuan Chen, Huanhuan Chen, Mengling Chen, Liang-Kung Chen, Ming-Huei Chen, Hongshan Chen, Cuncun Chen, Qingchao Chen, Yanzi Chen, Lingli Chen, Shiqian Chen, Liangwan Chen, Lexia Chen, Wei-Ting Chen, Zhencong Chen, Tzy-Yen Chen, Mingcong Chen, Honglei Chen, Yuyan Chen, Huachen Chen, Yu Chen, Li-Juan Chen, Aozhou Chen, Xinlin Chen, Wai Chen, Dake Chen, Bo-Sheng Chen, Meilin Chen, Kequan Chen, Hong Yang Chen, Yan Chen, Bowei Chen, Silian Chen, Jian Chen, Yongmei Chen, Ling Chen, Jinbo Chen, Yingxi Chen, Ge Chen, Max Jl Chen, C Z Chen, Weitao Chen, Xiaole L Chen, Yonglu Chen, Shih-Pin Chen, Jiani Chen, Huiru Chen, San-Yuan Chen, Bing Chen, Xiao-ping Chen, Feiyue Chen, Shuchun Chen, Zhaolin Chen, Qianxue Chen, Xiaoyang Chen, Bowang Chen, Yinghui Chen, Ting-Ting Chen, Xiao-Yang Chen, Chi-Yuan Chen, Zhi-zhe Chen, Ting-Tao Chen, Xiaoyun Chen, Min-Hsuan Chen, Kuan-Ting Chen, Yongheng Chen, Wenhao Chen, Shengyu Chen, Kai Chen, Yueh-Peng Chen, Guangju Chen, Minghua Chen, Hong-Sheng Chen, Qingmei Chen, Song-Mei Chen, Limei Chen, Yuqi Chen, Yuyang Chen, Yang-Ching Chen, Yu-Gen Chen, Peizhan Chen, Rucheng Chen, Jin-Xia Chen, Szu-Chieh Chen, Xiaojun Chen, Jialing Chen, Heni Chen, Yi Feng Chen, Sen Chen, Alice Ye A Chen, Wen Chen, Han-Chun Chen, Dawei Chen, Fangli Chen, Ai-Qun Chen, Zhaojun Chen, Gong Chen, Yishan Chen, Zhijing Chen, Qiuxuan Chen, Miao-Der Chen, Fengwu Chen, Weijie Chen, Weixin Chen, Mei-Ling Chen, Hung-Po Chen, Rui-Pei Chen, Nian-Ping Chen, Tielin Chen, Canyu Chen, Xiaotao Chen, Nan Chen, C Chen, Juanjuan Chen, Xinan Chen, Jiaping Chen, Xiao-Lin Chen, Jianping Chen, Yayun Chen, Le Qi Chen, Jen-Sue Chen, Mechi Chen, Miao-Yu Chen, Zhou Chen, Szu-Han Chen, Zhen Bouman Chen, Baihua Chen, Qingao Chen, Shao-Ke Chen, Feng Chen, Jiawen Chen, Lianmin Chen, Sifeng Chen, Mengxia Chen, Xueli Chen, Can Chen, Yibo Chen, Zinan Chen, Lei-Chin Chen, Carol Chen, Yanlin Chen, Zihang Chen, Zaozao Chen, Haiqin Chen, Lu Hua Chen, Zhiyuan Chen, Meiyu Chen, Du-Qun Chen, Keying Chen, Naifei Chen, Peixian Chen, Jin-Ran Chen, Yijun Chen, Yulin Chen, Fumei Chen, Zhanfei Chen, Zhe-Yu Chen, Xin-Qi Chen, Valerie Chen, Ru Chen, Mengqing Chen, Runsheng Chen, Tong Chen, Tan-Zhou Chen, Suet Nee Chen, Cuicui Chen, Yifan Chen, Tian Chen, XiangFan Chen, Lingyi Chen, Hsiao-Yun Chen, Kenneth L Chen, Ni Chen, Huishan Chen, Fang-Yu Chen, Ken Chen, Yongshen Chen, Qiong Chen, Mingfeng Chen, Shoudeng Chen, Qiao Chen, Qian Chen, Yuebing Chen, Xuehua Chen, Chang-Lan Chen, Min-Hu Chen, Hongbin Chen, Jingming Chen, Qing Chen, Yu-Fan Chen, Hao-Zhu Chen, Yunjia Chen, Zhongjian Chen, Mingyi Chen, Qianping Chen, Huaxin Chen, Dong-Mei Chen, Peize Chen, Leijie Chen, Ming-Yu Chen, Jiaxuan Chen, Xiao-chun Chen, Wei-Min Chen, Ruisen Chen, Xuanwei Chen, Guiquan Chen, Minyan Chen, Feng-Ling Chen, Yili Chen, Alvin Chen, Xiaodong Chen, Bohong Chen, Chih-Ping Chen, Xuanjing Chen, Shuhui Chen, Ming-Hong Chen, Tzu-Yu Chen, Brian Chen, Bowen Chen, Kai-En Chen, Szu-Chia Chen, Guangchun Chen, Fang Chen, Chuyu Chen, Haotian Chen, Xiaoting Chen, Shaoliang Chen, Chun-Houh Chen, Shali Chen, Yu-Cheng Chen, Zhijun Chen, B Chen, Yuan Chen, Zhanglin Chen, Chaoran Chen, Xing-Long Chen, Zhinan Chen, Yu-Hui Chen, Yuquan Chen, Andrew Chen, Fengming Chen, Guangyong Chen, Jun Chen, Wenshuo Chen, Yi-Guang Chen, Jing-Yuan Chen, Kuangyang Chen, Mingyang Chen, Shaofei Chen, Weicong Chen, Gonghai Chen, Di-Long Chen, Limin Chen, Jishun Chen, Yunfei Chen, Caihong Chen, Tongsheng Chen, Ligang Chen, Wenqin Chen, Shiyu Chen, Xiaoyong Chen, Christina Y Chen, Yushan Chen, Ginny I Chen, Guo-Jun Chen, Xianzhen Chen, Wanling Chen, Kuan-Jen Chen, Maorong Chen, Kaijian Chen, Erqu Chen, Shen Chen, Quan Chen, Zian Chen, Yi-Lin Chen, Juei-Suei Chen, Yi-Ting Chen, Huaiyong Chen, Minjian Chen, Qianzhi Chen, Jiahao Chen, Xikun Chen, Juan-Juan Chen, Xiaobo Chen, Tianzhen Chen, Ziming Chen, Qianbo Chen, Jindong Chen, Jiu-Chiuan Chen, Yinwei Chen, Carl Pc Chen, Li-Hsin Chen, Jenny Chen, Ruoyan Chen, Yanqiu Chen, Yen-Fu Chen, Haiyan Chen, Zhebin Chen, Si Chen, Jian-Qiao Chen, Yang-Yang Chen, Ningning Chen, Zhifeng Chen, Zhenyi Chen, Hangang Chen, Zihe Chen, Mengdi Chen, Zhichuan Chen, Xu Chen, Huixi Chen, Weitian Chen, Bao-Sheng Chen, Tien-Hsing Chen, Junchen Chen, Yan-yan Chen, Xiangning Chen, Sijia Chen, Xinyan Chen, Kuan-Yu Chen, Qunxiang Chen, Guangliang Chen, Bing-Huei Chen, Fei Xavier Chen, Zhangcheng Chen, Qianming Chen, Xianze Chen, Yanhua Chen, Qinghao Chen, Yanting Chen, Sijuan Chen, Chen-Mei Chen, Qiankun Chen, Jianan Chen, Rong Chen, Xiankai Chen, Kaina Chen, Gui-Hai Chen, Y-D Ida Chen, Quanjiao Chen, Shuang Chen, Lichang Chen, Xinyi Chen, Yong-Jun Chen, Zhaoli Chen, Chunnuan Chen, Jui-Chang Chen, Zhiang Chen, Weirui Chen, Zhenguo Chen, Jennifer F Chen, Zhiguo Chen, Kunmei Chen, Huan-Xin Chen, Mengyan Chen, Dongrong Chen, Siyue Chen, Xianyue Chen, Chien-Lun Chen, YiChung Chen, Guang Chen, Quanwei Chen, Zongming E Chen, Ting-Huan Chen, Michael C Chen, Jinli Chen, Beth L Chen, Yuh-Lien Chen, Peihong Chen, Qiaoling Chen, Jiale Chen, Shufeng Chen, Xiaowan Chen, Xian-Kai Chen, Ling-Yan Chen, Yen-Ling Chen, Guiying Chen, Guangyi Chen, Yuling Chen, Xiangqiu Chen, Haiquan Chen, Cuie Chen, Gui-Lai Chen, R Chen, Heng-Yu Chen, Yongxun Chen, Fuxiang Chen, Mingmei Chen, Hua-Pu Chen, Yulong Chen, Zhitao Chen, Guohua Chen, Cheng-Yi Chen, Hongxu Chen, Yuanhao Chen, Qichen Chen, Hualin Chen, Guo-Rong Chen, Rongsheng Chen, Xuesong Chen, Wei-Fei Chen, Bao-Bao Chen, Anqi Chen, Yi-Han Chen, Ying-Jung Chen, Jinhuang Chen, Guochao Chen, Lei Chen, S N Chen, Songfeng Chen, Chenyang Chen, Xing Chen, Letian Chen, Meng Xuan Chen, Xiang-Mei Chen, Xiaoyan Chen, Yi-Heng Chen, D F Chen, Bang Chen, Jiaxu Chen, Wei Chen, Sihui Chen, Shu-Hua Chen, I-M Chen, Xuxin Chen, Zhangxin Chen, Jin Chen, Yin-Huai Chen, Wuyan Chen, Bingqing Chen, Bao-Fu Chen, Zhen-Hua Chen, Dan Chen, Zhe-Sheng Chen, Ranyun Chen, Wanyin Chen, Xueyan Chen, Xiaoyu Chen, Tai-Tzung Chen, Xiaofang Chen, Yongxing Chen, Yanghui Chen, Hekai Chen, Yuanwei Chen, Liang Chen, Hui-Jye Chen, Chengchun Chen, Han-Bin Chen, Shuaijie Chen, Yibing Chen, Kehui Chen, Shuhai Chen, Xueling Chen, Ying-Jie Chen, Qingxing Chen, Fang-Zhi Chen, Mei-Hua Chen, Yutong Chen, Lixian Chen, Alex Chen, Qiuhong Chen, Qiuxia Chen, Liping Chen, Hou-Tsung Chen, Zhanghua Chen, Chun-Fa Chen, Chian-Feng Chen, Benjamin P C Chen, Yewei Chen, Mu-Hong Chen, Jianshan Chen, Xiaguang Chen, Meiling Chen, Heng Chen, Ying-Hsiang Chen, Longyun Chen, Dengpeng Chen, Jichong Chen, Shixuan Chen, Liaobin Chen, Everett H Chen, ZhuoYu Chen, Qihui Chen, Zhiyong Chen, Nuan Chen, Hongmei Chen, Guiqian Chen, Yan Q Chen, Fengling Chen, Hung-Chang Chen, Zhenghong Chen, Chengsheng Chen, Hegang Chen, Huei-Yan Chen, Liutao Chen, Meng-Lin Chen, Xi Chen, Qing-Juan Chen, Linna Chen, Xiaojing Chen, Lang Chen, Gengsheng Chen, Fengrong Chen, Weilun Chen, Shi Chen, Wan-Yi Chen, On Chen, Yufeng Chen, Benjamin Chen, Hui-Zhao Chen, Bo-Rui Chen, Kangyong Chen, Ruixiang Chen, Weiyong Chen, Ning-Hung Chen, Meng-Ping Chen, Huimei Chen, Ying Chen, Kang-Hua Chen, Pei-zhan Chen, Liujun Chen, Hanqing Chen, Chengchuan Chen, Guojun Chen, Yongfa Chen, Li Chen, Mingling Chen, Jacinda Chen, Jinlun Chen, Kun Chen, Yi Chen, Chiung Mei Chen, Shaotao Chen, Tianhong Chen, Chanjuan Chen, Yuhao Chen, Huizhi Chen, Chung-Hsing Chen, Qiuchi Chen, Haoting Chen, Luzhu Chen, Huanhua Chen, Long Chen, Jiang-hua Chen, Kai-Yang Chen, Jing-Zhou Chen, Yong-Syuan Chen, Lifang Chen, Ruonan Chen, Meimei Chen, Qingchuan Chen, Liugui Chen, Shaokun Chen, Yi-Yung Chen, Jintian Chen, Xuhui Chen, Dongyan Chen, Huei-Rong Chen, Xianmei Chen, Jinyan Chen, Yuxi Chen, Qingqing Chen, Weibo Chen, Qiwei Chen, Mingxia Chen, Hongmin Chen, Jiahui Chen, Yen-Jen Chen, Zihan Chen, Guozhou Chen, Fei Chen, Zhiting Chen, Denghui Chen, Gary Chen, Hongli Chen, Jack Chen, Zhigang Chen, Lie Chen, Siyuan Chen, Haojie Chen, Qing-Wei Chen, Maochong Chen, Mei-Jie Chen, Haining Chen, Xing-Zhen Chen, Weiqing Chen, Huanchun Chen, C-Y Chen, Tzu-An Chen, Jen-Hau Chen, Xiaojie Chen, Dongquan Chen, Gao B Chen, Daijie Chen, Zixi Chen, Lingfeng Chen, Jiayi Chen, Zan Chen, Shuming Chen, Mei-Hsiu Chen, Xueqin Chen, Huan Chen, Xiaoqing Chen, Hui-Xiong Chen, Ruoying Chen, Deying Chen, Huixian Chen, Zhezhe Chen, Lu Chen, Xiaolong Chen, Si-Yue Chen, Xinwei Chen, Wentao Chen, Yucheng Chen, Jiajing Chen, Allen Menglin Chen, Chixiang Chen, Shiqun Chen, Wenwu Chen, Chin-Chuan Chen, Ningbo Chen, Hsin-Hung Chen, Shenglan Chen, Jia-Feng Chen, Changya Chen, ZhaoHui Chen, Guo Chen, Juhai Chen, Xiao-Quan Chen, Cuimin Chen, Yongshuo Chen, Sai Chen, Fengyang Chen, Siteng Chen, Hualan Chen, Lian Chen, Yuan-Hua Chen, Minjie Chen, Shiyan Chen, Z Chen, Zhengzhi Chen, Jonathan Chen, H Chen, You-Yue Chen, Shu-Gang Chen, Hsuan-Yu Chen, Hongyue Chen, Weiyi Chen, Jiaqi Chen, Chengde Chen, Shufang Chen, Ze-Hui Chen, Xiuping Chen, Zhuojia Chen, Zhouji Chen, Lidian Chen, Yilan Chen, Kuan-Ling Chen, Alon Chen, Zi-Yue Chen, Hongmou Chen, Fang-Zhou Chen, Jianzhou Chen, Wenbiao Chen, Yujie Chen, Zhijian Chen, Zhouqing Chen, Xiuhui Chen, Qingguang Chen, Hanbei Chen, Qianyu Chen, Mengping Chen, Yongqi Chen, Sheng-Yi Chen, Siqi Chen, Yelin Chen, Shirui Chen, Yuan-Tsong Chen, Dongyin Chen, Lingxue Chen, Long-Jiang Chen, Yunshun Chen, Yahong Chen, Yaosheng Chen, Zhonghua Chen, Jingyao Chen, Pei-Yin Chen, Fusheng Chen, Xiaokai Chen, Shuting Chen, Miao-Hsueh Chen, Y-D I Chen, Zijie Chen, Haozhu Chen, Haodong Chen, Xiong Chen, Wenxi Chen, Feng-Jung Chen, Shangwu Chen, Zhiping Chen, Zhang-Yuan Chen, Wentong Chen, Ou Chen, Ruiming Chen, Xiyu Chen, Shuqiu Chen, Xiaoling Chen, Ruimin Chen, Hsiao-Wang Chen, Dongli Chen, Haibo Chen, Yiyun Chen, Luming Chen, Wenting Chen, Chongyang Chen, Qingqiu Chen, Wen-Pin Chen, Yuhui Chen, Lingxia Chen, Jun-Long Chen, Xingyu Chen, Haotai Chen, Bang-dang Chen, Qiuwen Chen, Rui Chen, K C Chen, Zhixuan Chen, Gaoyu Chen, Yitong Chen, Tzu-Ju Chen, Jingqing Chen, Huiqun Chen, Runsen Chen, Michelle Chen, Hanyong Chen, Xiaolin Chen, Ke Chen, Yangchao Chen, Y D I Chen, Jinghua Chen, Jia Wei Chen, Man-Hua Chen, H T Chen, Zheyi Chen, Lihong Chen, Guangyao Chen, Rujun Chen, Ming-Fong Chen, Haiyun Chen, Dexiong Chen, Huiqin Chen, Ching Kit Chen, En-Qiang Chen, Wanjia Chen, Xiangliu Chen, Meiting Chen, Szu-Chi Chen, Yii-der Ida Chen, Jian-Hua Chen, Yanjie Chen, Yingying Chen, Paul Chih-Hsueh Chen, Si-Ru Chen, Mingxing Chen, Rui-Zhen Chen, Changjie Chen, Qu Chen, Yintong Chen, Jingde Chen, Mao Chen, Xinghai Chen, Mei-Chih Chen, Xueqing Chen, Chun-An Chen, Cheng Chen, Ruijing Chen, Huayu Chen, Yunqin Chen, Yan-Gui Chen, Ruibing Chen, Size Chen, Qi-An Chen, Yuan-Zhen Chen, J Chen, Heye Chen, T Chen, Junpeng Chen, Tan-Huan Chen, Shuaijun Chen, Hao Yu Chen, Fahui Chen, Lan Chen, Dong-Yi Chen, Xianqiang Chen, Shi-Sheng Chen, Qiao-Yi Chen, Pei-Chen Chen, Xueying Chen, Yi-Wen Chen, Guohong Chen, Zhiwei Chen, Zuolong Chen, Erfei Chen, Yuqing Chen, Zhenyue Chen, Qiongyun Chen, Jianghua Chen, Yingji Chen, Xiuli Chen, Xiaowei Chen, Hengyu Chen, Sheng-Xi Chen, Haiyi Chen, Shao-Peng Chen, Yi-Ru Chen, Zhaoran Chen, Xiuyan Chen, Jinsong Chen, Sunny Chen, Xiaolan Chen, S-D Chen, Ruofan Chen, Qiujing Chen, Yun Chen, Wei-Cheng Chen, Chun-Wei Chen, Liechun Chen, Lulu Chen, Hsiu-Wen Chen, Yanping Chen, Jiayao Chen, Xuejiao Chen, Guan-Wei Chen, Yusi Chen, Yijiang Chen, Chi-Hua Chen, Qixian Chen, Ziqing Chen, Peiyou Chen, Chunhai Chen, Zheren Chen, Qiuyun Chen, Xiaorong Chen, Chaoqun Chen, Dan-Dan Chen, Xuechun Chen, Yafang Chen, Mystie X Chen, Jina Chen, Wei-Kai Chen, Yule Chen, Bo Chen, Kaili Chen, Junqin Chen, Jia Min Chen, Chen Chen, Guoliang Chen, Xiaonan Chen, Guangjie Chen, Xiao Chen, Jeanne Chen, Danyang Chen, Minjiang Chen, Jiyuan Chen, Zheng-Zhen Chen, Shou-Tung Chen, Ouyang Chen, Xiu Chen, H Q Chen, Peiyu Chen, Yuh-Min Chen, Youmeng Chen, Shuoni Chen, Peiqin Chen, Xinji Chen, Chih-Ta Chen, Shang-Hung Chen, Robert Chen, Suet N Chen, Yun-Tzu Chen, Suming Chen, Ye Chen, Yao Chen, Yi-Fei Chen, Ruixue Chen, Tianhang Chen, Suning Chen, Jingnan Chen, Xiaohong Chen, Kun-Chieh Chen, Tuantuan Chen, Mei Chen, He-Ping Chen, Zhi Bin Chen, Yuewu Chen, Mengying Chen, Po-See Chen, Xue Chen, Jian-Jun Chen, Xiyao Chen, Jeremy J W Chen, Jiemei Chen, Daiwen Chen, Christina Yingxian Chen, Qinian Chen, Chih-Wei Chen, Wensheng Chen, Yingcong Chen, Zhishi Chen, Duo Chen, Jiansu Chen, Keping Chen, Min Chen, Yi-Hui Chen, Yun-Ju Chen, Gaoyang Chen, Renjin Chen, Kui Chen, Shuai-Ming Chen, Hui-Fen Chen, Zi-Yun Chen, Shao-Yu Chen, Meiyang Chen, Jiahua Chen, Zongyou Chen, Yen-Rong Chen, Huaping Chen, Yu-Xin Chen, Bohe Chen, Kehua Chen, Zilin Chen, Zhang-Liang Chen, Ziqi Chen, Yinglian Chen, Hui-Wen Chen, Peipei Chen, Baolin Chen, Zugen Chen, Kangzhen Chen, Yanhan Chen, Sung-Fang Chen, Zheping Chen, Zixuan Chen, Jiajia Chen, Yuanjian Chen, Lili Chen, Xiangli Chen, Ban Chen, Yuewen Chen, X Chen, Yan-Qiong Chen, Chider Chen, Yung-Hsiang Chen, Hanlin Chen, Xiangjun Chen, Haibing Chen, Le Chen, Xuan Chen, Xue-Ying Chen, Zexiao Chen, Chen-Yu Chen, Zhe-Ling Chen, Fan Chen, Hsin-Yi Chen, Feilong Chen, Zilong Chen, Yi-Jen Chen, Zhiyun Chen, Ning Chen, Wenxu Chen, Chuanbing Chen, Yaxi Chen, Yi-Hong Chen, Eleanor Y Chen, Yuexin Chen, Kexin Chen, Shoujun Chen, Yen-Ju Chen, Yu-Chuan Chen, Yen-Teen Chen, Bao-Ying Chen, Xiaopeng Chen, Danli Chen, Katharine Y Chen, Jingli Chen, Qianyi Chen, Zihua Chen, Ya-xi Chen, Xuanxu Chen, Chung-Hung Chen, Yajie Chen, Cindi Chen, Hua Chen, Shuliang Chen, Elizabeth H Chen, Gen-Der Chen, Bingyu Chen, Keyang Chen, Siyu S Chen, Xinpu Chen, Yau-Hung Chen, Hsueh-Fen Chen, Han-Hsiang Chen, Wei Ning Chen, Guopu Chen, Zhujun Chen, Yurong Chen, Yuxian Chen, Wanjun Chen, Qiu-Jing Chen, Qifang Chen, Yuhan Chen, Jingshen Chen, Zhongliang Chen, Ching-Hsuan Chen, Zhaoyao Chen, Yongning Chen, Marcus Y Chen, Ping Chen, Junfei Chen, Yung-Wu Chen, Xueting Chen, Yingchun Chen, Wan-Yan Chen, Yuxin Chen, Yisheng Chen, Chun-Yuan Chen, Yulian Chen, Yan-Jun Chen, Guoxun Chen, Ding Chen, Yu-Fen Chen, Jason A Chen, Shuyi Chen, Cuilan Chen, Ruijuan Chen, Kevin Chen, Xuanmao Chen, Shen-Ming Chen, Ya-Nan Chen, Sean Chen, Zhaowei Chen, Xixi Chen, Yu-Chia Chen, Xuemin Chen, Binlong Chen, Weina Chen, Xuemei Chen, Di Chen, P P Chen, Yubin Chen, Chunhua Chen, Li-Chieh Chen, Ping-Chung Chen, Zhihao Chen, Xinyang Chen, Chan Chen, Yan Jie Chen, Shi-Qing Chen, Ivy Xiaoying Chen, Ying-Cheng Chen, Jia-Shun Chen, Shao-Wei Chen, Aiping Chen, Dexiang Chen, Qianfen Chen, Hongyu Chen, Wei-Kung Chen, Danlei Chen, Hongen Chen, Shipeng Chen, Jake Y Chen, Dongsheng Chen, Chien-Ting Chen, Shouzhen Chen, Hehe Chen, Yu-Tung Chen, Yilin Chen, Joy J Chen, Zhong Chen, Zhenfeng Chen, Zhongzhu Chen, Feiyang Chen, Xingxing Chen, Keyan Chen, Huimin Chen, Guanyu Chen, D. Chen, Dianke Chen, Zhigeng Chen, Sien-Tsong Chen, Yii-Der Chen, Chi-Yun Chen, Beidong Chen, Wu-Xian Chen, Zhihang Chen, Yuanqi Chen, Jianhua Chen, Xian Chen, Xiangding Chen, Jingteng Chen, Shuaiyu Chen, Xue-Mei Chen, Yu-Han Chen, Hongqiao Chen, Weili Chen, Yunzhu Chen, Guo-qing Chen, Miao Chen, Zhi Chen, Junhui Chen, Jing-Xian Chen, Zhiquan Chen, Shuhuang Chen, Shaokang Chen, Irwin Chen, Xiang Chen, Chuo Chen, Siting Chen, Keyuan Chen, Xia-Fei Chen, Zhihai Chen, Yuanyu Chen, Po-Sheng Chen, Qingjiang Chen, Yi-Bing Chen, Rongrong Chen, Katherine C Chen, Shaoxing Chen, Lifen Chen, Luyi Chen, Sisi Chen, Ning-Bo Chen, Yihong Chen, Guanjie Chen, Li-Hua Chen, Xiao-Hui Chen, Ting Chen, Chun-Han Chen, Xuzhuo Chen, Junming Chen, Zheng Chen, Wen-Jie Chen, Bingdi Chen, Jiang Ye Chen, Yanbin Chen, Duoting Chen, Shunyou Chen, Shaohua Chen, Jien-Jiun Chen, Jiaohua Chen, Shaoze Chen, Yifang Chen, Chiqi Chen, Yen-Hao Chen, Rui-Fang Chen, Hung-Sheng Chen, Kuey Chu Chen, Y S Chen, Xijun Chen, Chaoyue Chen, Heng-Sheng Chen, Lianfeng Chen, Yen-Ching Chen, Yuhong Chen, Yixin Chen, Yuanli Chen, Cancan Chen, Yanming Chen, Yajun Chen, Chaoping Chen, F-K Chen, Menglan Chen, Zi-Yang Chen, Yongfang Chen, Hsin-Hong Chen, Hongyan Chen, Chao-Wei Chen, Jijun Chen, Xiaochun Chen, Yazhuo Chen, Zhixin Chen, YongPing Chen, Jui-Yu Chen, Mian-Mian Chen, Liqiang Chen, Y P Chen, D-F Chen, Jinhao Chen, Yanyan Chen, Chang-Zheng Chen, Shao-long Chen, Guoshun Chen, Lo-Yun Chen, Yen-Lin Chen, Bingqian Chen, Dafang Chen, Yi-Chung Chen, Liming Chen, Qiuli Chen, Shuying Chen, Chih-Mei Chen, Renyu Chen, Wei-Hao Chen, Lihua Chen, Hang Chen, Hai-Ning Chen, Hu Chen, Yu-Fu Chen, Yalan Chen, Wan-Tzu Chen, Benjamin Jieming Chen, Yingting Chen, Jiacai Chen, Ning-Yuan Chen, Shuo-Bin Chen, Yu-Ling Chen, Jian-Kang Chen, Hengsan Chen, Yu-Ting Chen, Y Chen, Qingjie Chen, Jiong Chen, Chaoyi Chen, Yunlin Chen, Gang Chen, Hui-Chun Chen, Li-Tzong Chen, Zhangliang Chen, Qiangpu Chen, Xianbo Chen, Jinxuan Chen, Hebing Chen, Ran Chen, Zhehui Chen, Carol X-Q Chen, Yuping Chen, Xiangyu Chen, Xinyu Chen, Qianyun Chen, Junyi Chen, B-S Chen, Zhesheng Chen, Man Chen, Dali Chen, Danyu Chen, Huijiao Chen, Naisong Chen, Qitong Chen, Chueh-Tan Chen, Kai-Ming Chen, Jiarou Chen, Huang Chen, Chunjie Chen, Weiping Chen, Po-Min Chen, Guang-Chao Chen, Danxia Chen, Youran Chen, Chuanzhi Chen, Peng-Cheng Chen, Wen-Tsung Chen, Linxi Chen, Si-guo Chen, Zike Chen, Zhiyu Chen, Wanting Chen, Jiangxia Chen, Wenhua Chen, Roufen Chen, Shi-You Chen, Fang-Pei Chen, Chu Chen, Feifeng Chen, Chunlin Chen, Yunwei Chen, Wenbing Chen, Xuejun Chen, Meizhen Chen, Li Jia Chen, Tianhua Chen, Xiangmei Chen, Kewei Chen, Yuh-Ling Chen, Dejuan Chen, Jiyan Chen, Xinzhuo Chen, Yue-Lai Chen, Hsiao-Jou Cortina Chen, Weiqin Chen, Huey-Miin Chen, Elizabeth Suchi Chen, Kai-Ting Chen, Lizhen Chen, Xiaowen Chen, Chien-Yu Chen, Lingjun Chen, Gonglie Chen, Jiao Chen, Zhuo-Yuan Chen, Wei-Peng Chen, Xiangna Chen, Jiade Chen, Lanmei Chen, Siyu Chen, Kunpeng Chen, Hung-Chi Chen, Jia Chen, Shuwen Chen, Siqin Chen, Zhenlei Chen, Wen-Yi Chen, Si-Yuan Chen, Yidan Chen, Tianfeng Chen, Fu Chen, Leqi Chen, Jiamiao Chen, Shasha Chen, Qingyi Chen, Ben-Kuen Chen, Haitao Chen, Qi Chen, Yihao Chen, Yunfeng Chen, Elizabeth S Chen, Yiming Chen, Youwei Chen, Lichun Chen, Yanfei Chen, Hongxing Chen, Muh-Shy Chen, Yingyu Chen, Weihong Chen, Ming Chen, Kelin Chen, Duan-Yu Chen, Shi-Yi Chen, Shih-Yu Chen, Yanling Chen, Shuanghui Chen, Ya Chen, Yusheng Chen, Yuting Chen, Shiming Chen, Xinqiao Chen, Hongbo Chen, Mien-Cheng Chen, Jiacheng Chen, Herbert Chen, Ji-ling Chen, Sun Chen, Chen-Sheng Chen, Na Chen, Chih-Yi Chen, Wenfang Chen, Yii-Der I Chen, Qinghua Chen, Shuai Chen, Hsi-Hsien Chen, F Chen, Guo-Chong Chen, Zhe Chen, Beijian Chen, Roger Chen, You-Ming Chen, Hongzhi Chen, Zhen-Yu Chen, Xianxiong Chen, Chang Chen, Chujie Chen, Chuannan Chen, Kan Chen, Lu-Biao Chen, Yupei Chen, Qiu-Sheng Chen, Shangduo Chen, Yuan-Yuan Chen, Yundai Chen, Binzhen Chen, Cai-Long Chen, Yen-Chen Chen, Xue-Xin Chen, Yanru Chen, Chunxiu Chen, Yifa Chen, Xingdong Chen, Ruey-Hwa Chen, Shangzhong Chen, Ching-Wen Chen, Danna Chen, Jingjing Chen, Yafei Chen, Dandan Chen, Pei-Yi Chen, Shan Chen, Guanghao Chen, Longqing Chen, Yen-Cheng Chen, Zhanjuan Chen, Jinguo Chen, Zhongxiu Chen, Rui-Min Chen, Shunde Chen, Xun Chen, Jianmin Chen, Linyi Chen, Ying-Ying Chen, Chien-Hsiun Chen, Li-Nan Chen, Yu-Ming Chen, Qianqian Chen, Xue-Yan Chen, Shengdi Chen, Huali Chen, Xinyue Chen, Ching-Yi Chen, Honghai Chen, Baosheng Chen, Pingguo Chen, Yike Chen, Yuxiang Chen, Qing-Hui Chen, Yuanwen Chen, Yongming Chen, Zongzheng Chen, Ruiying Chen, Huafei Chen, Tingen Chen, Zhouliang Chen, Shih-Yin Chen, Shanyuan Chen, Yiyin Chen, Feiyu Chen, Zitao Chen, Constance Chen, Zhoulong Chen, Haide Chen, Jiang Chen, Ray-Jade Chen, Shiuhwei Chen, Chih-Chieh Chen, Chaochao Chen, Lijuan Chen, Qianling Chen, Jian-Min Chen, Xihui Chen, Yuli Chen, Wu-Jun Chen, Diyun Chen, Alice P Chen, Jingxuan Chen, Chiung-Mei Chen, Shibo Chen, M L Chen, Lena W Chen, Xiujuan Chen, Christopher S Chen, Yeh Chen, Xingyong Chen, Feixue Chen, Boyu Chen, Weixian Chen, Tingting Chen, Bosong Chen, Junjie Chen, Han-Min Chen, Szu-Yun Chen, Qingliang Chen, Huatao Chen, Bin Chen, L B Chen, Xuanyi Chen, Chun Chen, Dong Chen, Yinjuan Chen, Jiejian Chen, Lu-Zhu Chen, Alex F Chen, Pei-Chun Chen, Chien-Jen Chen, Y M Chen, Xiao-Chen Chen, Tania Chen, Yang Chen, Yangxin Chen, Mark I-Cheng Chen, Haiming Chen, Shuo Chen, Yong Chen, Hsiao-Tan Chen, Erzhen Chen, Jiaye Chen, Fangyan Chen, Guanzheng Chen, Haoyun Chen, Jiongyu Chen, Baofeng Chen, Yuqin Chen, Juan Chen, Haobo Chen, Shuhong Chen, Fu-Shou Chen, Wei-Yu Chen, Haw-Wen Chen, Feifan Chen, Deqian Chen, Linlin Chen, Xiaoshan Chen, Hui Chen, Wenwen Chen, Yanli Chen, Yuexuan Chen, Xiaoyin Chen, Yen-Chang Chen, Tiantian Chen, Ruiai Chen, Alice Y Chen, Jinglin Chen, Zifan Chen, Wantao Chen, Shanshan Chen, Jianjun Chen, Xiaoyuan Chen, Xuefei Chen, Runfeng Chen, Weisan Chen, Guangnan Chen, Junpan Chen, An Chen, Lankai Chen, Yiding Chen, Tianpeng Chen, Ya-Ting Chen, Lijin Chen, Ching-Yu Chen, Y Eugene Chen, Guanglong Chen, Rongyuan Chen, Yali Chen, Yanan Chen, Liyun Chen, Shuai-Bing Chen, Zhixue Chen, Xiaolu Chen, Xiao-he Chen, Hongxiang Chen, Bing-Feng Chen, Gary K Chen, Xiaohui Chen, Jin-Wu Chen, Qiuxiang Chen, Huaqiu Chen, X Steven Chen, Xiaoqian Chen, Chao-Jung Chen, Zhengjun Chen, Yong-Ping Chen, Zhelin Chen, Xuancai Chen, Yi-Hsuan Chen, Daiyu Chen, Gui Mei Chen, Hongqi Chen, Zhizhong Chen, Mengting Chen, Guofang Chen, Jian-Guo Chen, Hou-Zao Chen, Yuyao Chen, Lixia Chen, Yu-Yang Chen, Zhengling Chen, Qinfen Chen, Jiajun Chen, Xue-Qing Chen, Shenghui Chen, Yii-Derr Chen, Linbo Chen, Yanjing Chen, S Pl Chen, Chi-Long Chen, Jiawei Chen, Rong-Hua Chen, Shu-Fen Chen, Yu-San Chen, Ying-Lan Chen, Xiaofen Chen, Weican Chen, Xin Chen, Yumei Chen, Ruohong Chen, You-Xin Chen, Tse-Ching Chen, Xiancheng Chen, Yu-Pei Chen, Weihao Chen, Baojiu Chen, Haimin Chen, Zhihong Chen, Jion Chen, Yi-Chun Chen, Ping-Kun Chen, Wan Jun Chen, Willian Tzu-Liang Chen, Qingshi Chen, Ren-Hui Chen, Weihua Chen, Hanjing Chen, Guihao Chen, Xiao-Qing Chen, Po-Yu Chen, Liangsheng Chen, Fred K Chen, Haiying Chen, Tzu-Chieh Chen, Wei J Chen, Zhen Chen, Shu Chen, Jie Chen, Chung-Hao Chen, Zi-Qing Chen, Yu-Xia Chen, Weijia Chen, Ming-Han Chen, Yaodong Chen, Yong-Zhong Chen, Jinquan Chen, Haijiao Chen, Tom Wei-Wu Chen, Jingzhou Chen, Ya-Peng Chen, Shiwei Chen, Xiqun Chen, Yingjie Chen, Wenjun Chen, Linjie Chen, Hung-Chun Chen, Xiaoping Chen, Haoran Chen, Qiang Chen, Sy-Jou Chen, Y U Chen, Weineng Chen, Li-hong Chen, Cheng-Fong Chen, Yajing Chen, Song Chen, Qiaoli Chen, Yiru Chen, Guang-Yu Chen, Zhi-bin Chen, Deyu Chen, C Y Chen, Junhong Chen, Yonghui Chen, Chaoli Chen, Syue-Ting Chen, Sufang Chen, I-Chun Chen, Shangsi Chen, Xiao-Wei Chen, Qinsheng Chen, Zhao-Xia Chen, Yun-Yu Chen, Chi-Chien Chen, Wenxing Chen, Meng Chen, Zixin Chen, Jianhui Chen, Yuanyuan Chen, Jiamin Chen, Wei-Wei Chen, Xingyi Chen, Yen-Ni Chen, Danxiang Chen, Po-Ju Chen, Mei-Ru Chen, Ziying Chen, E S Chen, Tailai Chen, Qingyang Chen, Miaomiao Chen, Shuntai Chen, Wei-Lun Chen, Xuanli Chen, Zhengwei Chen, Fengju Chen, Chengwei Chen, Xujia Chen, Faye H Chen, Xiaoxiao Chen, Shengpan Chen, Shin-Yu Chen, Shiyao Chen, Yuan-Shen Chen, Shengzhi Chen, Shaohong Chen, Ching-Jung Chen, Zihao Chen, Duo-Xue Chen, Xiaochang Chen, Siping Chen, Rongfeng Chen, Jiali Chen, Hsin-Han Chen, Xiaohua Chen, Delong Chen, Wenjie Chen, Huijia Chen, Yunn-Yi Chen, Siyi Chen, Zhengming Chen, Chu-Huang Chen, Zhuchu Chen, Yuanbin Chen, Jinyong Chen, Yunzhong Chen, Pan Chen, Bihong T Chen, Yunyun Chen, Shujuan Chen, M Chen, Mulan Chen, Jiaren Chen, Zechuan Chen, Jian-Qing Chen, Wei-Hui Chen, Lifeng Chen, Geng Chen, Yan-Ming Chen, Zhijian J Chen, Honghui Chen, Wenfan Chen, Zhongbo Chen, Rouxi Chen, Ye-Guang Chen, Zhimin Chen, Tzu-Ting Chen, Xiaolei Chen, Ziyuan Chen, Shilan Chen, Ruiqi Chen, Xiameng Chen, Huijie Chen, Jiankui Chen, Yuhang Chen, Jianzhong Chen, Wen-Qi Chen, Fa Chen, Shu-Jen Chen, Li-Mien Chen, Xing-Lin Chen, Xuxiang Chen, Erbao Chen, Jiaqing Chen, Hsiang-Wen Chen, Jiaxin Chen
articles

MACF1, versatility in tissue-specific function and in human disease.

Lifang Hu, Yunyun Xiao, Zhipeng Xiong +9 more · 2017 · Seminars in cell & developmental biology · Elsevier · added 2026-04-24
Spectraplakins are a family of evolutionarily conserved gigantic proteins and play critical roles in many cytoskeleton-related processes. Microtubule actin crosslinking factor 1 (MACF1) is one of the Show more
Spectraplakins are a family of evolutionarily conserved gigantic proteins and play critical roles in many cytoskeleton-related processes. Microtubule actin crosslinking factor 1 (MACF1) is one of the most versatile spectraplakin with multiple isoforms. As a broadly expressed mammalian spectraplakin, MACF1 is important in maintaining normal functions of many tissues. The loss-of-function studies using knockout mouse models reveal the pivotal roles of MACF1 in embryo development, skin integrity maintenance, neural development, bone formation, and colonic paracellular permeability. Mutation in the human MACF1 gene causes a novel myopathy genetic disease. In addition, abnormal expression of MACF1 is associated with schizophrenia, Parkinson's disease, cancer and osteoporosis. This demonstrates the crucial roles of MACF1 in physiology and pathology. Here, we review the research advances of MACF1's roles in specific tissue and in human diseases, providing the perspectives of MACF1 for future studies. Show less
no PDF DOI: 10.1016/j.semcdb.2017.05.017
MACF1

Novel polymorphism in FADS1 gene and fish consumption on risk of oral cancer: A case-control study in southeast China.

Fa Chen, Tao Lin, Lingjun Yan +8 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
The aim of this study was to investigate the independent and combined effects of fatty acid desaturase 1 (FADS1) gene polymorphism and fish consumption on oral cancer. A hospital-based case-control st Show more
The aim of this study was to investigate the independent and combined effects of fatty acid desaturase 1 (FADS1) gene polymorphism and fish consumption on oral cancer. A hospital-based case-control study was performed including 305 oral cancer patients and 579 cancer-free controls. The genotypes were determined by TaqMan genotyping assay. Non-conditional logistic regression model was used to assess the effects of FADS1 rs174549 polymorphism and fish intake. Subjects carrying A allele of rs174549 significantly reduced the risk of oral cancer (AA VS GG, OR: 0.65, 95% CI: 0.42-0.99; AA VS AG+GG, OR: 0.67, 95% CI: 0.46-0.98). Moreover, the statistically significant reverse associations were especially evident in men, smokers, alcohol drinkers and those age ≤ 60 years. Additionally, fish intake ≥7 times/week showed a 73% reduction in risk for oral cancer compared to those who ate fish less than 2 times/week (OR: 0.27, 95% CI: 0.18-0.42). Furthermore, a significant gene-diet multiplicative interaction was observed between FADS1 rs174549 polymorphism and fish intake for oral cancer (P=0.028). This preliminary study suggests that FADS1 rs174549 polymorphism and fish consumption may be protective factors for oral cancer, with a gene-diet multiplicative interaction. Functional studies with larger samples are required to confirm our findings. Show less
📄 PDF DOI: 10.18632/oncotarget.15069
FADS1

Exome-wide association study of plasma lipids in >300,000 individuals.

Dajiang J Liu, Gina M Peloso, Haojie Yu +229 more · 2017 · Nature genetics · Nature · added 2026-04-24
Dajiang J Liu, Gina M Peloso, Haojie Yu, Adam S Butterworth, Xiao Wang, Anubha Mahajan, Danish Saleheen, Connor Emdin, Dewan Alam, Alexessander Couto Alves, Philippe Amouyel, Emanuele Di Angelantonio, Dominique Arveiler, Themistocles L Assimes, Paul L Auer, Usman Baber, Christie M Ballantyne, Lia E Bang, Marianne Benn, Joshua C Bis, Michael Boehnke, Eric Boerwinkle, Jette Bork-Jensen, Erwin P Bottinger, Ivan Brandslund, Morris Brown, Fabio Busonero, Mark J Caulfield, John C Chambers, Daniel I Chasman, Y Eugene Chen, Yii-der Ida Chen, Rajiv Chowdhury, Cramer Christensen, Audrey Y Chu, John M Connell, Francesco Cucca, L Adrienne Cupples, Scott M Damrauer, Gail Davies, Ian J Deary, George Dedoussis, Joshua C Denny, Anna Dominiczak, Marie-Pierre Dubé, Tapani Ebeling, Gudny Eiriksdottir, Tõnu Esko, Aliki-Eleni Farmaki, Mary F Feitosa, Marco Ferrario, Jean Ferrieres, Ian Ford, Myriam Fornage, Paul W Franks, Timothy M Frayling, Ruth Frikke-Schmidt, Lars G Fritsche, Philippe Frossard, Valentin Fuster, Santhi K Ganesh, Wei Gao, Melissa E Garcia, Christian Gieger, Franco Giulianini, Mark O Goodarzi, Harald Grallert, Niels Grarup, Leif Groop, Megan L Grove, Vilmundur Gudnason, Torben Hansen, Tamara B Harris, Caroline Hayward, Joel N Hirschhorn, Oddgeir L Holmen, Jennifer Huffman, Yong Huo, Kristian Hveem, Sehrish Jabeen, Anne U Jackson, Johanna Jakobsdottir, Marjo-Riitta Jarvelin, Gorm B Jensen, Marit E Jørgensen, J Wouter Jukema, Johanne M Justesen, Pia R Kamstrup, Stavroula Kanoni, Fredrik Karpe, Frank Kee, Amit V Khera, Derek Klarin, Heikki A Koistinen, Jaspal S Kooner, Charles Kooperberg, Kari Kuulasmaa, Johanna Kuusisto, Markku Laakso, Timo Lakka, Claudia Langenberg, Anne Langsted, Lenore J Launer, Torsten Lauritzen, David C M Liewald, Li An Lin, Allan Linneberg, Ruth J F Loos, Yingchang Lu, Xiangfeng Lu, Reedik Mägi, Anders Malarstig, Ani Manichaikul, Alisa K Manning, Pekka Mäntyselkä, Eirini Marouli, Nicholas G D Masca, Andrea Maschio, James B Meigs, Olle Melander, Andres Metspalu, Andrew P Morris, Alanna C Morrison, Antonella Mulas, Martina Müller-Nurasyid, Patricia B Munroe, Matt J Neville, Jonas B Nielsen, Sune F Nielsen, Børge G Nordestgaard, Jose M Ordovas, Roxana Mehran, Christoper J O'Donnell, Marju Orho-Melander, Cliona M Molony, Pieter Muntendam, Sandosh Padmanabhan, Colin N A Palmer, Dorota Pasko, Aniruddh P Patel, Oluf Pedersen, Markus Perola, Annette Peters, Charlotta Pisinger, Giorgio Pistis, Ozren Polasek, Neil Poulter, Bruce M Psaty, Daniel J Rader, Asif Rasheed, Rainer Rauramaa, Dermot F Reilly, Alex P Reiner, Frida Renström, Stephen S Rich, Paul M Ridker, John D Rioux, Neil R Robertson, Dan M Roden, Jerome I Rotter, Igor Rudan, Veikko Salomaa, Nilesh J Samani, Serena Sanna, Naveed Sattar, Ellen M Schmidt, Robert A Scott, Peter Sever, Raquel S Sevilla, Christian M Shaffer, Xueling Sim, Suthesh Sivapalaratnam, Kerrin S Small, Albert V Smith, Blair H Smith, Sangeetha Somayajula, Lorraine Southam, Timothy D Spector, Elizabeth K Speliotes, John M Starr, Kathleen E Stirrups, Nathan Stitziel, Konstantin Strauch, Heather M Stringham, Praveen Surendran, Hayato Tada, Alan R Tall, Hua Tang, Jean-Claude Tardif, Kent D Taylor, Stella Trompet, Philip S Tsao, Jaakko Tuomilehto, Anne Tybjaerg-Hansen, Natalie R van Zuydam, Anette Varbo, Tibor V Varga, Jarmo Virtamo, Melanie Waldenberger, Nan Wang, Nick J Wareham, Helen R Warren, Peter E Weeke, Joshua Weinstock, Jennifer Wessel, James G Wilson, Peter W F Wilson, Ming Xu, Hanieh Yaghootkar, Robin Young, Eleftheria Zeggini, He Zhang, Neil S Zheng, Weihua Zhang, Yan Zhang, Wei Zhou, Yanhua Zhou, Magdalena Zoledziewska, Charge Diabetes Working Group, EPIC-InterAct Consortium, EPIC-CVD Consortium, GOLD Consortium, VA Million Veteran Program, Joanna M M Howson, John Danesh, Mark I McCarthy, Chad A Cowan, Goncalo Abecasis, Panos Deloukas, Kiran Musunuru, Cristen J Willer, Sekar Kathiresan Show less
We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated w Show more
We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD. Show less
📄 PDF DOI: 10.1038/ng.3977
ANGPTL4

Metabolome-wide association study identified the association between a circulating polyunsaturated fatty acids variant rs174548 and lung cancer.

Cheng Wang, Na Qin, Meng Zhu +12 more · 2017 · Carcinogenesis · Oxford University Press · added 2026-04-24
Quantitative trait loci (QTLs) are widely used as instruments to infer causal risk factors of diseases based on the idea of mendelian randomization. Plasma metabolites can serve as risk factors of can Show more
Quantitative trait loci (QTLs) are widely used as instruments to infer causal risk factors of diseases based on the idea of mendelian randomization. Plasma metabolites can serve as risk factors of cancer, and the heritability of many circulating metabolites was high. We conducted a metabolome-wide association study (MWAS) to systematically investigate the effects of genetic variants on metabolites and lung cancer based on published genome-wide association study (GWASs) and metabolic-QTL (mQTL) study. Then we confirmed the results by subsequent genetic and metabolic validations and inferred the causal relationship between identified metabolites and lung cancer through genetic variant(s). We firstly identified six polyunsaturated fatty acids (PUFAs) represented by rs174548-linked haplotype were significantly associated with lung cancer risk in a Chinese GWAS (2311 cases and 3077 controls). Rs174548 was further confirmed to be associated with lung cancer in 13 821 Europeans and 18 471 Asians (ORmeta = 0.87, Pmeta = 1.76 × 10-15) and the effect was much stronger in females (Pinteraction = 6.00 × 10-4). We next validated rs174548-plasma PUFA association in 253 Chinese subjects (β = -0.57, P = 1.68 × 10-3). Rs174548 was also found associated with FADS1 (the major fatty acid desaturase of identified PUFAs) expression in liver tissues. Taken together, we found that rs174548 was associated with both PUFAs and lung cancer. Because rs174548 was the only mQTL variant of PUFAs reported by previous GWASs and explained a large proportion of heritability, we proposed that plasma PUFAs could be causally associated with lung cancer based on the idea of mendelian randomization. These findings provide a diet-related risk factor and may have important implications for prevention on lung cancer. Show less
no PDF DOI: 10.1093/carcin/bgx084
FADS1

The effect of glucose-dependent insulinotropic polypeptide (GIP) variants on visceral fat accumulation in Han Chinese populations.

T Wang, X Ma, T Tang +13 more · 2017 · Nutrition & diabetes · Nature · added 2026-04-24
We aim to validate the effects of glucose-dependent insulinotropic polypeptide (GIP) on fat distribution and glucose metabolism in Han Chinese populations. We genotyped six tag single-nucleotide polym Show more
We aim to validate the effects of glucose-dependent insulinotropic polypeptide (GIP) on fat distribution and glucose metabolism in Han Chinese populations. We genotyped six tag single-nucleotide polymorphisms (SNPs) of GIP and four tag SNPs of glucose-dependent insulinotropic polypeptide receptor (GIPR) among 2884 community-based individuals from Han Chinese populations. Linear analysis was applied to test the associations of these variants with visceral fat area (VFA) and subcutaneous fat area (SFA) quantified by magnetic resonance imaging as well as glucose-related traits. We found that the C allele of rs4794008 of GIP tended to increase the VFA and the VFA/SFA ratio in all subjects (P=0.050 and P=0.054, respectively), and rs4794008 was associated with the VFA/SFA ratio in males (P=0.041) after adjusting for the BMI. The VFA-increasing allele of rs4794008 was not related to any glucose metabolism traits. However, rs9904288 of GIP was associated with the SFA in males as well as glucose-related traits in all subjects (P range, 0.004-0.049), and the GIPR variants displayed associations with both fat- and glucose-related traits. The results could provide the evidence that GIP might modulate visceral fat accumulation via incretin function or independent of incretin. Show less
📄 PDF DOI: 10.1038/nutd.2017.28
GIPR

AXIN1 protects against testicular germ cell tumors via the PI3K/AKT/mTOR signaling pathway.

Hailiang Xu, Yunyun Feng, Zhankui Jia +7 more · 2017 · Oncology letters · added 2026-04-24
Axis inhibition protein 1 (AXIN1) is characterized as a tumor suppressor in numerous types of cancer. However, the functional role of AXIN1 in the testicular germ cell tumors (TGCTs) remains unclear. Show more
Axis inhibition protein 1 (AXIN1) is characterized as a tumor suppressor in numerous types of cancer. However, the functional role of AXIN1 in the testicular germ cell tumors (TGCTs) remains unclear. The human embryonal carcinoma-derived cell line NTera2 was transfected with a recombinant AXIN1 expression vector (pcDNA3.1-AXIN1) and/or a small interfering RNA (siRNA) directed against AXIN1 (siAXIN). Following transfection, the mRNA and protein levels of AXIN1 were determined via reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. In addition, cell viability, apoptosis and the expression of apoptosis-associated proteins [apoptosis regulator Bax (Bax) and B-cell lymphoma (Bcl)-2] and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins [phosphorylated (p)-mTOR, mTOR, p-AKT, AKT, P-70S ribosomal protein S6 (S6) and S6] were assessed. AXIN1 mRNA and protein levels were increased following transfection with pcDNA3.1-AXIN1 and decreased following transfection with siAXIN1 compared with their respective control groups. After overexpression of AXIN1, NTera2 cell viability and expression of Bcl-2, p-mTOR p-AKT and p-S6 protein was decreased, while apoptosis and Bax protein levels were increased, compared with the control group. However, there was no significant difference in AXIN1 mRNA expression, apoptosis or Bax/Bcl-2 protein expression when NTera2 cells were simultaneously transfected with pcDNA3.1-AXIN1+siAXIN1. In conclusion, the results of the present study indicate that overexpression of AXIN1 protects against TGCTs via inhibiting the PI3K/AKT/mTOR signaling pathway, suggesting that AXIN1 may be a potential target for gene therapy in TGCTs. Show less
no PDF DOI: 10.3892/ol.2017.6214
AXIN1

Achieving efficient digestion faster with Flash Digest: potential alternative to multi-step detergent assisted in-solution digestion in quantitative proteomics experiments.

Vinit Shah, Michael E Lassman, Ying Chen +2 more · 2017 · Rapid communications in mass spectrometry : RCM · Wiley · added 2026-04-24
In quantitative analysis of protein biomarkers and therapeutic proteins by liquid chromatography/mass spectrometry (LC/MS), it is a preferred and well-established approach to digest with proteolytic e Show more
In quantitative analysis of protein biomarkers and therapeutic proteins by liquid chromatography/mass spectrometry (LC/MS), it is a preferred and well-established approach to digest with proteolytic enzymes to produce smaller peptide fragments which are more suitable for LC/MS analysis than the intact protein. In-solution digestion is one widely used method for protein digestion. Proteolytically resistant proteins often require digestion times that extend beyond normal working hours and prohibit same day analysis. We evaluated the performance of an immobilized enzyme reactor (IMER) to determine if this technology could reduce method development time, digestion time and increase throughput. We digested human plasma samples using a commercially available IMER, Flash Digest, and compared it to an in-solution digestion method for analysis of three different apolipoprotein biomarkers APOE, APOC2, and APOC3. The plasma digests were analyzed via LC/MS using electrospray ionization (ESI) and multiple reaction monitoring (MRM). Value assigned calibrators were selected over a relevant physiological concentration range for each protein of interest. Quality control samples (QCs) and 'unknown' human plasma samples were analyzed with both methods. Flash Digest significantly reduced digestion time for APOC3, the most proteolytically resistant of the three proteins, to 30 min compared with overnight used with in-solution digestion. The Flash Digest achieved comparable digestion efficiency with minimal method development and reduced sample preparation time. Both methods showed linearity over a physiologically relevant concentration range. Precision was evaluated and a percentage coefficient of variance (% CV) less than 8% was obtained during intra-day reproducibility evaluation for all three apolipoproteins with Flash Digest. Concentrations observed for QCs and unknown samples using Flash Digest were comparable to the in-solution method. An IMER such as Flash Digest may be a potential alternative to in-solution digestion to accelerate digestion of proteolytically resistant proteins in a quantitative proteomics experiments, reduce method development time and increase throughput. Copyright © 2016 John Wiley & Sons, Ltd. Show less
no PDF DOI: 10.1002/rcm.7778
APOC3

The activity of the carbamoyl phosphate synthase 1 promoter in human liver-derived cells is dependent on hepatocyte nuclear factor 3-beta.

Zhanfei Chen, Nanhong Tang, Xiaoqian Wang +1 more · 2017 · Journal of cellular and molecular medicine · Blackwell Publishing · added 2026-04-24
Carbamoyl phosphate synthase 1 (CPS1) is the rate-limiting enzyme in the first step of the urea cycle and an indispensable enzyme in the metabolism of human liver. However, CPS1 epigenetic regulation Show more
Carbamoyl phosphate synthase 1 (CPS1) is the rate-limiting enzyme in the first step of the urea cycle and an indispensable enzyme in the metabolism of human liver. However, CPS1 epigenetic regulation involves promoter analysis and the role of liver-enriched transcription factors (LETFs), which is not fully elucidated. In this work, the promoter region of hCPS1 gene was cloned, and its activity was investigated. An LETF, hepatocyte nuclear factor 3-beta (HNF3β), was found to promote the transcriptional expression of CPS1 in liver-derived cell lines. In addition, dual-luciferase reporter assay shows that the essential binding sites of the HNF3β may exist in the oligonucleotide -70 nt to +73 nt. Two putative binding sites are available for HNF3β. Mutation analysis results show that the binding site 2 of HNF3β was effective, and the transcriptional activity of CPS1 promoter significantly decreased after mutation. Electrophoretic mobile shift assay (EMSA) and ChIP assay confirmed that HNF3β can interact with the binding site in the CPS1 promoter region of -70 nt to +73 nt promoter region in vivo and in vitro to regulate the transcription of CPS1. Moreover, HNF3β overexpression enhanced the transcription of CPS1 and consequently improved the mRNA and protein levels of CPS1, whereas the knockdown of HNF3β showed the opposite effects. Finally, urea production in cells was measured, and ammonia detoxification improved significantly in cells after transfection with HNF3β. HNF3β plays a vital role in regulation of CPS1 gene and could promote the metabolism of ammonia by regulating CPS1 expression. Show less
📄 PDF DOI: 10.1111/jcmm.13123
CPS1

Studies on the regulation of lipid metabolism and the mechanism of the aqueous and ethanol extracts of Usnea.

Jiali Zhu, Xuemei Zhang, Xiu Chen +5 more · 2017 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · Elsevier · added 2026-04-24
Usnea is a lichen of Usnea diffracta Vain and Usnea longissima Ach, which belongs to the genus Usnea Adans of Usneaceae. Usnea exerts numerous pharmacological activities, while its lipid regulatory ac Show more
Usnea is a lichen of Usnea diffracta Vain and Usnea longissima Ach, which belongs to the genus Usnea Adans of Usneaceae. Usnea exerts numerous pharmacological activities, while its lipid regulatory activities remain unreported. This study aims to evaluate the effects of aqueous and ethanol extracts of Usnea on the regulation of lipid metabolism and to explore the possible mechanism. Hyperlipidemia rat model was established by feeding with high-fat diet for 45days. Therapy rats were intragastrically administered with simvastatin (0.004g/kg/d), Usnea aqueous extract (2.766g/kg/d), or Usnea ethanol extract (2.766g/kg/d) for 20days. Pharmacodynamic effects, including body weight, serum and liver lipid levels, total bile acid (TBA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), liver index, and hepatic morphological changes were evaluated. To explore the mechanisms, the lipase activities and protein expressions related to lipid metabolism were detected. Compared with the model group, aqueous and ethanol extracts of Usnea can slow down the weight gain of rats, significantly reduce the serum levels of total cholesterol, triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and the liver contents of TG, LDL-C, as well as significantly increase the contents of high-density lipoprotein cholesterol in serum. In addition, aqueous and ethanol extracts of Usnea can significantly reduce the serum contents of AST and ALT. Furthermore, ethanol extract of Usnea can also significantly reduce the TBA content in serum and liver index. Liver tissue pathological observation showed that aqueous and ethanol extracts of Usnea can improve cell degeneration to a certain extent. Aqueous and ethanol extracts of Usnea can significantly reduce sterol regulatory element-binding proteins-1c, and liver X receptor α (LXR-α) protein expressions. Furthermore, aqueous extract of Usnea can significantly increase hepatic lipase activity and promote apoprotein A5 (ApoA5) protein expression. These findings strongly suggest that the aqueous and ethanol extracts of Usnea play significant roles in regulating lipid metabolism, and the ethanol extract exhibits higher activity than the aqueous extract. The mechanism of the regulation of lipid metabolism by Usnea aqueous extract may involve the increased ApoA5 protein expression via inhibition of the LXR-α signal pathway; however, the mechanism of the regulation of lipid metabolism by Usnea ethanol extract remains to be further studied. Show less
no PDF DOI: 10.1016/j.biopha.2017.08.012
APOA5

Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF-1α synthesis, and decreases breast cancer metastasis.

Zhonghong Wei, Yunlong Shan, Li Tao +7 more · 2017 · Molecular carcinogenesis · Wiley · added 2026-04-24
Intratumoral hypoxia promotes the distant metastasis of cancer subclones. The clinical expression level of hypoxia-inducible factor-1α (HIF-1α) reflects the prognosis of a variety of cancers, especial Show more
Intratumoral hypoxia promotes the distant metastasis of cancer subclones. The clinical expression level of hypoxia-inducible factor-1α (HIF-1α) reflects the prognosis of a variety of cancers, especially breast cancer. Histone deacetylase (HDAC) inhibitors can target HIF-1α protein due to von Hippel-Lindau (VHL) protein-dependent degradation. Dietary organosulfur compounds, such as those in garlic, have been reported as HDAC inhibitors. The effects of diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS) on the ratio of firefly/Renilla luciferase activity in hypoxic MDA-MB-231 cells were determined. The mRNA expressions of HIF-1α target genes ANGPTL4, LOXL4, and LOX in hypoxic MDA-MB-231 cells were significantly down-regulated by DATS. DATS attenuated the metastatic potential of MDA-MB-231 cells in hypoxia-induced embryonic zebrafish, xenograft, and orthotopic tumors. Endothelial cell-cancer cell adhesion, wound healing, transwell, and tube formation assays showed that DATS dose-dependently inhibited the migration and angiogenesis of MDA-MB-231 cells in vitro. The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS. DATS dose-dependently inhibited HIF-1α transcriptional activity and hypoxia-induced hematogenous metastasis of MDA-MB-231 cells. It reduced the protein expression of HIF-1α, which did not involve inhibition of HIF-1α mRNA expression or ubiquitin proteasome degradation. Efficient inhibition of HIF-1α expression was required for DATS to resist breast cancer. Show less
no PDF DOI: 10.1002/mc.22686
ANGPTL4

FADS1 rs174549 Polymorphism May Predict a Favorable Response to Chemoradiotherapy in Oral Cancer Patients.

Fa Chen, Baochang He, Lingjun Yan +3 more · 2017 · Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · Elsevier · added 2026-04-24
The fatty acid desaturase 1 (FADS1) gene variant is a novel susceptibility marker for laryngeal squamous cell carcinoma identified by a recent genome-wide association study, but it is still unclear wh Show more
The fatty acid desaturase 1 (FADS1) gene variant is a novel susceptibility marker for laryngeal squamous cell carcinoma identified by a recent genome-wide association study, but it is still unclear whether this genetic variant continues to influence oral cancer recurrence or death. The purpose of this study was to evaluate the role of FADS1 rs174549 polymorphism and its interaction with postoperative chemoradiotherapy in the prognosis of oral cancer. A prospective cohort study involving 304 oral cancer patients with surgical resection was conducted in Fujian, China. Demographic and clinical data (adjuvant therapy types, histologic types, clinical stage, etc.) were extracted from medical records, and follow-up data were obtained by telephone interviews. We collected 5 to 8 mL of venous blood from all patients for DNA extraction, and rs174549 genotypes were determined by TaqMan assays (Life Technologies, Carlsbad, CA). A Cox proportional hazards model and Kaplan-Meier curve were used to assess the association between FADS1 rs174549 polymorphism and progression-free survival (PFS), as well as overall survival, in oral cancer. Carrying the AA genotype was significantly associated with a decreased risk of PFS: The hazard ratio was 0.52 (95% confidence interval, 0.29 to 0.93) for the codominant model and 0.54 (95% confidence interval, 0.31 to 0.94) for the recessive model. Moreover, better PFS was particularly obvious in patients who had received chemoradiotherapy. A positive multiplicative interaction between FADS1 rs174549 polymorphism and chemoradiotherapy was observed for PFS (P = .036). No significant association was found between FADS1 rs174549 polymorphism and overall survival. Our study suggests, for the first time, that FADS1 rs174549 polymorphism is a potentially independent and favorable factor in predicting oral cancer PFS especially for patients who undergo chemoradiotherapy, and it may serve as a potential target for individualized treatment in the future. Show less
no PDF DOI: 10.1016/j.joms.2016.07.005
FADS1

[MACF1 knockdown in glioblastoma multiforme cells increases temozolomide-induced cytotoxicity].

Si-di Xie, Zi-Yang Chen, Hai Wang +6 more · 2017 · Nan fang yi ke da xue xue bao = Journal of Southern Medical University · added 2026-04-24
To investigate the role of microtubule-actin crosslinking factor 1 (MACF1) in the response of glioma cells to temozolomide (TMZ). TMZ was applied to a human gliomablastoma cell line (U87) and changes Show more
To investigate the role of microtubule-actin crosslinking factor 1 (MACF1) in the response of glioma cells to temozolomide (TMZ). TMZ was applied to a human gliomablastoma cell line (U87) and changes in the protein expression and cellular localization were determined with Western blot, RT-PCR, and immunofluorescence. The responses of the cells with MACF1 expression knockdown by RNA interference to TMZ were assessed. TMZ-induced effects on MACF1 expression were also assessed by immunohistochemistry in a nude mouse model bearing human glioblastoma xenografts. TMZ resulted in significantly increased MACF1 expression (by about 2 folds) and changes in its localization in the gliomablastoma cells both in vitro and in vivo (P<0.01). Knockdown of MACF1 reduced the proliferation (by 45%) of human glioma cell lines treated with TMZ (P<0.01). TMZ-induced changes in MACF1 expression was accompanied by cytoskeletal rearrangement. MACF1 may be a potential therapeutic target for glioblastoma. Show less
no PDF DOI: 10.3969/j.issn.1673-4254.2017.09.07
MACF1

Association of BTBD9 and MAP2K5/SKOR1 With Restless Legs Syndrome in Chinese Population.

Gen Li, Huidong Tang, Cheng Wang +4 more · 2017 · Sleep · Oxford University Press · added 2026-04-24
The aim of the study was to investigate the relationship between genetic factors and primary restless legs syndrome (RLS) in Chinese population. A total of 116 RLS patients and 200 controls were recru Show more
The aim of the study was to investigate the relationship between genetic factors and primary restless legs syndrome (RLS) in Chinese population. A total of 116 RLS patients and 200 controls were recruited and the diagnosis of RLS was based on the criteria of International RLS Study Group. Polymer chain reaction (PCR) and sequencing were used to detect 19 single nucleotide polymorphisms (SNPs) in six genetic loci (MEIS1, BTBD9, PTPRD, MAP2K5/SKOR1, TOX3, and Intergenic region of 2p14). Our study found that one SNP increased the risk of RLS in Chinese population: rs6494696 of MAP2K5/SKOR1 (odds ratio [OR] = 0.09, p < .0001, recessive model). A further meta-analysis of RLS in Asian population found that two SNPs of BTBD9 increased the risk of RLS: rs9296249 of BTBD9 (OR = 1.44, p = .000, T allele), rs9357271 of BTBD9 (OR = 1.38, p = .021, dominant model). Our results confirmed the association of BTBD9 and MAP2K5/SKOR1 with primary RLS in Chinese population. Show less
no PDF DOI: 10.1093/sleep/zsx028
MAP2K5

The role of lncRNA MALAT1 in the regulation of hepatocyte proliferation during liver regeneration.

Cuicui Li, Lei Chang, Zhiquan Chen +3 more · 2017 · International journal of molecular medicine · added 2026-04-24
Exploring the biological functions of long non-coding RNAs (lncRNAs) has come to the foreground in recent years. Studies have indicated that the lncRNA metastasis‑associated lung adenocarcinoma transc Show more
Exploring the biological functions of long non-coding RNAs (lncRNAs) has come to the foreground in recent years. Studies have indicated that the lncRNA metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) not only regulates tumorigenesis in hepatocellular carcinoma, but also controls cell cycle progression in hematopoietic cells. The present study was designed to investigate the biological role of lncRNA MALAT1 in liver regeneration. We carried out a series of assays during liver regeneration following 2/3 partial hepatectomy in mice. We explored the functions of lncRNA MALAT1 with a series of functional analyses in vitro. We found that MALAT1 was upregulated during liver regeneration. Moreover, MALAT1 accelerated hepatocyte proliferation by stimulating cell cycle progression from the G1 to the S phase and inhibiting apoptosis in vitro. In addition, our findings also demonstrated that MALAT1 was regulated by p53 during liver regeneration, and that p53 may be a key upstream regulator of MALAT1 activity. Mechanistically, we found that MALAT1 activated the Wnt/β‑catenin pathway by inhibiting the expression of Axin1 and adenomatous polyposis coli (APC), and subsequently promoting the expression of cyclin D1. On the whole, the findings of this study suggest that MALAT1 is a critical molecule for liver regeneration. Pharmacological interventions targeting MALAT1 may thus prove to be therapeutically beneficial in liver failure or liver transplantation by promoting liver regeneration. Show less
📄 PDF DOI: 10.3892/ijmm.2017.2854
AXIN1

Association of the S2 allele of the SstI polymorphism in the apoC3 gene with plasma apoCIII interacts with unfavorable lipid profiles to contribute to atherosclerosis in the Li ethnic group in China.

Minzeng Sun, Lin Chen, Hui Liu +3 more · 2017 · Lipids in health and disease · BioMed Central · added 2026-04-24
The SstI polymorphism in the apolipoprotein 3 gene (apoC3) has been identified in many ethnic groups. In addition, the S2 allele of the SstI polymorphism is shown to be associated with increased plasm Show more
The SstI polymorphism in the apolipoprotein 3 gene (apoC3) has been identified in many ethnic groups. In addition, the S2 allele of the SstI polymorphism is shown to be associated with increased plasma triglyceride (TG) levels. Plasma apoCIII is an important atherogenic factor, which interrupts lipid metabolism and is positively associated with plasma TG levels. However, the existence of the SstI polymorphism in the Li ethnic group in China remains to be confirmed. The relationship between the S2 allele of the SstI polymorphism and plasma apoCIII or TG and their roles in atherosclerosis are also unknown. A cohort of 628 participants was recruited (316 atherosclerotic patients and 312 healthy controls) from both the Li and Han ethnic groups. Blood samples were obtained to evaluate the SstI polymorphism in the apoC3 and lipid profiles. Chi-squared and t-tests and multiple unconditional logistic regression were employed to analyze the genotypic and allelic frequencies and lipid profiles using SPSS version 20.0 software. The SstI polymorphism in the apoC3 was identified in the Li ethnic group. The S2 allele and plasma apoCIII and TG levels were associated with the development of atherosclerosis (P < 0.01, S2 allele and apoCIII; P < 0.05, TG) in the Li ethnic group. The S2 allele was associated with increased plasma apoCIII levels in the atherosclerotic group (P < 0.01), but with increased plasma apoCIII and TG levels in control group (both P < 0.01). In addition to the increases in the S2 allele frequency and plasma TG and apoCIII levels, atherosclerotic patients in the Li ethnic group also exhibited increased apoB, decreased HDL-C and apoAI and a lower apoAI:apoB ratio (all P < 0.01). Our results indicate that the S2 allele of the SstI polymorphism in the apoC3 gene is associated with plasma apoCIII levels in the Li population. In combination with unfavorable lipid profiles, this might contribute to susceptibility to atherosclerosis. Show less
📄 PDF DOI: 10.1186/s12944-017-0614-3
APOC3

FADS Gene Polymorphisms, Fatty Acid Desaturase Activities, and HDL-C in Type 2 Diabetes.

Meng-Chuan Huang, Wen-Tsan Chang, Hsin-Yu Chang +5 more · 2017 · International journal of environmental research and public health · MDPI · added 2026-04-24
Polyunsaturated fatty acids (PUFA) correlate with risk of dyslipidemia and cardiovascular diseases. Fatty acid desaturase (
📄 PDF DOI: 10.3390/ijerph14060572
FADS1

Inhibition Role of Atherogenic Diet on Ethyl Carbamate Induced Lung Tumorigenesis in C57BL/6J Mice.

Ting Chen, Lei Lu, Cai Xu +5 more · 2017 · Scientific reports · Nature · added 2026-04-24
With emerging evidence connecting cholesterol dysregulation with disturbed pulmonary homeostasis, we are wondering if diet induced hypercholesterolemia would influence the susceptibility to chemical i Show more
With emerging evidence connecting cholesterol dysregulation with disturbed pulmonary homeostasis, we are wondering if diet induced hypercholesterolemia would influence the susceptibility to chemical induced lung tumorigenesis in mice. Six to eight week-old male C57BL/6J mice were fed with either a high-cholesterol atherogenic diet (HCD) or matching normal diet (ND), respectively. Following 3 weeks diet adapting, a multi-dose intraperitoneal injections of ethyl carbamate (urethane, 1 g/kg body weight) were established and lung tumorigenesis assessments were taken after 15 weeks latency period. Compared to the urethane treated ND-fed mice, the HCD-fed mice exhibited significantly decreased lung tumor multiplicity and attenuated pulmonary inflammation, which including reduced influx of leukocytes and down regulated tumor-promoting cyto-/chemokine profile in bronchoalveolar lavage fluid, decreased TLR2/4 expression and NF-κB activation in the lung. As a sensor regulating intracellular cholesterol homeostasis, nuclear receptor LXR-α was up-regulated significantly in the urethane treated HCD-fed mice lungs compared to the ND-fed mice lungs, accompanied with decreased pulmonary free cholesterol content and suppressed tumor cell proliferation. These results suggested that intrapulmonary cholesterol homeostasis, other than systematic cholesterol level, is important in lung tumorigenesis, and LXR activation might partly contribute to the inhibitory role of atherogenic diet on lung tumorigenesis. Show less
no PDF DOI: 10.1038/s41598-017-05053-1
NR1H3

Proteome-based identification of apolipoprotein A-IV as an early diagnostic biomarker in liver fibrosis.

Pei-Wen Wang, Yu-Ching Hung, Tung-Ho Wu +3 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
Hepatic fibrosis may ultimately result in organ failure and death, a reality compounded by the fact that most drugs for liver fibrosis appear to be effective only if given as a prophylactic or early t Show more
Hepatic fibrosis may ultimately result in organ failure and death, a reality compounded by the fact that most drugs for liver fibrosis appear to be effective only if given as a prophylactic or early treatment. In a dimethylnitrosamine-induced liver fibrotic model, aspartate aminotransferase/alanine aminotransferase levels could not precisely distinguish the differences between the initial stage of liver fibrosis and normal control, whereas histological examination indicated that dimethylnitrosamine treatment for two weeks has resulted in hepatic fibrogenesis. Comprehensive proteomics identified 12 proteins mainly associated with the interleukin 6-stimulated inflammatory pathway. Coordinately, cytokine profiles showed that dimethylnitrosamine administration would stimulate various signaling pathways leading to liver fibrosis. Of note, apolipoprotein A4 in serum samples obtained from patients in the early stage of liver fibrosis were significantly increased compared to the healthy controls ( Show less
📄 PDF DOI: 10.18632/oncotarget.21627
APOA4

Vitamin D receptor is a novel transcriptional regulator for Axin1.

Dapeng Jin, Yong-Guo Zhang, Shaoping Wu +6 more · 2017 · The Journal of steroid biochemistry and molecular biology · Elsevier · added 2026-04-24
Axin1 is a scaffold protein in the β-catenin destruction complex, which, if disrupted, contributes to pathogenesis of various human diseases, including colorectal carcinogenesis and inflammatory bowel Show more
Axin1 is a scaffold protein in the β-catenin destruction complex, which, if disrupted, contributes to pathogenesis of various human diseases, including colorectal carcinogenesis and inflammatory bowel diseases (IBD). We have previously demonstrated that Salmonella infection promotes the degradation and plasma sequestration of Axin1, leading to bacterial invasiveness and inflammatory responses. Vitamin D and the vitamin D receptor (VDR) appear to be important regulators of IBD and colon cancer. Although VDR and Axin1 are all involved in intestinal inflammation, it remains unclear whether these processes are related or function independently. In the current study, we hypothesize that VDR is an important regulator for the maintenance of physiological level of Axin1. Using the intestinal epithelial conditional VDR knockout mouse model (VDR We found that VDR deletion led to lower protein and mRNA levels of Axin1, whereas knockdown of Axin1 did not change the expression level of VDR protein. Immunoprecipitation data did not support physical interaction between VDR and Axin1. The VDR regulation of Axin1 was through a VDR genomic binding site for Axin1 gene on the regulatory region. Fractionation data showed that cytosolic Axin1 was significantly reduced due to VDR deletion, leaving the nuclear fraction unchanged. In ileum, Axin1 was distributed in the cytosol of apical epithelium and crypts. VDR is important for the maintenance of physiological level of Axin1. The discovery of Axin1 as a VDR target gene provides novel and fundamental insights into the interactions between the VDR and β-catenin signaling pathways. Show less
📄 PDF DOI: 10.1016/j.jsbmb.2016.09.002
AXIN1

Fragment-based design, synthesis, biological evaluation, and SAR of 1H-benzo[d]imidazol-2-yl)-1H-indazol derivatives as potent PDK1 inhibitors.

Ting Chen, Venkataswamy Sorna, Susie Choi +7 more · 2017 · Bioorganic & medicinal chemistry letters · Elsevier · added 2026-04-24
In this work, we describe the use of the rule of 3 fragment-based strategies from biochemical screening data of 1100 in-house, small, low molecular weight fragments. The sequential combination of in s Show more
In this work, we describe the use of the rule of 3 fragment-based strategies from biochemical screening data of 1100 in-house, small, low molecular weight fragments. The sequential combination of in silico fragment hopping and fragment linking based on S160/Y161/A162 hinge residues hydrogen bonding interactions leads to the identification of novel 1H-benzo[d]imidazol-2-yl)-1H-indazol class of Phosphoinositide-Dependent Kinase-1 (PDK1) inhibitors. Consequent SAR and follow-up screening data led to the discovery of two potent PDK1 inhibitors: compound 32 and 35, with an IC Show less
no PDF DOI: 10.1016/j.bmcl.2017.10.041
DUSP6

[Gene Analysis for the Sudden Death of Hypertrophic Cardiomyopathy by Whole Exome Sequencing.].

C C Xu, Y Z Bai, X S Xu +5 more · 2017 · Fa yi xue za zhi · added 2026-04-24
To analyze the related pathogenicity gene mutations in a sudden death of hypertrophic cardiomyopathy （HCM） on whole exome level. Whole exome sequencing （WES） was been performed on a sudden death case Show more
To analyze the related pathogenicity gene mutations in a sudden death of hypertrophic cardiomyopathy （HCM） on whole exome level. Whole exome sequencing （WES） was been performed on a sudden death case sample with pathological features of HCM by Illumina® Hiseq 2500 platform. Using hg19 as the reference sequences, the sequencing data were analyzed. Suspicious single nucleotide variants （SNV） were screened, and the conservatism and function were analyzed by the software such as PhyloP, PolyPhen-2, SIFT, etc. After screening, a heterozygous mutation C719R was finally identified in the gene The molecular anatomy on whole exome level by second generation sequencing technology can help to define the molecular mechanism of HCM and provide a new mothed and thought for analysis of death cause. Show less
no PDF DOI: 10.3969/j.issn.1004-5619.2017.04.001
MYBPC3

Human microcephaly protein RTTN interacts with STIL and is required to build full-length centrioles.

Hsin-Yi Chen, Chien-Ting Wu, Chieh-Ju C Tang +3 more · 2017 · Nature communications · Nature · added 2026-04-24
Mutations in many centriolar protein-encoding genes cause primary microcephaly. Using super-resolution and electron microscopy, we find that the human microcephaly protein, RTTN, is recruited to the p Show more
Mutations in many centriolar protein-encoding genes cause primary microcephaly. Using super-resolution and electron microscopy, we find that the human microcephaly protein, RTTN, is recruited to the proximal end of the procentriole at early S phase, and is located at the inner luminal walls of centrioles. Further studies demonstrate that RTTN directly interacts with STIL and acts downstream of STIL-mediated centriole assembly. CRISPR/Cas9-mediated RTTN gene knockout in p53-deficient cells induce amplification of primitive procentriole bodies that lack the distal-half centriolar proteins, POC5 and POC1B. Additional analyses show that RTTN serves as an upstream effector of CEP295, which mediates the loading of POC1B and POC5 to the distal-half centrioles. Interestingly, the naturally occurring microcephaly-associated mutant, RTTN (A578P), shows a low affinity for STIL binding and blocks centriole assembly. These findings reveal that RTTN contributes to building full-length centrioles and illuminate the molecular mechanism through which the RTTN (A578P) mutation causes primary microcephaly.Mutations in many centriolar protein-encoding genes cause primary microcephaly. Here the authors show that human microcephaly protein RTTN directly interacts with STIL and acts downstream of STIL-mediated centriole assembly, contributing to building full-length centrioles. Show less
no PDF DOI: 10.1038/s41467-017-00305-0
POC5

Genetic Polymorphisms in Estrogen Metabolic Pathway Associated with Risks of Alzheimer's Disease: Evidence from a Southern Chinese Population.

Lu Hua Chen, Yan Hui Fan, Patrick Yu Ping Kao +4 more · 2017 · Journal of the American Geriatrics Society · Blackwell Publishing · added 2026-04-24
To investigate whether genetic variations on the estrogen metabolic pathway would be associated with risk of Alzheimer's disease (AD). Cross-sectional study. Individuals were recruited at the Memory C Show more
To investigate whether genetic variations on the estrogen metabolic pathway would be associated with risk of Alzheimer's disease (AD). Cross-sectional study. Individuals were recruited at the Memory Clinic, Queen Mary Hospital, Hong Kong. Chinese individuals with (n = 426) and without (n = 350) AD. All subjects underwent a standardized cognitive assessment and genotyping of four candidate genes on the estrogen metabolic pathway (estrogen receptor α gene (ESR1), estrogen receptor β gene (ESR2), cytochrome P450 19A1 gene (CYP19A1), cytochrome P450 11A1 gene (CYP11A1)). Apart from consistent results showing an association between apolipoprotein (APO)E and AD, strong evidence of disease associations were found for polymorphisms in ESR2 and CYP11A1 based on the entire data set. For ESR2, significant protective effects were found for A alleles of rs4986938 (permuted P = .02) and rs867443 (permuted P = .02). For CYP11A1, significant risk effects were found for G alleles of rs11638442 (permuted P = .03) and rs11632698 (permuted P = .03). Stratifying subjects according to APOE ε4 status, their genetic effects continued to be significant in the APOE ε4-negative subgroup. Associations between CYP11A1 polymorphisms (rs2279357, rs2073475) and risk of AD were detected in women but not men. Further gene-level analysis confirmed the above association between ESR2 and CYP11A1, and pathway-level analysis highlighted the genetic effect of the estrogen metabolic pathway on disease susceptibility (permuted pathway-level P = .03). Consistent with previous biological findings for sex steroid hormones in the central nervous system, genetic alterations on the estrogen metabolic pathway were revealed in the Chinese population. Confirmation of these present findings in an independent population is warranted to elucidate disease pathogenesis and to explore the potential of hormone therapy in the treatment of AD. Show less
no PDF DOI: 10.1111/jgs.14537
APOA4

Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.

Dongyin Chen, Xin Huang, Hongwen Zhou +10 more · 2017 · European journal of medicinal chemistry · Elsevier · added 2026-04-24
A series of pentacyclic triterpene 3β-ester derivatives were designed, synthesized and evaluated as a new class of cholesteryl ester transfer protein (CETP) inhibitors for the treatment of dyslipidemi Show more
A series of pentacyclic triterpene 3β-ester derivatives were designed, synthesized and evaluated as a new class of cholesteryl ester transfer protein (CETP) inhibitors for the treatment of dyslipidemia. In vitro screening assay showed that 5 out of 30 compounds displayed moderate inhibiting human CETP activity with IC Show less
no PDF DOI: 10.1016/j.ejmech.2017.08.012
CETP

Biomimetic tendon extracellular matrix composite gradient scaffold enhances ligament-to-bone junction reconstruction.

Huanhuan Liu, Long Yang, Erchen Zhang +11 more · 2017 · Acta biomaterialia · Elsevier · added 2026-04-24
Management of ligament/tendon-to-bone-junction healing remains a formidable challenge in the field of orthopedic medicine to date, due to deficient vascularity and multi-tissue transitional structure Show more
Management of ligament/tendon-to-bone-junction healing remains a formidable challenge in the field of orthopedic medicine to date, due to deficient vascularity and multi-tissue transitional structure of the junction. Numerous strategies have been employed to improve ligament-bone junction healing, including delivery of stem cells, bioactive factors, and synthetic materials, but these methods are often inadequate at recapitulating the complex structure-function relationships at native tissue interfaces. Here, we developed an easily-fabricated and effective biomimetic composite to promote the regeneration of ligament-bone junction by physically modifying the tendon extracellular matrix (ECM) into a Random-Aligned-Random composite using ultrasound treatment. The differentiation potential of rabbit bone marrow stromal cells on the modified ECM were examined in vitro. The results demonstrated that the modified ECM enhanced expression of chondrogenesis and osteogenesis-associated epigenetic genes (Jmjd1c, Kdm6b), transcription factor genes (Sox9, Runx2) and extracellular matrix genes (Col2a1, Ocn), resulting in higher osteoinductivity than the untreated tendon ECM in vitro. In the rabbit anterior cruciate ligament (ACL) reconstruction model in vivo, micro-computed tomography (Micro-CT) and histological analysis showed that the modified Random-Aligned-Random composite scaffold enhanced bone and fibrocartilage formation at the interface, more efficaciously than the unmodified tendon ECM. Therefore, these results demonstrated that the biomimetic Random-Aligned-Random composite could be a promising scaffold for ligament/tendon-bone junction repair. The native transitional region consists of several distinct yet contiguous tissue regions, composed of soft tissue, non-calcified fibrocartilage, calcified fibrocartilage, and bone. A stratified graft whose phases are interconnected with each other is essential for supporting the formation of functionally continuous multi-tissue regions. Various techniques have been attempted to improve adherence of the ligament/tendon graft to bone, including utilization of stem cells, growth factors and biomaterials, but these methods are often inadequate at recapitulating the complex structure-function relationships at native tissue interfaces. Here, we developed an easily-fabricated and effective biomimetic composite to promote the regeneration of ligament-bone junction by physically modifying the tendon extracellular matrix (ECM) into a Random-Aligned-Random composite using ultrasound treatment. The modified ECM enhanced expression of chondrogenesis and osteogenesis-associated epigenetic genes expression in vitro. In the rabbit anterior crucial ligament reconstruction model in vivo, results showed that the modified Random-Aligned-Random composite enhances the bone and fibrocartilage formation in the interface, proving to be more efficient than the unmodified tendon ECM. Therefore, these results demonstrated that the biomimetic Random-Aligned-Random composite could be a promising scaffold for ligament/tendon-bone junction repair. Show less
no PDF DOI: 10.1016/j.actbio.2017.05.027
JMJD1C

Metformin improves nonalcoholic fatty liver disease in obese mice via down-regulation of apolipoprotein A5 as part of the AMPK/LXRα signaling pathway.

Min-Jie Lin, Wen Dai, Melanie J Scott +5 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
Apolipoprotein A5 (apoA5) has been implicated in the formation of hepatocyte lipid droplets, a histological hallmark of non-alcoholic fatty liver disease (NAFLD). Recent evidence demonstrated that liv Show more
Apolipoprotein A5 (apoA5) has been implicated in the formation of hepatocyte lipid droplets, a histological hallmark of non-alcoholic fatty liver disease (NAFLD). Recent evidence demonstrated that liver X receptor α (LXRα), a transcription factor involved in down-regulation of Show less
📄 PDF DOI: 10.18632/oncotarget.22163
APOA5

YAP promotes myogenic differentiation

Ting-Huan Chen, Chen-Yu Chen, Hui-Chin Wen +4 more · 2017 · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · added 2026-04-24
Yes-associated protein (YAP) is a transcriptional coactivator in the Hippo pathway that regulates cell proliferation, differentiation, and apoptosis. The MEK5/ERK5 MAPK cascade is essential for the ea Show more
Yes-associated protein (YAP) is a transcriptional coactivator in the Hippo pathway that regulates cell proliferation, differentiation, and apoptosis. The MEK5/ERK5 MAPK cascade is essential for the early step of myogenesis. In this study, we generated C2C12 stable cell lines that expressed YAP (C2C12-YAP cells) and found that ERK5 and MEK5 were activated in C2C12-YAP cells compared with control C2C12 (C2C12-vector) cells. C2C12-YAP stable cells also differentiated into myotubes better than C2C12-vector cells, and expressed elevated levels of myogenin, a transcription factor that regulates myogenesis, as well as elevated levels of myosin heavy chain, a skeletal muscle marker. Western blot analysis revealed that Src and c-Abl (Abelson murine leukemia viral oncogene homolog 1) activation were enhanced in C2C12-YAP cells. Conversely, treatment of inhibitors of c-Abl, Src, or MEK5 inhibited activation of MEK5 and ERK5 and myogenesis of C2C12 myoblasts. Specific interactions between YAP and proteins in the ERK5 pathway, such as MEK kinase 3 (MEKK3) and ERK5, were illustrated by coimmunoprecipitation experiments. MEKK3 contains the PPGY motif (aa 178-181), which may interact with YAP. Site-directed mutagenesis experiments revealed that expression of MEKK3 Y181F mutant inhibited MEK5/ERK5 activation and myogenic differentiation. These results suggest that YAP promotes muscle differentiation by activating the Abl/Src/MEKK3/MEK5/ERK5 kinase cascade.-Chen, T.-H., Chen, C.-Y., Wen, H.-C., Chang, C.-C., Wang, H.-D., Chuu, C.-P., Chang, C.-H. YAP promotes myogenic differentiation Show less
no PDF DOI: 10.1096/fj.201601090R
MAP2K5

The Nogo receptor inhibits proliferation, migration and axonal extension by transcriptionally regulating WNK1 in PC12 cells.

Tao Yang, Kai Zhao, Haifeng Shu +6 more · 2017 · Neuroreport · added 2026-04-24
Neuronal regeneration and axonal regrowth mechanisms in the injured mammalian central nervous system are largely unknown. As part of a major pathway for inhibiting axonal regeneration, activated neuro Show more
Neuronal regeneration and axonal regrowth mechanisms in the injured mammalian central nervous system are largely unknown. As part of a major pathway for inhibiting axonal regeneration, activated neuronal glycosylphosphatidylinositol-anchored Nogo receptor (NgR) interacts with LINGO-1 and p75NTR to form a complex at the cell surface. However, it was found in our previous report that upregulation of NgR stimulated by injury plays a key role in neuronal regeneration in the neonatal cortex freeze-lesion model, but its downstream signalling remains elusive. In the present study, the novel regulatory role of NgR in a serine-threonine kinase WNK1 was identified. NgR's transcriptional regulation of WNK1 was identified by RT-qPCR and semiquantitative western blot after the overexpression or knockdown of NgR, and the regulation is specific to WNK1, which is not the same for its family members, WNK2, WNK3 and WNK4. Furthermore, NgR inhibition by NEP fails to affect WNK1, which indicates that WNK1 functions outside of the Nogo-A/NgR pathway. By performing a proliferation, migration and axonal extension assay, we also identified that overexpressed NgR critically regulated these processes and impairment by overexpressing NgR was rescued with coexpression of WNK1, indicating the partial role of WNK1 in NgR-mediated morphological regulation. Our study identifies a separation of functions for the NgR-regulated WNK1 in mediating proliferation, migration and axonal extension in PC12 cells as well as a specific regulatory role between NgR and WNK1 that is important for recovery from central nervous system injury. Show less
no PDF DOI: 10.1097/WNR.0000000000000800
LINGO1

Endothelial Cells Promote Formation of Medulloblastoma Stem-Like Cells via Notch Pathway Activation.

Yong Wang, Yushe Wang, Hang Chen +1 more · 2017 · Journal of molecular neuroscience : MN · Springer · added 2026-04-24
The aim of the study is to investigate whether endothelial cells (ECs) promoted the capacity of stem-like cell formation in medulloblastoma (MB) and whether the mechanism of action was associated with Show more
The aim of the study is to investigate whether endothelial cells (ECs) promoted the capacity of stem-like cell formation in medulloblastoma (MB) and whether the mechanism of action was associated with mediation of Notch signaling pathway. Co-culture experiment was conducted to particularly understand the potential role of ECs in promoting phenotype and gene expression of MB stem-like cells. Self-renewal capacity and tumor cell population were measured by sphere-forming assay and flow cytometry, respectively. To further clarify the effects of ECs on the formation of MB stem-like cells, the expression of genes and protein in MB stem-like cells (CCND1, CDK6, c-MYC, and Bmi-1) and Notch (Notch2, Jagged 1, Hes-1, and Hey-2) was quantified by quantitative real-time PCR (qRT-PCR) and western blot, respectively. Also, observed mediation of ECs in regulation of tumor cell stemness by Notch activation was observed when the co-cultures were treated with γ-secretase inhibitor (N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT)). Further investigation was conducted for the effects of ECs on the tumorigenesis in vivo of MB cells when co-cultures were inoculated into a nude mouse after treated with DAPT. Afterwards, tumor size and volume were measured. The sphere-forming rate and cell ratio of stem-like cells were significantly increased. Furthermore, the expression of genes and protein in stem-like cells and Notch was obviously upregulated although treated with γ-secretase inhibitor. Moreover, tumor size and volume were dramatically magnified. This study revealed that Notch pathway activation played a key role in the formation of stem-like cells in MB and had valuable meaning for further investigation of targeted therapies. Show less
no PDF DOI: 10.1007/s12031-017-0965-2
HEY2

Discovery and fine-mapping of loci associated with MUFAs through trans-ethnic meta-analysis in Chinese and European populations.

Yao Hu, Toshiko Tanaka, Jingwen Zhu +30 more · 2017 · Journal of lipid research · added 2026-04-24
MUFAs are unsaturated FAs with one double bond and are derived from endogenous synthesis and dietary intake. Accumulating evidence has suggested that plasma and erythrocyte MUFA levels are associated Show more
MUFAs are unsaturated FAs with one double bond and are derived from endogenous synthesis and dietary intake. Accumulating evidence has suggested that plasma and erythrocyte MUFA levels are associated with cardiometabolic disorders, including CVD, T2D, and metabolic syndrome (MS). Previous genome-wide association studies (GWASs) have identified seven loci for plasma and erythrocyte palmitoleic and oleic acid levels in populations of European origin. To identify additional MUFA-associated loci and the potential functional variant at each locus, we performed ethnic-specific GWAS meta-analyses and trans-ethnic meta-analyses in more than 15,000 participants of Chinese and European ancestry. We identified novel genome-wide significant associations for vaccenic acid at Show less
📄 PDF DOI: 10.1194/jlr.P071860
FADS1