👤 Di-Long Chen

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2981
Articles
1996
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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, 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, Kaiquan 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

Genetic inactivation of ANGPTL4 improves glucose homeostasis and is associated with reduced risk of diabetes.

Viktoria Gusarova, Colm O'Dushlaine, Tanya M Teslovich +78 more · 2018 · Nature communications · Nature · added 2026-04-24
Angiopoietin-like 4 (ANGPTL4) is an endogenous inhibitor of lipoprotein lipase that modulates lipid levels, coronary atherosclerosis risk, and nutrient partitioning. We hypothesize that loss of ANGPTL Show more
Angiopoietin-like 4 (ANGPTL4) is an endogenous inhibitor of lipoprotein lipase that modulates lipid levels, coronary atherosclerosis risk, and nutrient partitioning. We hypothesize that loss of ANGPTL4 function might improve glucose homeostasis and decrease risk of type 2 diabetes (T2D). We investigate protein-altering variants in ANGPTL4 among 58,124 participants in the DiscovEHR human genetics study, with follow-up studies in 82,766 T2D cases and 498,761 controls. Carriers of p.E40K, a variant that abolishes ANGPTL4 ability to inhibit lipoprotein lipase, have lower odds of T2D (odds ratio 0.89, 95% confidence interval 0.85-0.92, p = 6.3 × 10 Show less
📄 PDF DOI: 10.1038/s41467-018-04611-z
ANGPTL4

Neurexin gene family variants as risk factors for autism spectrum disorder.

Jia Wang, Jianhua Gong, Li Li +7 more · 2018 · Autism research : official journal of the International Society for Autism Research · Wiley · added 2026-04-24
Increasing evidence suggests that abnormal synaptic function leads to neuronal developmental disorders and is an important component of the etiology of autism spectrum disorder (ASD). Neurexins are pr Show more
Increasing evidence suggests that abnormal synaptic function leads to neuronal developmental disorders and is an important component of the etiology of autism spectrum disorder (ASD). Neurexins are presynaptic cell-adhesion molecules that affect the function of synapses and mediate the conduction of nerve signals. Thus, neurexins are attractive candidate genes for autism. Since gene families have greater power to reveal genetic association than single genes, we designed this case-control study to investigate six genetic variants in three neurexin genes (NRXN1, NRXN2, and NRXN3) in a Chinese population including 529 ASD patients and 1,923 healthy controls. We found that two SNPs were significantly associated with ASD after false discovery rate (FDR) adjustment for multiple comparisons. The NRXN2 rs12273892 polymorphism T allele and AT genotype were significantly associated with increased risk of ASD (respectively: OR = 1.328, 95% CI = 1.133-1.557, P < 0.001; OR = 1.528; 95% CI = 1.249-1.868, P < 0.001). The dominant model showed the same association (OR = 1.495, 95% CI = 1.231-1.816, P < 0.001). The NRXN3 rs12879016 polymorphism played a significant role in ASD susceptibility under the dominant model (OR = 0.747, 95% CI= 0.615-0.908, P = 0.023), with the same trend detected for the G allele and GT genotype (respectively: OR = 0.811, 95% CI = 0.699-0.941, P = 0.036; OR = 0.755, 95% CI = 0.615-0.928, P = 0.035). In conclusion, this study supports the importance of two genetic variants in the neurexin gene family in ASD susceptibility in China. Autism Res 2018, 11: 37-43. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is highly heritable, and studies have found a number of candidate genes that might contribute to ASD. Neurexins are presynaptic cell-adhesion molecules that affect the function of synapses and mediate the conduction of nerve signals, and they play an important role in normal brain development and become candidate genes for autism. The purpose of our study is to explore the association between variants of the neurexins gene family and ASD in a Chinese population through a case-control study. Show less
no PDF DOI: 10.1002/aur.1881
NRXN3

Wnt/β-catenin signaling pathway is involved in regulating the migration by an effective natural compound brucine in LoVo cells.

Xianpeng Shi, Man Zhu, Yuan Kang +3 more · 2018 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Colorectal cancer remains the third most common malignancies and migration is one of the main factors for its high mortality rate. Brucine, a natural plant alkaloid, has been proved to possess a varie Show more
Colorectal cancer remains the third most common malignancies and migration is one of the main factors for its high mortality rate. Brucine, a natural plant alkaloid, has been proved to possess a variety of pharmacological functions including anti-tumor activities. The aim of this study was to investigate the inhibitory effect of brucine on the colorectal cancer and the underlying mechanism. In this study, colony formation assay and transwell assay were used to investigate the effect of brucine on LoVo cells viability and migration. Immunofluorescence assay, western blot assay and Gelatin zymography assay were used to study the mechanism of brucine. Xenograft model in nude mice was induced to investigate the in vivo effect of brucine on LoVo cells. Brucine could significantly decrease the viability, inhibit the colony formation and induce the apoptosis of LoVo cells. Brucine could also suppress the migration of LoVo cells in a dose-dependent manner. Western blot analysis elucidated that the inhibition of migration was associated with the decreasing expression of matrix metalloproteinases including MMP2, MMP3 and MMP9. Moreover, we found that treatment of brucine could downregulate the expression of Frizzled-8, Wnt5a, APC and GSNK1A1, and increase the expression of AXIN1. Meanwhile, brucine also decreased the phosphorylation level of LRP5/6 and GSK3β, and increased the level of p-β-catenin. Xenografted model in nude mice study also revealed that oral administration of brucine could inhibit the growth and migration of LoVo cells by activating the expression of AXIN1 and p-β-catenin. Brucine could suppress the migration of the colorectal cancer in vitro and in vivo and the effect was associated with the inhibition of the Wnt/β-catenin signaling pathway. Show less
no PDF DOI: 10.1016/j.phymed.2018.04.019
AXIN1

DLG2, but not TMEM229B, GPNMB, and ITGA8 polymorphism, is associated with Parkinson's disease in a Taiwanese population.

Hsiu-Chuan Wu, Chiung-Mei Chen, Yi-Chun Chen +3 more · 2018 · Neurobiology of aging · Elsevier · added 2026-04-24
Transmembrane or membrane-associated protein dysfunction is increasingly recognized as an important mechanism of pathogenesis in Parkinson's disease (PD). Previous genome-wide association studies and Show more
Transmembrane or membrane-associated protein dysfunction is increasingly recognized as an important mechanism of pathogenesis in Parkinson's disease (PD). Previous genome-wide association studies and their meta-analysis in PD genes have identified several risk foci in transmembrane protein-encoding genes. Herein, we investigated the effect of 4 such PD-associated genetic variants reported in Caucasians, including discs-large membrane-associated guanylate kinase scaffolding protein 2 (DLG2 rs3793947), transmembrane protein 229B (TMEM229B rs1555399), glycoprotein nonmetastatic melanoma protein B (GPNMB rs199347), and integrin subunit alpha 8 (ITGA8 rs7077361). A total of 1185 Taiwanese subjects comprising 592 PD patients and 593 unrelated age-matched controls were genotyped. DLG2 rs3793947 AA genotype showed a significantly lower prevalence in female PD patients compared to the female controls (p = 0.019). The recessive model analysis also demonstrated a reduced PD risk for females in AA genotype (odds ratio = 0.573, 95% confidence interval: 0.379-0.868, p = 0.008). The frequencies of TMEM229B rs1555399 and GPNMB rs199347 genotypes and alleles were similar in PD patients and controls. ITG8 rs7077361 was not polymorphic in all subjects of this study. These data suggested that DLG2, but not TMEM229B, GPNMB, and ITGA8, influenced the risk of PD in Taiwan. Show less
no PDF DOI: 10.1016/j.neurobiolaging.2017.11.016
DLG2

A novel

Zhonghua Chen, Qing Bi, Mingxiang Kong +2 more · 2018 · Oncology letters · added 2026-04-24
Multiple osteochondromas (MO) is an autosomal inherited disease that is characterized by benign bone tumors. However, the underlying mechanism of MO at a molecular level requires further investigation Show more
Multiple osteochondromas (MO) is an autosomal inherited disease that is characterized by benign bone tumors. However, the underlying mechanism of MO at a molecular level requires further investigation. The majority of mutations associated with MO occur in the exostosin glycosyltransferase genes ( Show less
📄 PDF DOI: 10.3892/ol.2018.9248
EXT1

Dual Inhibition of PIK3C3 and FGFR as a New Therapeutic Approach to Treat Bladder Cancer.

Chun-Han Chen, Chun A Changou, Tsung-Han Hsieh +9 more · 2018 · Clinical cancer research : an official journal of the American Association for Cancer Research · added 2026-04-24
no PDF DOI: 10.1158/1078-0432.CCR-17-2066
PIK3C3

Impact of gender and age on the association of the BUD13-ZNF259 rs964184 polymorphism with coronary heart disease.

Xiaofeng Xu, Yirun Li, Yi Huang +10 more · 2018 · Anatolian journal of cardiology · added 2026-04-24
Coronary heart disease (CHD) is the most common cause of death worldwide. This study aimed to validate the association of the rs964184 polymorphism with the CHD risk and included 874 CHD patients and Show more
Coronary heart disease (CHD) is the most common cause of death worldwide. This study aimed to validate the association of the rs964184 polymorphism with the CHD risk and included 874 CHD patients and 776 controls. rs964184 polymorphism genotyping was performed using Tm-shift polymerase chain reaction. A strong association of the rs964184 polymorphism with CHD was found (genotype: X Our results indicate that both gender and age have great impacts on the association of the rs964184 polymorphism with CHD among Chinese. Show less
no PDF DOI: 10.14744/AnatolJCardiol.2017.8002
ZPR1

Association of Genes in the High-Density Lipoprotein Metabolic Pathway with Polypoidal Choroidal Vasculopathy in Asian Population: A Systematic Review and Meta-Analysis.

Ming-Zhen Yuan, Ruo-An Han, Chen-Xi Zhang +1 more · 2018 · Journal of ophthalmology · added 2026-04-24
To assess the association of genes in the high-density lipoprotein metabolic pathway (HDLMP) with polypoidal choroidal vasculopathy (PCV) and the genetic difference in the HDLMP between PCV and age-re Show more
To assess the association of genes in the high-density lipoprotein metabolic pathway (HDLMP) with polypoidal choroidal vasculopathy (PCV) and the genetic difference in the HDLMP between PCV and age-related macular degeneration (AMD). We performed a literature search in EMBASE, PubMed, and Web of Science for genetic studies on 7 single nucleotide polymorphisms (SNPs) from 5 genes in the HDLMP including cholesteryl ester transfer protein (CETP), hepatic lipase (LIPC), lipoprotein lipase (LPL), ATP-binding cassette transporter A1 (ABCA1), and ATP-binding cassette transporter G1 (ABCG1) in PCV. All studies were published before September 30, 2017, without language restriction. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) of each polymorphism were estimated. We also compared the association profiles between PCV and AMD and performed a sensitivity analysis. Our result is based on 43 articles. After excluding duplicates and articles without complete information, 7 studies were applicable to meta-analysis. 7 polymorphisms were meta-analyzed: CETP rs2303790/rs3764261, LIPC rs10468017/rs493258, LPL rs12678919, ABCA1 rs1883025, and ABCG1 rs57137919. We found that in Asian population, CETP rs3764261 (T allele; OR = 1.46; 95% CI: 1.28-1.665, Our study revealed 7 polymorphisms in 5 genes. Among them, CETP (rs3764261/rs2303790) and ABCG1 (rs57137919) were the major susceptibility genes for PCV in Asian population and ABCG1 (rs57137919) showed allelic diversity between PCV and AMD. Since the size for PCV and AMD was small, we need to study these genes genotyping in larger samples. Show less
📄 PDF DOI: 10.1155/2018/9538671
CETP

The Plasma LncRNA Acting as Fingerprint in Hilar Cholangiocarcinoma.

Jian Shi, Xiaohua Li, Fan Zhang +9 more · 2018 · Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · added 2026-04-24
Current studies have indicated that long non-coding RNAs (lncRNAs) could act as tumor biomarkers for disease diagnosis and prognosis prediction. In this study, we mainly focused on determining the exp Show more
Current studies have indicated that long non-coding RNAs (lncRNAs) could act as tumor biomarkers for disease diagnosis and prognosis prediction. In this study, we mainly focused on determining the expression of circulating lncRNAs in patients suffering for hilar cholangiocarcinoma (HC), aiming to reveal the potential lncRNA as a fingerprint. A total 12 lncRNAs were previously proven to be aberrantly expressed in HC tumor tissues. All of the 12 lncRNAs were selected as candidate targets for subsequent circulating lncRNA assay. The candidate lncRNAs were validated by qRT-PCR arranged in training and validation sets. The risk score analysis was employed. Data was presented with receiver operating characteristic curve (ROC). Circulating PCAT1, MALAT1, and CPS1-IT1 were significantly increased in plasma samples of HC patients in both the training set and validation set. Through ROC analysis, we found that the three plasmatic lncRNAs presented the area under ROC curve value (AUC) as 0.784, 0.860, and 0.677. Further combination with the three factors indicated a higher power (AUC, 0.893; sensitivity, 85.5%; specificity, 93.2%). This was the first time to reveal the potential circulating fingerprints for predicting HC. PCAT1, MALAT1, and CPS1-IT1 may act as novel early diagnosis biomarkers for predicting HC. Show less
no PDF DOI: 10.1159/000493613
CPS1

Molecular Mechanistic Insights into Drosophila DHX36-Mediated G-Quadruplex Unfolding: A Structure-Based Model.

Wei-Fei Chen, Stephane Rety, Hai-Lei Guo +8 more · 2018 · Structure (London, England : 1993) · Elsevier · added 2026-04-24
Helicase DHX36 plays essential roles in cell development and differentiation at least partially by resolving G-quadruplex (G4) structures. Here we report crystal structures of the Drosophila homolog o Show more
Helicase DHX36 plays essential roles in cell development and differentiation at least partially by resolving G-quadruplex (G4) structures. Here we report crystal structures of the Drosophila homolog of DHX36 (DmDHX36) in complex with RNA and a series of DNAs. By combining structural, small-angle X-ray scattering, molecular dynamics simulation, and single-molecule fluorescence studies, we revealed that positively charged amino acids in RecA2 and OB-like domains constitute an elaborate structural pocket at the nucleic acid entrance, in which negatively charged G4 DNA is tightly bound and partially destabilized. The G4 DNA is then completely unfolded through the 3'-5' translocation activity of the helicase. Furthermore, crystal structures and DNA binding assays show that G-rich DNA is preferentially recognized and in the presence of ATP, specifically bound by DmDHX36, which may cooperatively enhance the G-rich DNA translocation and G4 unfolding. On the basis of these results, a conceptual G4 DNA-resolving mechanism is proposed. Show less
no PDF DOI: 10.1016/j.str.2018.01.008
DHX36

The long non-coding RNA PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell.

Yetao Xu, Yifan Lian, Yuanyuan Zhang +6 more · 2018 · Journal of cellular and molecular medicine · Blackwell Publishing · added 2026-04-24
Despite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of ev Show more
Despite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of evidence have emphasized long non-coding RNAs (lncRNAs) which function as an innovative regulator of biological behaviour, as exemplified by proliferation, apoptosis and metastasis. However, the role of lncRNAs has not been well described in preeclampsia. Here, we identified a lncRNA, PVT1, whose expression was down-regulated in qRT-PCR analyses in severe preeclampsia. The effects of PVT1 on development were studied after suppression and overexpression of PVT1 in HTR-8/SVneo and JEG3 cells. PVT1 knockdown notably inhibited cell proliferation and stimulated cell cycle accumulation and apoptosis. Exogenous PVT1 significantly increased cell proliferation. Based on analysis of RNAseq data, we found that PVT1 could affect the expression of numerous genes, and then investigated the function and regulatory mechanism of PVT1 in trophoblast cells. Further mechanistic analyses implied that the action of PVT1 is moderately attributable to its repression of ANGPTL4 via association with the epigenetic repressor Ezh2. Altogether, our study suggests that PVT1 could play an essential role in preeclampsia progression and probably acts as a latent therapeutic marker; thus, it might be a useful prognostic marker when evaluating new therapies for patients with preeclampsia. Show less
📄 PDF DOI: 10.1111/jcmm.13405
ANGPTL4

DUSP6 mediates T cell receptor-engaged glycolysis and restrains T

Wei-Chan Hsu, Ming-Yu Chen, Shu-Ching Hsu +10 more · 2018 · Proceedings of the National Academy of Sciences of the United States of America · National Academy of Sciences · added 2026-04-24
Activated T cells undergo metabolic reprogramming and effector-cell differentiation but the factors involved are unclear. Utilizing mice lacking DUSP6 (DUSP6
no PDF DOI: 10.1073/pnas.1800076115
DUSP6

The Role of YB1 in Renal Cell Carcinoma Cell Adhesion.

Yong Wang, Jing Su, Donghe Fu +6 more · 2018 · International journal of medical sciences · added 2026-04-24
no PDF DOI: 10.7150/ijms.25580
NRXN3

MicroRNA-134 Promotes the Development of Atherosclerosis Via the ANGPTL4/LPL Pathway in Apolipoprotein E Knockout Mice.

Qiong Ye, Guo-Ping Tian, Hai-Peng Cheng +17 more · 2018 · Journal of atherosclerosis and thrombosis · added 2026-04-24
Atherosclerosis is the most common cause of cardiovascular disease, such as myocardial infarction and stroke. Previous study revealed that microRNA (miR)-134 promotes lipid accumulation and proinflamm Show more
Atherosclerosis is the most common cause of cardiovascular disease, such as myocardial infarction and stroke. Previous study revealed that microRNA (miR)-134 promotes lipid accumulation and proinflammatory cytokine secretion through angiopoietin-like 4 (ANGPTL4)/lipid lipoprotein (LPL) signaling in THP-1 macrophages. ApoE KO male mice on a C57BL/6 background were fed a high-fat/high-cholesterol Western diet, from 8 to 16 weeks of age. Mice were divided into four groups, and received a tail vein injection of miR-134 agomir, miR-134 antagomir, or one of the corresponding controls, respectively, once every 2 weeks after starting the Western diet. After 8 weeks we measured aortic atherosclerosis, LPL Activity, mRNA and protein levels of ANGPTL4 and LPL, LPL/ low-density lipoprotein receptor related protein 1 Complex Formation, proinflammatory cytokine secretion and lipid levels. Despite this finding, the influence of miR-134 on atherosclerosis in vivo remains to be determined. Using the well-characterized mouse atherosclerosis model of apolipoprotein E knockout, we found that systemic delivery of miR-134 agomir markedly enhanced the atherosclerotic lesion size, together with a significant increase in proinflammatory cytokine secretion and peritoneal macrophages lipid contents. Moreover, overexpression of miR-134 decreased ANGPTL4 expression but increased LPL expression and activity in both aortic tissues and peritoneal macrophages, which was accompanied by increased formation of LPL/low-density lipoprotein receptor-related protein 1 complexes in peritoneal macrophages. However, an opposite effect was observed in response to miR-134 antagomir. These findings suggest that miR-134 accelerates atherogenesis by promoting lipid accumulation and proinflammatory cytokine secretion via the ANGPTL4/LPL pathway. Therefore, targeting miR-134 may offer a promising strategy for the prevention and treatment of atherosclerotic cardiovascular disease. Show less
📄 PDF DOI: 10.5551/jat.40212
ANGPTL4

Upregulation of 24(R/S),25-epoxycholesterol and 27-hydroxycholesterol suppresses the proliferation and migration of gastric cancer cells.

Fenghua Guo, Wenting Hong, Mingjie Yang +4 more · 2018 · Biochemical and biophysical research communications · Elsevier · added 2026-04-24
Gastric cancer (GC) is one of the most common cancers and is the second-leading cause of cancer-associated morbidity worldwide. Oxysterols are oxidized derivatives of cholesterol that may be important Show more
Gastric cancer (GC) is one of the most common cancers and is the second-leading cause of cancer-associated morbidity worldwide. Oxysterols are oxidized derivatives of cholesterol that may be important in many biological processes, but the levels and roles of oxysterols in gastric tumours remain to be elucidated. The levels of cholesterol, oxysterols and sulfated oxysterols in human gastric tumour tissues, adjacent normal mucosal tissues, cancerous gastric juice and gastric juice obtained from healthy subjects were detected by LC-MS. It was found that the levels of 24(R/S),25-EC and 27HC in human gastric tumour tissues and cancerous gastric juice were significantly increased compared with those of adjacent normal mucosal tissues and gastric juice from healthy subjects. Compared with normal gastric mucosal tissue, the levels of sulfated 25-hydroxycholesterol (25HC3S) and the ratio of 25HC3S/25HC were decreased in human gastric tumour tissues, which might be related to the dramatically decreased SULT2A1 expression in gastric tumour tissue. Both 24(R/S),25-EC and 27HC suppressed gastric cancer proliferation, which was not altered by LXRα-siRNA treatment. The suppression of cell proliferation induced by 27HC was attenuated by LXRβ-siRNA, but the suppression of cell proliferation induced by 24(R/S),25-EC was intensified by LXRβ-siRNA. Both 24(R/S),25-EC and 27HC dramatically inhibited HGC-27 cell migration, which was attenuated by the co-transfection of cells with LXRα-siRNA and LXRβ-siRNA, but not LXRα-siRNA or LXRβ-siRNA alone. In conclusion, the accumulated 24(R/S),25-EC and 27HC in human gastric tumour tissues might play important roles in gastric cancer development. Show less
no PDF DOI: 10.1016/j.bbrc.2018.09.058
NR1H3

Genome-wide association study identifies novel susceptibility loci for migraine in Han Chinese resided in Taiwan.

Shih-Pin Chen, Jong-Ling Fuh, Ming-Yi Chung +15 more · 2018 · Cephalalgia : an international journal of headache · SAGE Publications · added 2026-04-24
Background Susceptibility genes for migraine, despite it being a highly prevalent and disabling neurological disorder, have not been analyzed in Asians by genome-wide association study (GWAS). Methods Show more
Background Susceptibility genes for migraine, despite it being a highly prevalent and disabling neurological disorder, have not been analyzed in Asians by genome-wide association study (GWAS). Methods We conducted a two-stage case-control GWAS to identify susceptibility genes for migraine without aura in Han Chinese residing in Taiwan. In the discovery stage, we genotyped 1005 clinic-based Taiwanese migraine patients and 1053 population-based sex-matched controls using Axiom Genome-Wide CHB Array. In the replication stage, we genotyped 27 single-nucleotide polymorphisms with p < 10 Show less
no PDF DOI: 10.1177/0333102417695105
DLG2

Silica-induced initiation of circular ZC3H4 RNA/ZC3H4 pathway promotes the pulmonary macrophage activation.

Xiyue Yang, Jing Wang, Zewei Zhou +8 more · 2018 · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · added 2026-04-24
Phagocytosis of silicon dioxide (SiO
no PDF DOI: 10.1096/fj.201701118R
ZC3H4

MACF1 Overexpression by Transfecting the 21 kbp Large Plasmid PEGFP-C1A-ACF7 Promotes Osteoblast Differentiation and Bone Formation.

Yan Zhang, Chong Yin, Lifang Hu +14 more · 2018 · Human gene therapy · added 2026-04-24
Microtubule actin crosslinking factor 1 (MACF1) is a large spectraplakin protein known to have crucial roles in regulating cytoskeletal dynamics, cell migration, growth, and differentiation. However, Show more
Microtubule actin crosslinking factor 1 (MACF1) is a large spectraplakin protein known to have crucial roles in regulating cytoskeletal dynamics, cell migration, growth, and differentiation. However, its role and action mechanism in bone remain unclear. The present study investigated optimal conditions for effective transfection of the large plasmid PEGFP-C1A-ACF7 (∼21 kbp) containing full-length human MACF1 cDNA, as well as the potential role of MACF1 in bone formation. To enhance MACF1 expression, the plasmid was transfected into osteogenic cells by electroporation in vitro and into mouse calvaria with nanoparticles. Then, transfection efficiency, osteogenic marker expression, calvarial thickness, and bone formation were analyzed. Notably, MACF1 overexpression triggered a drastic increase in osteogenic gene expression, alkaline phosphatase activity, and matrix mineralization in vitro. Mouse calvarial thickness, mineral apposition rate, and osteogenic marker protein expression were significantly enhanced by local transfection. In addition, MACF1 overexpression promoted β-catenin expression and signaling. In conclusion, MACF1 overexpression by transfecting the large plasmid containing full-length MACF1 cDNA promotes osteoblast differentiation and bone formation via β-catenin signaling. Current data will provide useful experimental parameters for the transfection of large plasmids and a novel strategy based on promoting bone formation for prevention and therapy of bone disorders. Show less
no PDF DOI: 10.1089/hum.2017.153
MACF1

A novel index including SNPs for the screening of nonalcoholic fatty liver disease among elder Chinese: A population-based study.

Huanhuan Yang, Guochong Chen, Chunli Song +4 more · 2018 · Medicine · added 2026-04-24
Presently noninvasive methods were employed to the diagnosis of nonalcoholic fatty liver disease (NAFLD), including fatty liver index (FLI), hepatic steatosis index (HSI), product of fasting triglycer Show more
Presently noninvasive methods were employed to the diagnosis of nonalcoholic fatty liver disease (NAFLD), including fatty liver index (FLI), hepatic steatosis index (HSI), product of fasting triglyceride and glucose levels (TyG), and single nucleotide polymorphism (SNP), whereas the accuracy of those indexes need to be improved. Our study aimed to investigate the feasibility of a new index comprehensive index (CI), consisting of 6 serum biomarkers and anthropometric parameters through multivariate logistic regression analysis, to the earlier detection of NAFLD, and the diagnostic value of 5 SNPs (S1: rs2854116 of apolipoprotein C3 [APOC3], S2: rs4149267 of ATP-binding cassette transporter [ABCA1], S3: rs13702 of lipoprotein lipase [LPL], S4: rs738409 of protein 3 [patatin-like phospholipase domain containing protein 3 (PNPLA3)], S5: rs780094 of glucokinase regulatory protein gene [GCKR]) for NAFLD were also explored. Area under the receiver operating characteristic curves (AUROC) and Youden index (YI) were calculated to assess the diagnostic value. The AUROC of CI was higher than FLI, HSI, and TyG (CI: 0.897, FLI: 0.873, HSI: 0.855, TyG: 0.793). Therefore, CI might be a better index for the diagnosis of NAFLD. Although there had no statistical significance (P = .123), the AUROC and YI were increased when CI combined with rs2854116 (S1) (AUROC = 0.902, YI = 0.6844). The combination of CI with S1 showed even better diagnostic accuracy than CI, which suggests the potential value of rs2854116 for the diagnosis of NAFLD. Show less
📄 PDF DOI: 10.1097/MD.0000000000010272
APOC3

Genome-wide analysis of disease progression in age-related macular degeneration.

Qi Yan, Ying Ding, Yi Liu +15 more · 2018 · Human molecular genetics · Oxford University Press · added 2026-04-24
Family- and population-based genetic studies have successfully identified multiple disease-susceptibility loci for Age-related macular degeneration (AMD), one of the first batch and most successful ex Show more
Family- and population-based genetic studies have successfully identified multiple disease-susceptibility loci for Age-related macular degeneration (AMD), one of the first batch and most successful examples of genome-wide association study. However, most genetic studies to date have focused on case-control studies of late AMD (choroidal neovascularization or geographic atrophy). The genetic influences on disease progression are largely unexplored. We assembled unique resources to perform a genome-wide bivariate time-to-event analysis to test for association of time-to-late-AMD with ∼9 million variants on 2721 Caucasians from a large multi-center randomized clinical trial, the Age-Related Eye Disease Study. To our knowledge, this is the first genome-wide association study of disease progression (bivariate survival outcome) in AMD genetic studies, thus providing novel insights to AMD genetics. We used a robust Cox proportional hazards model to appropriately account for between-eye correlation when analyzing the progression time in the two eyes of each participant. We identified four previously reported susceptibility loci showing genome-wide significant association with AMD progression: ARMS2-HTRA1 (P = 8.1 × 10-43), CFH (P = 3.5 × 10-37), C2-CFB-SKIV2L (P = 8.1 × 10-10) and C3 (P = 1.2 × 10-9). Furthermore, we detected association of rs58978565 near TNR (P = 2.3 × 10-8), rs28368872 near ATF7IP2 (P = 2.9 × 10-8) and rs142450006 near MMP9 (P = 0.0006) with progression to choroidal neovascularization but not geographic atrophy. Secondary analysis limited to 34 reported risk variants revealed that LIPC and CTRB2-CTRB1 were also associated with AMD progression (P < 0.0015). Our genome-wide analysis thus expands the genetics in both development and progression of AMD and should assist in early identification of high risk individuals. Show less
no PDF DOI: 10.1093/hmg/ddy002
POC5

G1 and S phase arrest in Candida albicans induces filamentous growth via distinct mechanisms.

Cuilan Chen, Guisheng Zeng, Yue Wang · 2018 · Molecular microbiology · Blackwell Publishing · added 2026-04-24
Candida albicans is an opportunistic fungal pathogen. In immunocompromised individuals, it can cause bloodstream infections with high mortality rates. The ability to switch between yeast and hyphal mo Show more
Candida albicans is an opportunistic fungal pathogen. In immunocompromised individuals, it can cause bloodstream infections with high mortality rates. The ability to switch between yeast and hyphal morphologies is a critical virulence factor of C. albicans. In response to diverse environmental cues, several signaling pathways are activated resulting in filamentous growth. Interestingly, cell cycle arrest can also trigger filamentous growth although the pathways involved are not well-understood. Here, we demonstrate that the cAMP-PKA pathway is involved in the filamentous growth caused by G1 arrest due to the depletion of the G1 cyclin Cln3 and S phase arrest due to hydroxyurea treatment. The downstream mechanisms involved in filamentation are different between the two cell cycle arrest phenomena. Cln3-depleted cells require HGC1 and UME6 for filamentous growth, but hydroxyurea-induced filamentation does not. Also, the hyphal repressor Nrg1 is not involved in the suppression of Cln3-depletion and hydroxyurea-induced filamentous growth. The findings highlight the complexity of the signaling networks that control filamentous growth in which different mechanisms downstream of the cAMP-PKA pathway are activated based on the nature of the inducing signals. Show less
no PDF DOI: 10.1111/mmi.14097
CLN3

Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose.

Yan Chen, Yan-Jun Wang, Ying Zhao +1 more · 2018 · Bioscience reports · added 2026-04-24
Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix-loop-helix leucine zipper transcrip Show more
Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix-loop-helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated the role of ChREBP in the pathogenesis of DN. The expression of ChREBP was detected in patients with type 2 diabetes mellitus (T2DM), diabetic mice, and mesangial cells. ELISA was used to measure cytokine production in mesangial cells. Flow cytometry analysis was performed to detect the apoptosis of mesangial cells in the presence of high glucose. The expression levels of ChREBP and several cytokines (TNF-α, IL-1β, and IL-6) were up-regulated in T2DM patients. The mRNA and protein levels of ChREBP were also significantly elevated in the kidneys of diabetic mice. Moreover, glucose treatment promoted mRNA levels of TNF-α, IL-1β, and IL-6 in mesangial cells. Glucose stimulation induced significant apoptosis of SV40 MES 13 cells. In addition, transfection with ChREBP siRNA significantly inhibited ChREBP expression. Consequently, the inflammatory responses and apoptosis were inhibited in SV40 MES 13 cells. These results demonstrated that ChREBP could mediate the inflammatory response and apoptosis of mesangial cells, suggesting that ChREBP may be involved in the pathogenesis of DN. Show less
📄 PDF DOI: 10.1042/BSR20180767
MLXIPL

SIRT1 activator E1231 protects from experimental atherosclerosis and lowers plasma cholesterol and triglycerides by enhancing ABCA1 expression.

Tingting Feng, Peng Liu, Xiao Wang +12 more · 2018 · Atherosclerosis · Elsevier · added 2026-04-24
Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent protein deacetylase. Recent studies have demonstrated that enhancing SIRT1 expression or activity may modulate cholesterol and lipid Show more
Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent protein deacetylase. Recent studies have demonstrated that enhancing SIRT1 expression or activity may modulate cholesterol and lipid metabolism. However, pharmacological and molecular regulators for SIRT1 are scarce. Here, we aimed to find novel small molecule modulators of SIRT1 to regulate cholesterol and lipid metabolism. A high-throughput screening assay was established to identify SIRT1 activators. Surface plasmon resonance and immunoprecipitation were performed to confirm the interaction of E1231 with SIRT1. Cholesterol assay was performed to demonstrate the in vitro effect of E1231. The in vivo effect of E1231 was evaluated in experimental models. E1231, a piperazine 1,4-diamide compound, was identified as a SIRT1 activator with EC We identified a novel SIRT1 activator E1231 and elucidated its beneficial effects on lipid and cholesterol metabolism. Our study suggests that E1231 might be developed as a novel drug for treating atherosclerosis. Show less
no PDF DOI: 10.1016/j.atherosclerosis.2018.04.039
NR1H3

MLLT10 promotes tumor migration, invasion, and metastasis in human colorectal cancer.

Xiaoqian Jing, Haoxuan Wu, Xi Cheng +6 more · 2018 · Scandinavian journal of gastroenterology · Taylor & Francis · added 2026-04-24
Colorectal cancer (CRC), one of the most aggressive gastrointestinal malignancies, is a frequently diagnosed life-threatening cancer worldwide. Most CRC patients have poor prognosis mainly because of Show more
Colorectal cancer (CRC), one of the most aggressive gastrointestinal malignancies, is a frequently diagnosed life-threatening cancer worldwide. Most CRC patients have poor prognosis mainly because of frequent metastasis and recurrence. Thus, it is crucial to find out some new biomarkers and to show deeper insights into the mechanisms of CRC. MLLT10, Myeloid/lymphoid or mixed-lineage leukemia translocated to 10, also known as AF10, a recurrent MLL partner. In this study, we found that MLLT10 promotes CRC tumor invasion and metastasis both in vitro and in vivo. Here, the expression of MLLT10 was evaluated by immunohistochemistry. Then, the plasmid and lentivirus particles for MLLT10 overexpression or knockdown were designed and constructed into SW620 and HT29 cells. Finally, cell proliferation assay, cell adhesion assay, transwell migration, and invasion assay were used to detect the migration and invasion ability of MLLT10 in CRC cells. A tail vein injection assay was employed to evaluate the role of MLLT10 in tumor metastases. MLLT10 expression was significantly higher in CRC tissues than in noncancerous tissues and was associated with some clinicopathological factors. In vitro, the overexpression of MLLT10 promoted CRC cell migration and invasion, while after MLLT10 was knocked down, the opposite results were observed. Furthermore, we used animal metastasis models to detect the function of MLLT10 in vivo, the results are same with the outcomes in vitro. In lung metastasis sites, the knockdown of MLLT10 in SW620 cells significantly inhibited Vimentin expression, whereas the E-Cadherin was increased. These results indicate that MLLT10 regulates the metastasis of CRC cells via EMT. Show less
no PDF DOI: 10.1080/00365521.2018.1481521
MLLT10

Chalcone Derivatives Enhance ATP-Binding Cassette Transporters A1 in Human THP-1 Macrophages.

I-Jou Teng, Min-Chien Tsai, Shao-Fu Shih +6 more · 2018 · Molecules (Basel, Switzerland) · MDPI · added 2026-04-24
Atherosclerosis is a process of imbalanced lipid metabolism in the vascular walls. The underlying pathology mainly involves the deposition of oxidized lipids in the endothelium and the accumulation of Show more
Atherosclerosis is a process of imbalanced lipid metabolism in the vascular walls. The underlying pathology mainly involves the deposition of oxidized lipids in the endothelium and the accumulation of cholesterol in macrophages. Macrophages export excessive cholesterol (cholesterol efflux) through ATP-binding cassette transporter A1 (ABCA1) to counter the progression of atherosclerosis. We synthesized novel chalcone derivatives and assessed their effects and the underlying mechanisms on ABCA1 expression in macrophages. Human THP-1 macrophages were treated with synthetic chalcone derivatives for 24 h. In Western blot and flow cytometry analyses, a chalcone derivative, ( Show less
no PDF DOI: 10.3390/molecules23071620
NR1H3

Two novel CPS1 mutations in a case of carbamoyl phosphate synthetase 1 deficiency causing hyperammonemia and leukodystrophy.

Xihui Chen, Lijuan Yuan, Mao Sun +2 more · 2018 · Journal of clinical laboratory analysis · Wiley · added 2026-04-24
Carbamoyl phosphate synthetase 1 deficiency (CPS1D) is a rare autosomal recessive disorder of the urea cycle, mostly characterized by hyperammonemia and the concomitant leukodystrophy. The onset of CP Show more
Carbamoyl phosphate synthetase 1 deficiency (CPS1D) is a rare autosomal recessive disorder of the urea cycle, mostly characterized by hyperammonemia and the concomitant leukodystrophy. The onset of CPS1D can be at any age, and the clinical manifestations are variable and atypical. Genetic tests are indispensable for accurate diagnosis of CPS1D on the basis of biochemical tests. Blood tandem mass spectrometric analysis and urea organic acidemia screening were performed on a Chinese neonatal patient with low activity, recurrent seizures, and hyperammonemia. Next-generation sequencing and Sanger sequencing were followed up for making a definite diagnosis. Bioinformatics tools were used for the conservation analysis and pathogenicity predictions of the identified mutations. Increased lactate in urea and decreased citrulline in blood were detected in the patient. Two novel mutations (c.173G>T, p.G58V in exon 2 and c.796G>A, p.G266R in exon 8) in CPS1 identified in the neonatal patient were found through coseparation verification. Both of the two mutations were predicted to be deleterious, and the two relevant amino acids exerted highly evolutionarily conserved. The final diagnosis of the patient was compound heterozygous CPS1D. This study described the specific clinical characteristics and the variations of physiological and biochemical indices in a Chinese neonatal patient with CPS1D, which facilitated the diagnosis and mechanism research of the disease. Two novel causative missense mutations were identified, which enriched the mutation spectrum of CPS1D in China and worldwide. Advice of prenatal diagnosis was given to the family for a new pregnancy. Show less
no PDF DOI: 10.1002/jcla.22375
CPS1

Screening and identification of potential protein biomarkers for evaluating the efficacy of intensive therapy in pulmonary tuberculosis.

Ting-Ting Jiang, Li-Ying Shi, Jing Chen +9 more · 2018 · Biochemical and biophysical research communications · Elsevier · added 2026-04-24
This research aimed to discover potential biomarkers for evaluating the therapeutic efficacy of intensive therapy in pulmonary tuberculosis (TB). Protein profiles in 2-months intensively treated TB pa Show more
This research aimed to discover potential biomarkers for evaluating the therapeutic efficacy of intensive therapy in pulmonary tuberculosis (TB). Protein profiles in 2-months intensively treated TB patients, untreated TB patients, and healthy controls were investigated with iTRAQ-2DLC-MS/MS technique. 71 differential proteins were identified in 2-months intensively treated TB patients. Significant differences in complement component C7 (CO7), apolipoprotein A-IV (APOA4), apolipoprotein C-II (APOC2), and angiotensinogen (ANGT) were found by ELISA validation. CO7 and ANGT were also found significantly different in sputum negative patients, compared with sputum positive patients after intensive treatment. Clinical analysis showed that after 2-months intensive treatment several indicators were significantly changed, and the one-year cure rate of sputum negative patients were significantly higher than sputum positive patients. Diagnostic models consisting of APOC2, CO7 and APOA4 were established to distinguish intensively treated TB patients from untreated TB patients and healthy controls with the AUC value of 0.910 and 0.935. Meanwhile, ANGT and CO7 were combined to identify sputum negative and sputum positive TB patients after intensive treatment with 89.36% sensitivity, 71.43% specificity, and the AUC value of 0.853. The results showed that APOC2, CO7, APOA4, and ANGT may be potential biomarkers for evaluating the efficacy of intensive anti-TB therapy. Show less
no PDF DOI: 10.1016/j.bbrc.2018.06.147
APOA4

Pleiotropic effects of n-6 and n-3 fatty acid-related genetic variants on circulating hemostatic variables.

Lu-Chen Weng, Weihua Guan, Lyn M Steffen +7 more · 2018 · Thrombosis research · Elsevier · added 2026-04-24
Data from epidemiological studies and clinical trials suggest an influence of dietary and circulating polyunsaturated fatty acids (PUFAs) on the hemostasis profile. Genome-wide association studies (GW Show more
Data from epidemiological studies and clinical trials suggest an influence of dietary and circulating polyunsaturated fatty acids (PUFAs) on the hemostasis profile. Genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) related to plasma PUFAs levels. We aimed to investigate whether the SNPs related to plasma PUFAs levels were also associated with plasma levels of hemostatic variables. We tested the associations between 9 PUFA-related SNPs and 6 hemostatic variables in 9035 European Americans (EAs) and 2702 African Americans (AAs) in the Atherosclerosis Risk in Communities (ARIC) Study. We then conducted a replication study by looking-up our novel observed associations in three published GWAS for hemostatic factors in different EA populations. We observed a novel linoleic acid-related locus at the JMJD1C region associated with factor VII activity (FVIIc): rs10740118 and rs1935, Beta (p) = -1.31 (1 × 10 Our study identified a novel association for FVIIc at JMJD1C, a histone demethylase that plays a role in DNA repair and possibly transcription regulation and RNA processing. Show less
📄 PDF DOI: 10.1016/j.thromres.2018.05.032
JMJD1C

Association of serum levels of antibodies against MMP1, CBX1, and CBX5 with transient ischemic attack and cerebral infarction.

Hao Wang, Xiao-Meng Zhang, Go Tomiyoshi +39 more · 2018 · Oncotarget · Impact Journals · added 2026-04-24
Transient ischemic attack (TIA) is a predictor for cerebral infarction (CI), and early diagnosis of TIA is extremely important for the prevention of CI. We set out to identify novel antibody biomarker Show more
Transient ischemic attack (TIA) is a predictor for cerebral infarction (CI), and early diagnosis of TIA is extremely important for the prevention of CI. We set out to identify novel antibody biomarkers for TIA and CI, and detected matrix metalloproteinase 1 (MMP1), chromobox homolog 1 (CBX1), and chromobox homolog 5 (CBX5) as candidate antigens using serological identification of antigens by recombinant cDNA expression cloning (SEREX) and Western blotting to confirm the presence of serum antibodies against the antigens. Amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA) revealed that serum antibody levels were significantly higher in patients with TIA or acute-phase CI (aCI) compared with healthy donors ( Show less
📄 PDF DOI: 10.18632/oncotarget.23789
CBX1

Characteristics of genomic alterations of lung adenocarcinoma in young never-smokers.

Wenxin Luo, Panwen Tian, Yue Wang +15 more · 2018 · International journal of cancer · Wiley · added 2026-04-24
Non-small-cell lung cancer (NSCLC) has been recognized as a highly heterogeneous disease with phenotypic and genotypic diversity in each subgroup. While never-smoker patients with NSCLC have been well Show more
Non-small-cell lung cancer (NSCLC) has been recognized as a highly heterogeneous disease with phenotypic and genotypic diversity in each subgroup. While never-smoker patients with NSCLC have been well studied through next generation sequencing, we have yet to recognize the potentially unique molecular features of young never-smoker patients with NSCLC. In this study, we conducted whole genome sequencing (WGS) to characterize the genomic alterations of 36 never-smoker Chinese patients, who were diagnosed with lung adenocarcinoma (LUAD) at 45 years or younger. Besides the well-known gene mutations (e.g., TP53 and EGFR), our study identified several potential lung cancer-associated gene mutations that were rarely reported (e.g., HOXA4 and MST1). The lung cancer-related copy number variations (e.g., EGFR and CDKN2A) were enriched in our cohort (41.7%, 15/36) and the lung cancer-related structural variations (e.g., EML4-ALK and KIF5B-RET) were commonly observed (22.2%, 8/36). Notably, new fusion partners of ALK (SMG6-ALK) and RET (JMJD1C-RET) were found. Furthermore, we observed a high prevalence (63.9%, 23/36) of potentially targetable genomic alterations in our cohort. Finally, we identified germline mutations in BPIFB1 (rs6141383, p.V284M), CHD4 (rs74790047, p.D140E), PARP1 (rs3219145, p.K940R), NUDT1 (rs4866, p.V83M), RAD52 (rs4987207, p.S346*), and MFI2 (rs17129219, p.A559T) were significantly enriched in the young never-smoker patients with LUAD when compared with the in-house noncancer database (p < 0.05). Our study provides a detailed mutational portrait of LUAD occurring in young never-smokers and gives insights into the molecular pathogenesis of this distinct subgroup of NSCLC. Show less
📄 PDF DOI: 10.1002/ijc.31542
JMJD1C