👤 Melody Zhang

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Also published as: Lanyue Zhang, Zemin Zhang, Kangning Zhang, Fan Zhang, Xianpeng Zhang, Xiaoxia Zhang, Suping Zhang, Jingtian Zhang, Jianzhao Zhang, Guoan Zhang, Bowei Zhang, Mengshi Zhang, Shijun Zhang, Nieke Zhang, Guoguo Zhang, J R Zhang, Hongbin Zhang, Xiao-Ming Zhang, Baojing Zhang, Linjing Zhang, Xiao-bo Zhang, Dai Zhang, Rongchao Zhang, Guang-Qiong Zhang, Jixing Zhang, Xiaomei Zhang, Honghua Zhang, Lixia Zhang, Jinhua Zhang, Xiaotong Zhang, Shu Zhang, Ming Zhang, Jianeng Zhang, Xintao Zhang, T Zhang, Li-Ke Zhang, Miaoran Zhang, Jinfeng Zhang, Shi Zhang, Lingxiao Zhang, Xiaoli Zhang, Hongjie Zhang, Bosheng Zhang, Qingfeng Zhang, Xiaofei Zhang, Tonghua Zhang, Huiting Zhang, Yuning Zhang, Yangfan Zhang, Guiping Zhang, Junying Zhang, Xiaojie Zhang, Yu-Chi Zhang, Yumin Zhang, Daming Zhang, Hongquan Zhang, Youzhong Zhang, Jianghong Zhang, Zhenzhen Zhang, Yixia Zhang, Yuebo Zhang, Yijing Zhang, Wenji Zhang, Xianjing Zhang, Menghuan Zhang, Xinwu Zhang, Xinyi Zhang, Fujun Zhang, Wen-Hong Zhang, Dayi Zhang, Xiongze Zhang, Qiaojun Zhang, F P Zhang, Sanbao Zhang, Nianxiang Zhang, Ya Zhang, Wenyang Zhang, Yunmei Zhang, Qingrun Zhang, Hailing Zhang, X X Zhang, Xiao-Yu Zhang, Zhihui Zhang, Youyi Zhang, Haokun Zhang, Jason Z Zhang, Jing-Nan Zhang, Han Zhang, Caiyu Zhang, Jianhong Zhang, Wenlu Zhang, Guang Zhang, Xinran Zhang, Xiaoxi Zhang, Kongyong Zhang, Xiuming Zhang, Jiaxing Zhang, Zhaobo Zhang, Wenkui Zhang, Yintang Zhang, Wen-Jie Zhang, Zhong-Yin Zhang, Ziding Zhang, XiaoLin Zhang, Xiao-Meng Zhang, Wenwen Zhang, Jinfang Zhang, Jinliang Zhang, Xiaoyuan Zhang, Jieming Zhang, Jiannan Zhang, Tianshu Zhang, Xinheng Zhang, Shitian Zhang, Su Zhang, Wen-Xuan Zhang, Qiuyue Zhang, Bohua Zhang, C Zhang, P Zhang, Huaqi Zhang, Fuqiang Zhang, Ruihong Zhang, Shanchun Zhang, Mingjun Zhang, Aiguo Zhang, Dong Zhang, Xipeng Zhang, Lingqiang Zhang, Yonglong Zhang, Haonan Zhang, Chengyu Zhang, Xutong Zhang, Cathy C Zhang, Zhao Zhang, Xinhan Zhang, Yulong Zhang, Guowei Zhang, Yi-Min Zhang, Lizhi Zhang, Licheng Zhang, Chunhai Zhang, Rui Long Zhang, Junwei Zhang, Zhao-Ming Zhang, Lianqin Zhang, Yiyao Zhang, X Zhang, Caiyi Zhang, Xiangwu Zhang, Haoxing Zhang, Ge Zhang, Shi-Qian Zhang, Ang Zhang, Zhi-Jun Zhang, Tao Zhang, Guofang Zhang, Yinzhi Zhang, Hu Zhang, Zhuzhen Zhang, Zewei Zhang, Qingqing Zhang, Liyi Zhang, S Y Zhang, Junjing Zhang, Yongjuan Zhang, Chao-Hua Zhang, Mingyu Zhang, Kaiyi Zhang, Xuelong Zhang, Juntai Zhang, Shanxiang Zhang, Liyuan Zhang, Siyuan Zhang, Ya-Long Zhang, Mingfa Zhang, Yashuo Zhang, Chengbo Zhang, Ziqi Zhang, Jianping Zhang, Chenmin Zhang, Juliang Zhang, Xingong Zhang, Kailing Zhang, Hengrui Zhang, Yachen Zhang, Changlong Zhang, Mo-Ruo Zhang, Hanyin Zhang, Jianyong Zhang, Boxiang Zhang, Jiangyan Zhang, Mingjiong Zhang, Guan-Yan Zhang, Mingming Zhang, Meng-Ying Zhang, Zhengfen Zhang, Gui-Ping Zhang, John Z H Zhang, Hai-Liang Zhang, Z Zhang, Kunning Zhang, Fukang Zhang, Yaping Zhang, Guangyong Zhang, Shasha Zhang, Hongrui Zhang, Jianwu Zhang, Shou-Peng Zhang, Nasha Zhang, Huiqing Zhang, Chuanxin Zhang, Ke Zhang, Anqi Zhang, Haomin Zhang, Yuanping Zhang, Mengmin Zhang, Junsheng Zhang, Xinmin Zhang, Enming Zhang, Chen-Yang Zhang, Qian Jun Zhang, Guo-Wei Zhang, Zhongqi Zhang, Yawei Zhang, Yang Zhang, Yueqi Zhang, Haitao Zhang, Zhen-Shan Zhang, Wencheng Zhang, Ai Zhang, Yuetong Zhang, Jinzhou Zhang, Guo-Fang Zhang, Jingmei Zhang, Fengxu Zhang, Lei Zhang, Quan Zhang, Zhenqiang Zhang, Shengchi Zhang, Shuer Zhang, Haiyang Zhang, Xiuzhen Zhang, Chenfei Zhang, Heping Zhang, Pingmei Zhang, Yichi Zhang, Junxing Zhang, Kainan Zhang, Long Zhang, Joyce Zhang, Cheng-Lin Zhang, Zhen-Dong Zhang, Fei-Ran Zhang, Tongran Zhang, F Zhang, Hongtao Zhang, Haijiao Zhang, Dongmei Zhang, Yuzhou Zhang, Zhiming Zhang, Shuangjie Zhang, Fuquan Zhang, M X Zhang, Chengkai Zhang, Chengshi Zhang, Luyun Zhang, Jinlong Zhang, Yanxia Zhang, Xiong Zhang, Luning Zhang, Jiayu Zhang, Zuoyi Zhang, H L Zhang, Pei-Zhuo Zhang, Geng Zhang, Caiying Zhang, Qifan Zhang, Wenya Zhang, Xiao-yan Zhang, Lijie Zhang, Fengwei Zhang, Yanhong Zhang, Leo H Zhang, Yongjiu Zhang, Jiachen Zhang, Jianmin Zhang, Zhaomin Zhang, Lechi Zhang, Bangzhou Zhang, Hongxia Zhang, Xuehui Zhang, Zhenglang Zhang, Qiyong Zhang, M M Zhang, Jianjun Zhang, Guangxin Zhang, Ninghan Zhang, Ruiqi Zhang, Jianduan Zhang, Yi-Ge Zhang, Qian-Qian Zhang, Pu-Hong Zhang, Meishan Zhang, Yun-Xiang Zhang, Lirong Zhang, Yan-Qing Zhang, Xiuwen Zhang, Yunhe Zhang, Shuxia Zhang, Kang Zhang, Yongping Zhang, Chen-Yan Zhang, Yihan Zhang, Yingmei Zhang, Jin-Yu Zhang, Xianhua Zhang, Xiao Zhang, Panpan Zhang, Haowen Zhang, Zhiqiang Zhang, Huili Zhang, Yushan Zhang, Yinzhuang Zhang, Zhiyan Zhang, Bingye Zhang, Ruihao Zhang, Kunyi Zhang, Lian-Lian Zhang, Jin-Jing Zhang, Yikai Zhang, Zhaohui Zhang, Hongxin Zhang, Leilei Zhang, Rong Zhang, Xiaonyun Zhang, Haotian Zhang, Chuankuo Zhang, Chong Zhang, Le-Le Zhang, Y Y Zhang, Chao Zhang, Hao-Chen Zhang, Yating Zhang, Jishui Zhang, Wenbo Zhang, Furen Zhang, Jinfan Zhang, Fen Zhang, Yajie Zhang, Chunxia Zhang, Xiu-Li Zhang, Tong-Cun Zhang, Tongxin Zhang, Le Zhang, Churen Zhang, Hongmei Zhang, Xin-Xin Zhang, Huiyuan Zhang, Yiqian Zhang, Aihua Zhang, Qingling Zhang, Yanman Zhang, Jianguang Zhang, Jiaying Zhang, Mingyang Zhang, Guangyuan Zhang, Xinping Zhang, Naixia Zhang, Yi-Hua Zhang, Xuebin Zhang, Tongxue Zhang, Jianshe Zhang, Chenyan Zhang, Yingying Zhang, Michael Zhang, Mengmeng Zhang, Fengshuo Zhang, Yi J Zhang, Cun Zhang, Xiuping Zhang, Shao Zhang, Dong-cui Zhang, Huijun Zhang, Yuan-Yuan Zhang, Chongguo Zhang, Huanxia Zhang, Niankai Zhang, Mengna Zhang, Lianjun Zhang, Anwei Zhang, Xiaoning Zhang, Huafeng Zhang, Xiao-Qi Zhang, Junmin Zhang, Jiecheng Zhang, Qi-Lei Zhang, Ruotian Zhang, Hejun Zhang, Yongsheng Zhang, Mengqi Zhang, Yuxin Zhang, Zengqiang Zhang, Lili Zhang, Ying Zhang, Yi-yi Zhang, Yanxiang Zhang, Hailin Zhang, Yi Ping Zhang, Zhongyang Zhang, Yunhai Zhang, Aimei Zhang, Sai Zhang, Ruixin Zhang, Naijin Zhang, Hanwen Zhang, Yanfei Zhang, Guangliang Zhang, Qihong Zhang, Kaitai Zhang, Xiao-Hua Zhang, Yanqiao Zhang, Xuan Zhang, Suyang Zhang, Jianchao Zhang, Rongcai Zhang, Weiping J Zhang, Chun-Lan Zhang, Duowen Zhang, Chenggang Zhang, Chao-Sheng Zhang, Xiangyang Zhang, Weizhou Zhang, Jianwen Zhang, Yan Zhang, Xijiang Zhang, Yi-Qi Zhang, Wanqi Zhang, Hengyuan Zhang, Zhewei Zhang, Haiwei Zhang, Guangqiong Zhang, Zhiyao Zhang, Ren Zhang, Mengdi Zhang, Shuangxin Zhang, Kan Zhang, Clarence K Zhang, Qishu Zhang, Jinyi Zhang, Tie-mei Zhang, Tuo Zhang, Runyun Zhang, Hongsen Zhang, Hong-Yu Zhang, Mingyuan Zhang, Jingmian Zhang, Lei-Sheng Zhang, Xinyue Zhang, Qingxue Zhang, Meng-Wen Zhang, YiJie Zhang, Xieyi Zhang, Guoxin Zhang, Xinling Zhang, Hengming Zhang, Jinquan Zhang, Zhangjin Zhang, Xi'an Zhang, Kejian Zhang, Liang-Rong Zhang, Baojun Zhang, Yanchao Zhang, Yan-Ling Zhang, Litao Zhang, Xia Zhang, Ruizhong Zhang, Tongwu Zhang, Lingling Zhang, Guicheng Zhang, Caihong Zhang, Yongyan Zhang, Guang-Xian Zhang, Q Y Zhang, Chris Zhiyi Zhang, Feng Zhang, Chuantao Zhang, Yanyi Zhang, Suzhen Zhang, Jimei Zhang, Shuo Zhang, Yue Zhang, W X Zhang, Xuefei Zhang, Haifeng Zhang, Xuehai Zhang, Richard Zhang, Qing-Hui Zhang, Runze Zhang, Chuchu Zhang, Minyue Zhang, Naiqi Zhang, Yong-Liang Zhang, Chang-Hua Zhang, Minying Zhang, Yuansheng Zhang, Maomao Zhang, Yixin Zhang, Hongyi Zhang, Qimin Zhang, Hongyuan Zhang, Quan-bin Zhang, Jianhui Zhang, Tingxue Zhang, Pili Zhang, Zhuohua Zhang, Yunfeng Zhang, Yanlin Zhang, X-T Zhang, Guofu Zhang, Yiren Zhang, Jingyu Zhang, Peiyi Zhang, S Z Zhang, Yajing Zhang, Juqing Zhang, Luzheng Zhang, Yuanzhuang Zhang, Kaihua Zhang, Ming-Liang Zhang, Weisen Zhang, Yupei Zhang, Luwen Zhang, Ruoxuan Zhang, Xiao Min Zhang, Yongxing Zhang, Muqing Zhang, Mingxue Zhang, Guolong Zhang, Jiquan Zhang, Wenjing Zhang, Ziyang Zhang, Changteng Zhang, Jieping Zhang, Jinglu Zhang, Honghe Zhang, Donna Zhang, Yandong Zhang, Chunjun Zhang, Fei Zhang, Jiajing Zhang, Xiaoming Zhang, Jingdan Zhang, Caiping Zhang, Mengzhao Zhang, Si Zhang, Jiankun Zhang, Boqing Zhang, Wang-Dong Zhang, Xindang Zhang, Jiahe Zhang, Qiannan Zhang, Zhibo Zhang, Zijing Zhang, Mei Zhang, Guiliang Zhang, Kaichuang Zhang, Dawei Zhang, Weihua Zhang, Yuhua Zhang, Xuezhi Zhang, Shu-Yang Zhang, Jun-Jie Zhang, Xin-Ye Zhang, Luoping Zhang, Yun Zhang, Jiayan Zhang, Yifan Zhang, Songying Zhang, Xinhua Zhang, Meng Zhang, Yani Zhang, Yuchao Zhang, Lijun Zhang, Zongwang Zhang, Pei Zhang, Peiqin Zhang, Guixiang Zhang, Ruiling Zhang, Liwen Zhang, Ming-Yu Zhang, Ziyu Zhang, Yanyu Zhang, Junping Zhang, Chu-Yue Zhang, Taoyuan Zhang, Lu-Pei Zhang, Junkai Zhang, Chunqing Zhang, S Zhang, Baohu Zhang, Songlin Zhang, Liu Zhang, H F Zhang, Ruixia Zhang, Zhi-Xin Zhang, Hongyan Zhang, Jingfa Zhang, Jing-Lve Zhang, Xiaochen Zhang, Xiangzheng Zhang, Jianbo Zhang, Yiliang Zhang, Yuanhui Zhang, Bo-Ya Zhang, Xiaofeng Zhang, Yanbing Zhang, K Zhang, Zhemei Zhang, Meixian Zhang, Hanqi Zhang, Fangmei Zhang, Mingyao Zhang, Fuxing Zhang, Mengxi Zhang, Yunjia Zhang, Lin Zhang, Weifeng Zhang, Guangji Zhang, Tian Zhang, Meiling Zhang, Xiaobao Zhang, Dongsheng Zhang, Luyao Zhang, Xiaopei Zhang, Zihan Zhang, Bing-Qi Zhang, Kui-ming Zhang, Yanru Zhang, Mingjie Zhang, Lupei Zhang, Junjie Zhang, Xiaocui Zhang, Yali Zhang, Yongheng Zhang, Guilin Zhang, Xiuse Zhang, Shu-Ming Zhang, Yuxia Zhang, Qiuting Zhang, Danning Zhang, Zhi-Jie Zhang, Siqi Zhang, Rongxu Zhang, Tingying Zhang, Claire Y Zhang, Mingxuan Zhang, Lianxin Zhang, Ding Zhang, Lichuan Zhang, Yuejuan Zhang, Dingkai Zhang, Li-Fen Zhang, Zhenyu Zhang, Yingna Zhang, Yuanhao Zhang, Linyou Zhang, Lintao Zhang, Shubing Zhang, Xufang Zhang, Lei-Lei Zhang, Zhi-Peng Zhang, Xiaomeng Zhang, Guoliang Zhang, Xujun Zhang, Ji Yao Zhang, Mengnan Zhang, Shenglan Zhang, Ningkun Zhang, Zhimin Zhang, Zhiwen Zhang, Jiming Zhang, Chuanfu Zhang, Yongwei Zhang, Mao Zhang, PeiFeng Zhang, Jia-Xuan Zhang, Shiyun Zhang, Genxi Zhang, Qingjiong Zhang, Duo Zhang, Qunyuan Zhang, Yan-Chun Zhang, Yongguo Zhang, Qi Zhang, Yaozhengtai Zhang, W G Zhang, Yu-Bo Zhang, Bowen Zhang, Wangping Zhang, Xinhe Zhang, Jinrui Zhang, Yuhan Zhang, Yangqianwen Zhang, Miao-Miao Zhang, Ya-Juan Zhang, Rui Xue Zhang, Dachuan Zhang, Ji Zhang, Chunxiao Zhang, Yaming Zhang, Xinrui Zhang, Bochuan Zhang, Yurou Zhang, Zhuoya Zhang, Ming-Zhu Zhang, Song-Yang Zhang, Ruiyang Zhang, Yang-Yang Zhang, Jinjin Zhang, Xinhong Zhang, Guijie Zhang, Jifa Zhang, Hai Zhang, Dong-Mei Zhang, Jian-Ping Zhang, Zi-Jian Zhang, Xixun Zhang, Haiying Zhang, Guoming Zhang, Jianfa Zhang, Zhi-Qing Zhang, Zhe Zhang, Qilong Zhang, Yingyi Zhang, Xincheng Zhang, Shiquan Zhang, Junhan Zhang, Hai-Ying Zhang, Xiuyun Zhang, Tiefeng Zhang, Chaoyue Zhang, Hailian Zhang, Yunqi Zhang, Zhanjie Zhang, Mei-Ya Zhang, Da-Qi Zhang, Yiheng Zhang, Qingjun Zhang, Wenting Zhang, Ruoshi Zhang, Xiaoyu Zhang, Chenhui Zhang, Baorong Zhang, Yong-Guo Zhang, Xuemin Zhang, Xu Dong Zhang, Jun-Xiao Zhang, Jingshuang Zhang, Zhi-Chang Zhang, Qihao Zhang, Tonghui Zhang, Guanglei Zhang, Jia Zhang, Shiyu Zhang, Hua Zhang, Xue-Ping Zhang, Xiao Bin Zhang, Chunhong Zhang, Huayong Zhang, Jixia Zhang, Tianxiao Zhang, Daoyong Zhang, Xinlei Zhang, Yilin Zhang, Rulin Zhang, Chi Zhang, Cuijuan Zhang, Shanshan Zhang, ChaoDong Zhang, Shaohua Zhang, Quanqi Zhang, Tianxi Zhang, Xinan Zhang, Q-D Zhang, Bingkun Zhang, Haiyue Zhang, Lihua Zhang, Simin Zhang, L Zhang, Nisi Zhang, Guanghui Zhang, Chen-Song Zhang, Rugang Zhang, H-F Zhang, Qi-Ai Zhang, Jiangtao Zhang, Cai Zhang, Youying Zhang, Guimin Zhang, Haopeng Zhang, Wanyu Zhang, Guo-Xiong Zhang, Wenru Zhang, Guoqiang Zhang, Xiuqing Zhang, K Y Zhang, Xinbo Zhang, Weilong Zhang, Tongcun Zhang, Ranran Zhang, Qing-Zhu Zhang, Wanying Zhang, Junpei Zhang, Yonghong Zhang, Hailou Zhang, Qingna Zhang, Tiehua Zhang, Hai-Gang Zhang, Shuwei Zhang, Jiahai Zhang, Hong-Sheng Zhang, Mo Zhang, Mengren Zhang, Renshuai Zhang, Xiao-Jun Zhang, Xinxin Zhang, Pengfei Zhang, Jin-Man Zhang, Shikai Zhang, Wenchao Zhang, Jianxin Zhang, Junzhi Zhang, Jiangang Zhang, Qian ZHANG, Peilin Zhang, Pengpeng Zhang, Daxin Zhang, Shuaishuai Zhang, Kai-Jie Zhang, Ruizhi Zhang, Yutong Zhang, Lanlan Zhang, Huijie Zhang, Jianxia Zhang, Yuxi Zhang, Dong-Hui Zhang, Hai-Bo Zhang, Zhonglin Zhang, Mengjie Zhang, Suya Zhang, Jinwei Zhang, Genglin Zhang, Yun-Feng Zhang, Yubin Zhang, Nong Zhang, Joe Z Zhang, Yupeng Zhang, De-Jun Zhang, Ganlin Zhang, Yanmin Zhang, Jin-Ge Zhang, Qingchuan Zhang, ShiSong Zhang, Yichen Zhang, Yafang Zhang, Lian Zhang, Liwei Zhang, Xuelian Zhang, Yinjiang Zhang, Xiaowan Zhang, Yeqian Zhang, Zaifeng Zhang, Zhehua Zhang, Jianing Zhang, Chen Zhang, Jiejie Zhang, Zhanhao Zhang, Donghui Zhang, Dinghu Zhang, Guochao Zhang, Guohui Zhang, Yingchao Zhang, Zikai Zhang, Danfeng Zhang, Hongmin Zhang, Jinming Zhang, Liying Zhang, Yu Zhang, Liguo Zhang, Yujing Zhang, Jun-Xiu Zhang, Yuanxi Zhang, Peichun Zhang, Yangyu Zhang, Xue-Qing Zhang, Fu-Ping Zhang, Terry Jianguo Zhang, Hongyou Zhang, Xuejiao Zhang, Zhijiao Zhang, Wenhong Zhang, Kezhong Zhang, Yihang Zhang, Qianhui Zhang, Sizhong Zhang, Mingchang Zhang, Shulong Zhang, Kaiming Zhang, Haiming Zhang, Bo-Heng Zhang, Yingzi Zhang, Chunxiang Zhang, Xiayin Zhang, Yumeng Zhang, Hongrong Zhang, Junyu Zhang, Peng-Fei Zhang, Yuanyuan Zhang, Ci Zhang, Zhanming Zhang, Yuanxiang Zhang, Hao-Yu Zhang, Jingzhe Zhang, Junxia Zhang, Xiaogang Zhang, Bingbing Zhang, Liyin Zhang, Shuang Zhang, Cuilin Zhang, Yi-Hang Zhang, Lichao Zhang, Chengnan Zhang, Chengcheng Zhang, Qianru Zhang, Bei Zhang, Manjin Zhang, Mengni Zhang, Hongyang Zhang, Yimin Zhang, Bojian Zhang, Junhui Zhang, Dianzheng Zhang, Chaoqiang Zhang, Huiyu Zhang, Wenjia Zhang, Xin-Yuan Zhang, Yun-Lin Zhang, Yangyang Zhang, Ning-Ping Zhang, Cheng-Wei Zhang, Yaoyao Zhang, Wenguang Zhang, Wei-Jia Zhang, Qiangsheng Zhang, Hongbing Zhang, Xuehong Zhang, Xin Zhang, Xueluo Zhang, Lining Zhang, Fugui Zhang, Hongzhou Zhang, Xinquan Zhang, Huhan Zhang, Gaoxin Zhang, Zhen-lin Zhang, Gong Zhang, Weiling Zhang, Yu-Qiu Zhang, Yulin Zhang, Zhengyun Zhang, Ting Ting Zhang, Xiaofan Zhang, Li Zhang, Zhiyong Zhang, Jieqiong Zhang, Tianlong Zhang, Yingang Zhang, Tianyang Zhang, Yahua Zhang, Weikang Zhang, Zhu-Qin Zhang, Junlong Zhang, Jingwei Zhang, Zenglei Zhang, Chuankuan Zhang, Liangliang Zhang, Guo-Fu Zhang, Wangang Zhang, Peng Zhang, Yaguang Zhang, Xinruo Zhang, Xu-Jun Zhang, Zhihong Zhang, Tianye Zhang, Zhiqiao Zhang, Zhuorong Zhang, Fa Zhang, Min Zhang, Ru Zhang, Yifang Zhang, Jin-Ru Zhang, Yibo Zhang, DanDan Zhang, M H Zhang, Shengnan Zhang, Jiayuan Zhang, Bao-Rong Zhang, Chengxiong Zhang, Ke-Wen Zhang, Zixiong Zhang, Q Zhang, Fred Zhang, G-Y Zhang, Ting-Ting Zhang, Shengli Zhang, Jie Zhang, Nan Yang Zhang, Zhijun Zhang, Bangke Zhang, Hui Z Zhang, Dekai Zhang, Xiaojia Zhang, Jiao Zhang, He Zhang, Bofang Zhang, Jiayi Zhang, Xianxian Zhang, Tianliang Zhang, Zhongheng Zhang, Shiyao Zhang, Xiaojing Zhang, Jinglan Zhang, Minfang Zhang, Xiujie Zhang, Xinhai Zhang, Wenkai Zhang, Feifei Zhang, Chunyan Zhang, Hong-Zhen Zhang, Tingting Zhang, Shuya Zhang, Chao-Yang Zhang, Shang Zhang, Jingrong Zhang, Zheyuan Zhang, Wen-Xin Zhang, Xueying Zhang, W Zhang, Jiangmei Zhang, Shuai-Nan Zhang, Shiping Zhang, Kai Zhang, Y L Zhang, Zhuo-Ya Zhang, Ling-Yu Zhang, Huan-Tian Zhang, Ying E Zhang, Mengliang Zhang, Jingying Zhang, Jingsong Zhang, Yunsheng Zhang, Xuxiang Zhang, Mengyuan Zhang, Xiang Yang Zhang, Hua-Min Zhang, Chenguang Zhang, Ziyue Zhang, Bohao Zhang, Xiulan Zhang, Xiaorong Zhang, Peng-Cheng Zhang, Famin Zhang, Hao Zhang, Yong-hong Zhang, Xiangbin Zhang, Weichen Zhang, Yuheng Zhang, Xu Zhang, Jiang Zhang, Xinjiang Zhang, Chen-Qi Zhang, Lingyan Zhang, Beiyu Zhang, Haipeng Zhang, Dongxin Zhang, Yuzhu Zhang, Cong Zhang, Haihong Zhang, Yanhua Zhang, Jitai Zhang, Shaozhen Zhang, Xinfu Zhang, Pengcheng Zhang, Ruth Zhang, Guangping Zhang, Ben Zhang, Run Zhang, Chan-na Zhang, Jiawen Zhang, Wuhu Zhang, Minhong Zhang, Jiyang Zhang, Dingyi Zhang, Guangxian Zhang, Haolin Zhang, Pei-Weng Zhang, Shu-Zhen Zhang, Yiqing Zhang, Xiu Qi Zhang, Jianguo Zhang, Zhixin Zhang, M Zhang, Muzi Zhang, Huayu Zhang, Jianwei Zhang, Xunming Zhang, Da-Wei Zhang, L F Zhang, Claire Zhang, Xiping Zhang, Yanan Zhang, Z-K Zhang, Jun-ying Zhang, Kaituo Zhang, Peijing Zhang, MeiLu Zhang, Zizhen Zhang, Fengxi Zhang, Yi-Yue Zhang, Melissa C Zhang, Bin Zhang, Xuebao Zhang, Dongjian Zhang, Sophia L Zhang, Anying Zhang, Siyue Zhang, Deyin Zhang, Yuehong Zhang, Lan Zhang, Xiao-Lei Zhang, Dongjie Zhang, Hailei Zhang, Jingting Zhang, Leli Zhang, Lichen Zhang, Haozheng Zhang, Shenqian Zhang, Yin-Hong Zhang, Xuejun C Zhang, Qiu Zhang, Kaiwen Zhang, Joshua Zhang, Fushun Zhang, Hailong Zhang, Haiyan Zhang, Chengfei Zhang, Xiaojian Zhang, Shangxiong Zhang, Zhijian Zhang, Zhishuai Zhang, Qingchao Zhang, Zhiwang Zhang, Liming Zhang, Baoren Zhang, Xiuyue Zhang, Huajia Zhang, Yaxin Zhang, Sibin Zhang, Anan Zhang, Linyuan Zhang, Mingai Zhang, Muxin Zhang, Zhongxu Zhang, Xinlin Zhang, Nana Zhang, Xiaoying Zhang, Guodong Zhang, Hong-Xing Zhang, Shaofei Zhang, Fomin Zhang, Jianhai Zhang, Xindong Zhang, Zhenfeng Zhang, Mei-Fang Zhang, Wanjiang Zhang, Naisheng Zhang, Xiaojun Zhang, Meixia Zhang, Hui Zhang, Dong-Wei Zhang, Qiuyang Zhang, Ming-Jun Zhang, Fangting Zhang, Jingxi Zhang, Ruixue Zhang, Mingyue Zhang, Zongxiang Zhang, Yingqi Zhang, Jingqi Zhang, Tong Xuan Zhang, Hanrui Zhang, You-Zhi Zhang, Wendi Zhang, Yunxia Zhang, Chuting Zhang, Xueguang Zhang, Hongliang Zhang, Haojie Zhang, Yanli Zhang, Huanmin Zhang, Zeng Zhang, H Y Zhang, Wancong Zhang, Yi-Xuan Zhang, Xu-Chao Zhang, Mei-Ling Zhang, Xiaoling Zhang, Qiang-Sheng Zhang, Cai-Ling Zhang, Chang Zhang, Xiaotun Zhang, Tianyi Zhang, Sainan Zhang, Guili Zhang, Weibo Zhang, Fangyuan Zhang, Yazhuo Zhang, Zeyuan Zhang, Xiujun Zhang, Stephen X Zhang, Zhaoxue Zhang, Ting Zhang, Rui-Ning Zhang, Xiaoxue Zhang, Hainan Zhang, Zhiye Zhang, Lanfang Zhang, Lingna Zhang, Weimin Zhang, Qingyue Zhang, Limei Zhang, Yuan-Wei Zhang, Haisan Zhang, Yinghui Zhang, Yujia Zhang, Ming-Ming Zhang, Shaoyang Zhang, Jing-Fa Zhang, Hui-Jun Zhang, Jian-Xu Zhang, Yunhui Zhang, Zhiyuan Zhang, Junhua Zhang, Qunfeng Zhang, Boping Zhang, Yaoyang Zhang, Mengxue Zhang, Yinhao Zhang, Hongying Zhang, Jingyue Zhang, Quanfu Zhang, Menghui Zhang, Xueqian Zhang, Keyong Zhang, Zian Zhang, Ning Zhang, Lishuang Zhang, Congen Zhang, Shurui Zhang, Shengding Zhang, Yuping Zhang, Mengyue Zhang, Yuyu Zhang, Ying-Qian Zhang, Huiru Zhang, Jingli Zhang, Wentao Zhang, Haoran Zhang, Sheng-Qiang Zhang, Zhikun Zhang, Yiwen Zhang, Daguo Zhang, R Zhang, June Zhang, Changjing Zhang, Yanna Zhang, Lingjie Zhang, Shuijun Zhang, Zhaohuai Zhang, Xudan Zhang, Jing-Qiu Zhang, Jieying Zhang, Zhihan Zhang, Jiasheng Zhang, Ningzhen Zhang, Menghao Zhang, Xin-Yan Zhang, Yiwei Zhang, Stanley Weihua Zhang, Hongjin Zhang, Shi-Yao Zhang, Zengfu Zhang, Yongfang Zhang, Hongzhong Zhang, Dongdong Zhang, Shuyang Zhang, Qiao-Xia Zhang, Meidi Zhang, Yanfen Zhang, Xinwei Zhang, An-Qi Zhang, Zhaotian Zhang, Yuyan Zhang, Yuwei Zhang, Yusen Zhang, Yin Jiang Zhang, Youti Zhang, Yingli Zhang, Yumei Zhang, Wenxiang Zhang, Yanfeng Zhang, Benyou Zhang, Tianxin Zhang, Duoduo Zhang, Xiao-Chang Zhang, Wei-Na Zhang, Jin Zhang, Ruiying Zhang, Liyu Zhang, Hongxing Zhang, Sen Zhang, Xuting Zhang, Qianjun Zhang, Yunfan Zhang, X-Y Zhang, Zu-Xuan Zhang, Yanbin Zhang, Xiao-Ling Zhang, Xinjun Zhang, An Zhang, Yanting Zhang, Shi-Han Zhang, Nan Zhang, Shaochun Zhang, Shi-Jie Zhang, Qiong Zhang, Xinyao Zhang, Yadong Zhang, Shushan Zhang, Jinying Zhang, Xiaotian Zhang, Jinhui Zhang, Shucong Zhang, Qiwei Zhang, Weiyu Zhang, X Y Zhang, Wenxi Zhang, Gang Zhang, Shan-Shan Zhang, Weilin Zhang, Chenglong Zhang, Andrew Zhang, Jingru Zhang, Zhaoqi Zhang, Yafeng Zhang, Bi-Tian Zhang, Liqian Zhang, Hefang Zhang, Meimei Zhang, Gan Zhang, Jinyu Zhang, Boxi Zhang, Jinghui Zhang, Zhengliang Zhang, Xiao-Xuan Zhang, Deyi Zhang, Chaoyang Zhang, Kunshan Zhang, Chen-Xi Zhang, Wenxin Zhang, Zhenzhu Zhang, Zaijun Zhang, Liyan Zhang, M J Zhang, Qiang Zhang, Zhentao Zhang, Wenzhong Zhang, Chenxi Zhang, Bo Zhang, Jianling Zhang, Vita Zhang, Ji-Yuan Zhang, Yonglian Zhang, Guorui Zhang, Junling Zhang, Xiao Yu Cindy Zhang, Haihua Zhang, Wenyi Zhang, Yidan Zhang, Tiejun Zhang, Yanjiao Zhang, Renhe Zhang, Ximei Zhang, Yiting Zhang, Menglu Zhang, Xiao-Chong Zhang, Jia-Bao Zhang, Shupeng Zhang, Ruilin Zhang, Donghua Zhang, Shiti Zhang, Zilu Zhang, Tiane Zhang, Xiang Zhang, Tongtong Zhang, Shengming Zhang, Y Zhang, Yu-Yu Zhang, Zengdi Zhang, Laihong Zhang, Ruxuan Zhang, Danhua Zhang, Youjin Zhang, Yuke Zhang, Sheng-Xiao Zhang, Zhongxin Zhang, Yuting Zhang, Shihan Zhang, Jinsong Zhang, Xiaolei Zhang, Yu Chen Zhang, Yefan Zhang, Jianmei Zhang, J-Y Zhang, Minghao Zhang, Yafei Zhang, Huawen Zhang, Junxiao Zhang, Jinsu Zhang, Yuxuan Zhang, Zhen Zhang, Cheng Cheng Zhang, Jingyao Zhang, Yi-Chi Zhang, Dongyan Zhang, Haoyuan Zhang, Yiyi Zhang, Yi-Ming Zhang, J Zhang, Mingdi Zhang, Huiping Zhang, Shuchen Zhang, Tongfu Zhang, Yaling Zhang, Huibing Zhang, Hugang Zhang, Danyang Zhang, Yuhao Zhang, Xibo Zhang, Keyi Zhang, Xiaozhe Zhang, Hongjia Zhang, Chenrui Zhang, Chaobao Zhang, Dan Zhang, Changhui Zhang, Wei-Yi Zhang, Simeng Zhang, Lianfeng Zhang, Qingtian Zhang, Xiuxing Zhang, Yongguang Zhang, Changjiang Zhang, Jinxiu Zhang, Xiling Zhang, Zhan-Xiong Zhang, Tianpeng Zhang, Mingzhao Zhang, Dan-Dan Zhang, Renbo Zhang, Yujin Zhang, Xiaochun Zhang, Xinjing Zhang, Yufang Zhang, Zhongwei Zhang, Lina Zhang, Enhui Zhang, Ningning Zhang, Yunfei Zhang, Jiqiang Zhang, Ping Zhang, Jing-Bo Zhang, Zeming Zhang, Jicai Zhang, Yikun Zhang, Fuyang Zhang, Yuanchao Zhang, Sihe Zhang, Haixia Zhang, Zaiqi Zhang, Shilei Zhang, Yayong Zhang, Wenlong Zhang, Zhiguo Zhang, Jiajia Zhang, Hansi Zhang, Yerui Zhang, Zhong-Yuan Zhang, Xiaoqing Zhang, Yuchi Zhang, Yu-Qi Zhang, Shun-Bo Zhang, Xueqin Zhang, Tian-Yu Zhang, Yanping Zhang, Fengxia Zhang, Tengfang Zhang, Shiyi Zhang, Li-ping Zhang, Changquan Zhang, Rusi Zhang, Xueqia Zhang, Yimei Zhang, Ziyin Zhang, Chungu Zhang, Yufeng Zhang, Lingyu Zhang, Sisi Zhang, Changhua Zhang, Xue Zhang, Wen Zhang, Changwang Zhang, XiaoYi Zhang, Keyu Zhang, Runxiang Zhang, C D Zhang, Xi-Feng Zhang, Dadong Zhang, XueWu Zhang, Ziguo Zhang, Zhuqing Zhang, Shuhong Zhang, Di Zhang, J B Zhang, Ningzhi Zhang, Yiwan Zhang, Jennifer Y Zhang, Jiaxin Zhang, Peiwen Zhang, Hanchao Zhang, Tao-Lan Zhang, Sujiang Zhang, Chenyi Zhang, Yizhi Zhang, H D Zhang, Xu-Mei Zhang, Longzhen Zhang, Shiwu Zhang, Longlong Zhang, Pumin Zhang, Fuhan Zhang, Yingjie Zhang, Yong Zhang, H P Zhang, Feixue Zhang, Yuyuan Zhang, Kai-Qiang Zhang, Ye Zhang, Yujiao Zhang, Ruiqian Zhang, Hanxu Zhang, Zhengyu Zhang, Xiuyin Zhang, Tongshuo Zhang, Aijun Zhang, Lanjun Zhang, Mi Zhang, Gu Zhang, JingZi Zhang, Sheng Zhang, Man Zhang, Xinqiao Zhang, Ruikun Zhang, Hai-Feng Zhang, Zongping Zhang, Da Zhang, Xingyu Zhang, Shuanglu Zhang, Shun Zhang, Haoyu Zhang, Chuanyong Zhang, Rey M Zhang, Dongying Zhang, Yunqiang Zhang, Huifang Zhang, Shengye Zhang, Mingxiang Zhang, Wenjuan Zhang, Pinggen Zhang, John H Zhang, Chong-Hui Zhang, Ran Zhang, Minghui Zhang, Wencong Zhang, Ruiyan Zhang, Tianfeng Zhang, Yihao Zhang, Nu Zhang, Shenqi Zhang, Yao-Hua Zhang, Ai-Min Zhang, Shaozhao Zhang, Zhao-Huan Zhang, Jiacheng Zhang, Shao-Qi Zhang, Tian-Guang Zhang, Jibin Zhang, Chenjie Zhang, Meiwei Zhang, Sixue Zhang, Yongchang Zhang, Ying-Lin Zhang, Hongju Zhang, Xianhong Zhang, Ming-Rong Zhang, Benjian Zhang, Binbin Zhang, Meiyu Zhang, Shuwan Zhang, Weizheng Zhang, Yuyanan Zhang, Zhen-Jie Zhang, Hong Zhang, Qian-Wen Zhang, Chuan Zhang, Zhijing Zhang, Xiaoxin Zhang, Yexiang Zhang, Yonghui Zhang, Mingying Zhang, Qin Zhang, Chengrui Zhang, Zijiao Zhang, Xueli Zhang, Yizhe Zhang, Qingyun Zhang, Nannan Zhang, Shuyuan Zhang, Linan Zhang, Jifeng Zhang, Qilu Zhang, Xudong Zhang, Zhanyi Zhang, Shenglei Zhang, Xueping Zhang, Rongguang Zhang, Bing Zhang, Y H Zhang, Yu-Fei Zhang, Zhaocong Zhang, Haibo Zhang, Guojun Zhang, Na Zhang, Lijian Zhang, Huixin Zhang, Yuanzhen Zhang, Yaxuan Zhang, Liangdong Zhang, Donglei Zhang, Huilin Zhang, Shanhong Zhang, Xinyu Zhang, Jianming Zhang, Jiehao Zhang, Weiqin Zhang, Huizhen Zhang, Xian-Li Zhang, Libo Zhang, Guomin Zhang, Jianglin Zhang, Yu-Jing Zhang, Fuming Zhang, Guangye Zhang, Zhezhe Zhang, Qingshuang Zhang, Xianglian Zhang, Saidan Zhang, Mei-Qing Zhang, Shunfen Zhang, Xueming Zhang, Ling Zhang, Hanyu Zhang, Bao-Fu Zhang, XiHe Zhang, Rongxin Zhang, Karen Zhang, Liang Zhang, Junqing Zhang, Yuanqiang Zhang, Pengbo Zhang, H Zhang, Jingdong Zhang, Wenxue Zhang, Xiaocong Zhang, Jia-Su Zhang, Ya-Li Zhang, Haisen Zhang, Meijia Zhang, Jingliang Zhang, Qianqian Zhang, Yonggen Zhang, Shunming Zhang, Aileen Zhang, Hanwang Zhang, Zhihao Zhang, Zhi-Shuai Zhang, Xinlong Zhang, Jintao Zhang, Jingxue Zhang, Yinci Zhang, L-S Zhang, Ailin Zhang, Shuli Zhang, Zhizhong Zhang, Kewen Zhang, Jishou Zhang, Lusha Zhang, Guosen Zhang, Qinghong Zhang, Mengqiu Zhang, Shichao Zhang, Suming Zhang, Chengxiang Zhang, Linlin Zhang, Zhengbin Zhang, Mianzhi Zhang, Ziyi Zhang, En Zhang, Zhiqian Zhang, Chonghe Zhang, Dong-Ying Zhang, Hong-Jie Zhang, Bingqiang Zhang, Jingyi Zhang, Jianan Zhang, Yuying Zhang, Chunling Zhang, Jianbin Zhang, Kaige Zhang, Ying-Jun Zhang, Yue-Bo Zhang, Zicheng Zhang, Cuiyu Zhang, Jiuwei Zhang, Zishuo Zhang, Yihui Zhang, Jia-Si Zhang, Chenlin Zhang, Deqiang Zhang, Zhengxiang Zhang, Luo Zhang, Lilei Zhang, Tianyu Zhang, Keshan Zhang, Qunchen Zhang, Xinlu Zhang, Yuqing Zhang, Guisen Zhang, Mengguo Zhang, N Zhang, Zhi-Shuo Zhang, Lv-Lang Zhang, Lucia Zhang, Hongjuan Zhang, Quanquan Zhang, Shuyi Zhang, Chuyue Zhang, Junfeng Zhang, Hai-Man Zhang, Chun Zhang, Lihong Zhang, Kui Zhang, Hongcai Zhang, Zhuqin Zhang, Yongliang Zhang, Yueru Zhang, Zufa Zhang, Xinye Zhang, Zhong-Bai Zhang, Kejun Zhang, Huimao Zhang, Ruo-Xin Zhang, Pengwei Zhang, Xinfeng Zhang, Zhaohuan Zhang, Shu-Fan Zhang, Lukuan Zhang, Xiu-Peng Zhang, Zhaohua Zhang, Yiping Zhang, Chengwu Zhang, Hang Zhang, Yao Zhang, Wenming Zhang, Luanluan Zhang, Haicheng Zhang, Yanming Zhang, Yajun Zhang, Xingen Zhang, Honglei Zhang, Xingyuan Zhang, Sumei Zhang, Wenyuan Zhang, Rong-Kai Zhang, Guixia Zhang, Jianliang Zhang, QiYue Zhang, Xinbao Zhang, Qinghua Zhang, Jianting Zhang, Xingxing Zhang, Xueyi Zhang, Yi-Wei Zhang, Weijian Zhang, Detao Zhang, Shaofeng Zhang, Yina Zhang, Yu-Hui Zhang, Zhou Zhang, Bo-Fei Zhang, Bixia Zhang, Yuyang Zhang, Chuanmao Zhang, Hongya Zhang, Shuai Zhang, XiaoPing Zhang, Huabing Zhang, Yili Zhang, Dianbo Zhang, Huiying Zhang, Qiuxia Zhang, Xiyu Zhang, Chenyang Zhang, Wanting Zhang, Ni Zhang, Rongying Zhang, Zebang Zhang, Fengshi Zhang, Wannian Zhang, Xiao-Yong Zhang, Xue-Qin Zhang, Chunli Zhang, Ti Zhang, Lifan Zhang, Guanqun Zhang, Erchen Zhang, Chenhong Zhang, Xiaopo Zhang, Dingyu Zhang, Lie Zhang, Mingfeng Zhang, Lu-Yang Zhang, M Q Zhang, Yvonne Zhang, Sheng-Hong Zhang, Li-Jie Zhang, Huanqing Zhang, Shen Zhang, Jun Zhang, Qiguo Zhang, Teng Zhang, Haikuo Zhang, Gary Zhang, Ziping Zhang, Bei-Bei Zhang, Changlin Zhang, Aimin Zhang, Xiao-Feng Zhang, Zepeng Zhang, Zixuan Zhang, Yuan Zhang, Xiaolong Zhang, Junpeng Zhang, Boya Zhang, Fuyuan Zhang, Xiao-Qian Zhang, Zongquan Zhang, Hongyun Zhang, Yaqi Zhang, Tinghu Zhang, Xingyi Zhang, Kejia Zhang, Qiaofang Zhang, Zhicong Zhang, Xiao-Lin Zhang, Gumuyang Zhang, Xingang Zhang, Honghong Zhang, Haoyue Zhang, Shuran Zhang, Hai-Han Zhang, Yihong Zhang, Zhishang Zhang, Qing Zhang, Wenhua Zhang, Chenlu Zhang, G Zhang, Yalan Zhang, Xiaodan Zhang, Geyang Zhang, Lianbo Zhang, Aixiang Zhang, Yujie Zhang, Xiushan Zhang, Xuening Zhang, Xiao-Wei Zhang, Lulu Zhang, Linda S Zhang, Jue Zhang, Linli Zhang, Hongting Zhang, Mengjia Zhang, Huayang Zhang, Cuihua Zhang, Liuwei Zhang, Jing Jing Zhang, Wen-Jing Zhang, Shimao Zhang, Xuewei Zhang, Jingning Zhang, Wanjun Zhang, Yaoxin Zhang, Mingzhen Zhang, Jingxuan Zhang, Mei-Zhen Zhang, Lin-Jie Zhang, Yongfeng Zhang, Lida Zhang, Xuemei Zhang, Ziheng Zhang, Sha Zhang, Jin-Rui Zhang, Wenhao Zhang, Yue-Ming Zhang, Ping-Fan Zhang, Wenjun Zhang, Yutian Zhang, Jiankang Zhang, Xiaobo Zhang, Xian-Man Zhang, Xilin Zhang, Chun-Mei Zhang, Junyan Zhang, Xiu-Juan Zhang, Bingxue Zhang, Liyun Zhang, Dingdong Zhang, Shuye Zhang, Zilong Zhang, Lijuan Zhang, Fang Zhang, Yunli Zhang, Yonggang Zhang, Jinze Zhang, Ling Xia Zhang, Xiaochang Zhang, Chenzi Zhang, Zi-Feng Zhang, Zai-Rong Zhang, Xueting Zhang, Liping Zhang, Xiupeng Zhang, Yanling Zhang, Qiaoxuan Zhang, Donna D Zhang, Zhenhua Zhang, Bohong Zhang, Wenhui Zhang, Shouyue Zhang, Chunguang Zhang, Jingwen Zhang, Jiuxuan Zhang, Xinke Zhang, David Y Zhang, Qun Zhang, Qingyu Zhang, Jian Zhang, Kejin Zhang, Shenglai Zhang, Jiupan Zhang, Xiaosheng Zhang, Mengzhen Zhang, Jinjing Zhang, Youwen Zhang, Yu-Jie Zhang, Alex R Zhang, Yanyan Zhang, Igor Ying Zhang, Kangjun Zhang, Guihua Zhang, Shaojun Zhang, Jianqiong Zhang, Xuexi Zhang, Sifan Zhang, Shuyan Zhang, Xin-Hui Zhang, Xiaobiao Zhang, Junyi Zhang, Susie Zhang, Fubo Zhang, Pan-Pan Zhang, Zhiyu Zhang, Taojun Zhang, Dongfeng Zhang, Dong-juan Zhang, Yi-Feng Zhang, Pan Zhang, Dapeng Zhang, Yukun Zhang, Yingnan Zhang, Yi-Wen Zhang, Tiantian Zhang, Weiwei Zhang, Yuanyi Zhang, Xiaotian Michelle Zhang, Bikui Zhang, Zhihua Zhang, Yadi Zhang, Xingan Zhang, Rui Zhang, Kang-Ling Zhang, Yiguo Zhang, Hongwu Zhang, Hua-Xiong Zhang, Wenqian Zhang, Caishi Zhang, Nan-Nan Zhang, Zhong Zhang, Jingxiao Zhang, Xiaoqi Zhang, Limin Zhang, Zhiyi Zhang, Xiongjun Zhang, Yunqing Zhang, Zhenhao Zhang, Xiuqin Zhang, Zhi Zhang, Chunying Zhang, Fengqing Zhang, Zhanjun Zhang, Zhengxing Zhang, Lixing Zhang, Haojun Zhang, Licui Zhang, Lele Zhang, YiPei Zhang, Shining Zhang, Xiaoyun Zhang, Yannan Zhang, Weili Zhang, Yitian Zhang, Hongfeng Zhang, Yanghui Zhang, Zhifei Zhang, Guo-Liang Zhang, Xiaoxian Zhang, Jiawei Zhang, Jimmy Zhang, Xingxu Zhang, Haohao Zhang, Leiying Zhang, Jihang Zhang, Hui-Wen Zhang, Yongbao Zhang, Ruohan Zhang, Zhuojun Zhang, Rui-fang Zhang, Youmin Zhang, Jing-Zhan Zhang, Dong-qiang Zhang, Yameng Zhang, Xuewen Zhang, Zhiyun Zhang, Jamie Zhang, Yunhang Zhang, Mingyi Zhang, Yujuan Zhang, Lanju Zhang, Longxin Zhang, Runcheng Zhang, Yiyuan Zhang, Hongfu Zhang, Xian-Bo Zhang, Xiao-Hong Zhang, Zhong-Yi Zhang, Si-Zhong Zhang, Yongfa Zhang, Qingcheng Zhang, Yeting Zhang, Guang-Ya Zhang, Juan-Juan Zhang, Mengxian Zhang, Hailiang Zhang, Yuzhi Zhang, Shuge Zhang, Peijun Zhang, Jian-Guo Zhang, Xiaowei Zhang, Yidong Zhang, Zheng Zhang, Zengtie Zhang, Xiangfei Zhang, Dengke Zhang, Xiaohui Zhang, Zhewen Zhang, Jing Zhang, Danyan Zhang, Juan Zhang, Mingyang A Zhang, Xiangsong Zhang, Yingze Zhang, Wen Jun Zhang, Wenbin Zhang, Qi-Min Zhang, X N Zhang, Junli Zhang, Jianying Zhang, Jiaqi Zhang, Yuemei Zhang, Huaiyong Zhang, Yuehua Zhang, Ruisan Zhang, Huihui Zhang, Dalong Zhang, Xiaohong Zhang, Zhongyi Zhang, Rongyu Zhang, Chenming Zhang, Yaru Zhang, Xueya Zhang, Jingping Zhang, Keke Zhang, YuHong Zhang, Junran Zhang, Xingwei Zhang, Biao Zhang, Song Zhang, Xiaodong Zhang, Shiwen Zhang, Kuo Zhang, Yongqiang Zhang, Xiao-Cheng Zhang, Ruyi Zhang, Tong Zhang, Shi-Meng Zhang, Junxiu Zhang, Jun-Feng Zhang, Guo-Guo Zhang, David Zhang, Zhiru Zhang, Kailin Zhang, Zhuo Zhang, Huiming Zhang, Zhuang Zhang, Caiqing Zhang, Jingchuan Zhang, Zixu Zhang, Ruxiang Zhang, Channa Zhang, Shu-Min Zhang, Xiaohan Zhang, Shengkun Zhang, Chunhua Zhang, Xixi Zhang, Xiaoyan Zhang, C H Zhang, Haijun Zhang, H X Zhang, Jingyuan Zhang, Weipeng Zhang, Yipeng Zhang, Ao Zhang, Yaodong Zhang, Mingxiu Zhang, Weiyi Zhang, Xiaoxiao Zhang, Delai Zhang, Mu Zhang, Yanquan Zhang, Liangming Zhang, Yuling Zhang, Jerry Z Zhang, Bicheng Zhang, Lijiao Zhang, Yige Zhang, Yanju Zhang, Shan Zhang, Kaihui Zhang, Chaoke Zhang, Zhenlin Zhang, Tangjuan Zhang, Lingli Zhang, Yuqi Zhang, Luo-Meng Zhang, Haiwang Zhang, Haibing Zhang, Miao Zhang, Miaomiao Zhang, Yimeng Zhang, Anli Zhang, Yun-Sheng Zhang, Yamin Zhang, Yongchao Zhang, Huize Zhang, Yingqian Zhang, Ruizhe Zhang, Wei Zhang, Yongci Zhang, Zhen-Tao Zhang, Daolai Zhang, Zeyan Zhang, Zhaoping Zhang, Xing Zhang, Zhicheng Zhang, Yuanqing Zhang, Zhiping Zhang, J Y Zhang, Yibin Zhang, Rui Yan Zhang, Lun Zhang, Yirong Zhang, Zewen Zhang, Yiming Zhang, Yongxiang Zhang, Xiaoyue Zhang, Xinlian Zhang, Baotong Zhang, Ruimin Zhang, Guohua Zhang, Xiao-Shuo Zhang, Ya-Meng Zhang, Zhenyang Zhang, Lifang Zhang, Shaochuan Zhang, Mingtong Zhang, Kefen Zhang, Tonghan Zhang, Xiaojin Zhang, Qiangyan Zhang, Renliang Zhang, Meng-Jie Zhang, Zhaofeng Zhang, Jiayin Zhang, Guoying Zhang, Guoping Zhang, Chumeng Zhang, Weixia Zhang, Yu-Zhe Zhang, A-Mei Zhang, YuHang Zhang, Xiaokui Zhang, Hui Hua Zhang, Rongrong Zhang, Boyan Zhang, Jiabi Zhang, Zijian Zhang, Xing Yu Zhang, Shou-Mei Zhang, Shu-Dong Zhang, Minzhu Zhang, Yongpeng Zhang, Yuchen Zhang, Yin Zhang, Hanting Zhang, Lantian Zhang, Jing-Chang Zhang, Jiahao Zhang, Zengrong Zhang, Shao Kang Zhang, Cheng Zhang, Jiuchun Zhang, Huawei Zhang, Xueyan Zhang, Huimin Zhang, Bei B Zhang, Saifei Zhang, Qinjun Zhang, Leili Zhang, Yuru Zhang, Huan Zhang, Haojian Zhang, Leitao Zhang, Minghang Zhang, Junru Zhang, Lu Zhang, Heng Zhang, Weiguo Zhang, Pingchuan Zhang, Amy L Zhang, Alaina Zhang, Fanghong Zhang, Yuzhe Zhang, Jinbiao Zhang, Junmei Zhang, Sheng-Dao Zhang, Liuming Zhang, Chenshuang Zhang, Mengying Zhang, Q L Zhang, Xian Zhang, Ke-lan Zhang, Rui-Nan Zhang, Huaqiu Zhang, Minzhi Zhang, Junhang Zhang, Chen-Ran Zhang, Wenli Zhang, Dian Ming Zhang, Jiachao Zhang, Yanjun Zhang, Linbo Zhang, Yunpeng Zhang, Y-H Zhang, Xiaolan Zhang, Yun-Mei Zhang, Bolin Zhang, Jianhua Zhang, Zhigang Zhang, Dongyang Zhang, Jingchun Zhang, Zekun Zhang, Huanyu Zhang, Guoli Zhang, Lufei Zhang, Qingquan Zhang, Deng-Feng Zhang, Xi Zhang, Yi Zhang, Yakun Zhang, Shu-Fang Zhang, Kun Zhang, Ruoying Zhang, Qun-Feng Zhang, Peizhen Zhang, Zhongjie Zhang, Yuhui Zhang, Yongyun Zhang, Xiaofang Zhang, Pengyuan Zhang, Guozhi Zhang, Lianmei Zhang, Jingjing Zhang, Xiaomin Zhang, Shujun Zhang, Weina Zhang, Mingqi Zhang, Sulin Zhang, Yongjie Zhang, Cuiping Zhang, Shiqi Zhang, Qingxiu Zhang, Chengsheng Zhang, Lunan Zhang, Jianxiang Zhang, Zengli Zhang, Haibei Zhang, Guoqing Zhang, Houbin Zhang, Jiaming Zhang, Chun-Qing Zhang, Zhixia Zhang, Xuhao Zhang, Xiangyu Zhang, Yan-Min Zhang, Xiuxiu Zhang, Guofeng Zhang, Bao Long Zhang, Chenan Zhang, Yucai Zhang, Can Zhang, Xingcai Zhang, Xinglai Zhang, H W Zhang, Zhu Zhang, Yuebin Zhang
articles
Qingrong Sun, Siyi Chen, Yingjian Hou +5 more · 2021 · Pathology, research and practice · Elsevier · added 2026-04-24
Metastatic renal cell carcinoma (mRCC) is the important factor for patient mortality, meanwhile gene mutation constantly changes cancer prognosis in tumor process. Exploring the driver mutation in mRC Show more
Metastatic renal cell carcinoma (mRCC) is the important factor for patient mortality, meanwhile gene mutation constantly changes cancer prognosis in tumor process. Exploring the driver mutation in mRCC process become more and more important. We obtained the 15 paired primary and metastatic mRCC samples and analyzed specific mutation genes in the metastatic foci (SMGs) by next generation sequencing. Moreover, we explored the Correlated networks, Pathway and Gene Ontology (GO) enrichment results, prediction analysis of AS sites and prognosis of survival. We identify EPCAM, TMEM127, EZH2, EXT1, CDKN2A, PRF1, AIP, CDK4, PRKARIA as SMGs and find that CDKN2A mutation sites affect the prognosis of mRCC by altering splicing elements. Based on the differential analysis for SMGs in KIRC, we found that EPCAM, PRF1 and EZH2 were differential expression in both primary tumors with metastasis compared to primary tumors without metastasis or metastatic tissues. By the AS prediction analysis, we suggest that CDKN2A mutation sites play an important role for RCC metastasis by affecting the p16/p14 expression. The SMGs could provide new molecular cues associated with tumor metastasis and have potential clinical implications for cancer prognosis and treatment. Definitive conclusions await further validation and follow up. Show less
no PDF DOI: 10.1016/j.prp.2021.153453
EXT1
Xiaowei Zheng, Suwen Shen, Aili Wang +11 more · 2021 · Annals of clinical and translational neurology · Wiley · added 2026-04-24
Angiopoietin-like protein 4 (ANGPTL-4) had been reported to be associated with the risk of ischemic stroke, but its prognostic value remained unclear. The aim of this study was to investigate the asso Show more
Angiopoietin-like protein 4 (ANGPTL-4) had been reported to be associated with the risk of ischemic stroke, but its prognostic value remained unclear. The aim of this study was to investigate the association between plasma ANGPTL-4 concentrations and prognosis of ischemic stroke. Baseline plasma ANGPTL-4 concentrations were measured in 3379 acute ischemic stroke patients. The primary outcome was a combination of death or major disability (modified Rankin Scale score, ≥3) at 3 months after ischemic stroke. At 3 months after ischemic stroke, 850 (26.16%) participants experienced major disability or died (750 major disabilities and 100 deaths). After adjusting for important covariates, odds ratios for the highest tertile of plasma ANGPTL-4 concentrations were 1.59 (1.22-2.06) for primary outcome, 1.53 (1.18-1.97) for major disability, and 2.03 (1.03-4.00) for death when compared with the lowest tertile of plasma ANGPTL-4 concentrations. For 1-SD increase in log-ANGPTL-4 concentrations (0.44 ng/mL), the adjusted odds ratios were 1.24 (1.11-1.38), 1.14 (1.03-1.27), and 1.72 (1.32-2.23), respectively. Adding ANGPTL-4 to a model containing conventional risk factors improved risk prediction for composite outcome of death and major disability. Higher plasma ANGPTL-4 concentration was associated with poor prognosis in acute ischemic stroke patients, suggesting that ANGPTL-4 might be a prognostic marker for ischemic stroke. Show less
📄 PDF DOI: 10.1002/acn3.51319
ANGPTL4
Yazhou Cui, Jing Wang, Genglin Zhang +2 more · 2021 · Stem cell research · Elsevier · added 2026-04-24
Multiple Osteochondroma is an abnormal skeleton development autosomal dominant genetic disease which caused by the mutation of EXT1 gene. In this study, we generated induced pluripotent stem cells (iP Show more
Multiple Osteochondroma is an abnormal skeleton development autosomal dominant genetic disease which caused by the mutation of EXT1 gene. In this study, we generated induced pluripotent stem cells (iPSCs) from the mesenchymal stem cells (MSCs) of a 12-year-old male patient by reprogramming MSCs with non-integrative vectors. The iPSCs line expresses pluripotent markers, has a normal male karyotype and can differentiate into the three germ layers. Show less
no PDF DOI: 10.1016/j.scr.2020.102111
EXT1
Yaxin Zhang, Yuyan Gu, Yihao Chen +12 more · 2021 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
Dingxin Recipe (DXR) is a traditional Chinese medicine formula that has been reported to be effective and safe treatment for cardiovascular diseases, such as arrhythmias, coronary heart disease. Dingx Show more
Dingxin Recipe (DXR) is a traditional Chinese medicine formula that has been reported to be effective and safe treatment for cardiovascular diseases, such as arrhythmias, coronary heart disease. Dingxin Recipe IV (DXR IV) was further improved from the DXR according to the traditional use. However, the mechanism of DXR IV in atherosclerosis is unclear. This study aimed to illustrate whether DXR IV improve atherosclerosis through modulating the lipid metabolism and gut microbiota in atherosclerosis mice. 40 male ApoE DXR IV exerted the anti-atherosclerosis effect by inhibiting the excessive cholesterol deposition in aorta and regulating the level of TG, TC, LDL-C and HDL-C. The composition of gut microbiota was changed. Interestingly, the relative abundance of Muribaculaceae and Ruminococcaceae increased after DXR IV administration, whereas the abundance of Erysipelotrichaceae decreased, which have been beneficial to lipid metabolism. Nine potential metabolic biomarkers, including acetate, butyrate, propionate, alanine, succinate, valerate, xylose, choline, glutamate, were identified, which were related to fatty acid metabolism. Further, the pathway of fatty acid was detected by the RT-qPCR and western blotting. Compared with model group, the level of LXR-α and SREBP1 decreased significantly in DXR IV group while LXR-β, SREBP2 showed no statistical significance. It indicated that DXR IV modulated lipid metabolism by LXR-α/SREBP1 but not LXRβ and SREBP2. DXR IV exhibits potential anti-atherosclerosis effect, which is closely related to lipid metabolism and the gut microbiota. This study may provide novel insights into the mechanism of DXR IV on atherosclerosis and a basis for promising clinical usage. Show less
no PDF DOI: 10.1016/j.jep.2020.113436
NR1H3
Minghui Li, Xuhan Yang, Liya Sun +10 more · 2021 · Journal of psychiatric research · Elsevier · added 2026-04-24
Recent evidence supports an association between lipid metabolism dysfunction and the pathology of schizophrenia which has led to the search for peripheral blood-based biomarkers. The purpose of this s Show more
Recent evidence supports an association between lipid metabolism dysfunction and the pathology of schizophrenia which has led to the search for peripheral blood-based biomarkers. The purpose of this study was to investigate the proteins involved in lipid metabolism (especially apolipoprotein) and to explore their potential as biomarkers for schizophrenia. Using multiple reaction monitoring mass spectrometry (MRM-MS), we quantified 22 proteins in serum samples of 109 healthy controls (HCs) and 111 patients with schizophrenia (SCZ), who were divided into discovery and validation sets. We found serum apolipoprotein A4 (ApoA4) to be significantly decreased in SCZ patients compared to HCs (p=1.61E-05). Moreover, the serum ApoA4 level served as an effective diagnostic tool, achieving area under the receiver operating characteristic curves (AUROC) of 0.840 in the discovery set and 0.791 in the validation set. Additionally, apolipoprotein F (ApoF), angiotensinogen (AGT), and alpha1-antichymotrypsin (ACT) levels were significantly higher in patients with schizophrenia than in healthy controls. These proteins combined with ApoA4, provided higher diagnostic accuracy for schizophrenia in the discovery set (AUROC=0.901) and in the validation set (AUROC=0.879). Our results suggest that the serum level of ApoA4 is a novel potential biomarker for schizophrenia. The proteins identified in this study expand the pool of biomarker candidates for schizophrenia and may be linked to the underlying mechanism of the disease. Show less
no PDF DOI: 10.1016/j.jpsychires.2021.02.016
APOA4
Qingxiu Zhang, Lei He, Mo Chen +8 more · 2021 · Journal of neurochemistry · Blackwell Publishing · added 2026-04-24
Post-synaptic density 93 (PSD-93) mediates glutamate excitotoxicity induced by ischemic brain injury, which then induces microglial inflammatory response. However, the underlying mechanisms of how PSD Show more
Post-synaptic density 93 (PSD-93) mediates glutamate excitotoxicity induced by ischemic brain injury, which then induces microglial inflammatory response. However, the underlying mechanisms of how PSD-93 mediates the crosstalk between neurons and microglia in the post-synaptic dense region remain elusive. CX3 chemokine ligand 1 (CX3CL1) is a chemokine specifically expressed in neurons while its receptor CX3CR1 is highly expressed in microglia. In this study, we examined the interaction of PSD-93 and CX3CL1 in the crosstalk between neurons and microglia in acute ischemic stroke. We utilized male C57BL/6 mice to establish the middle cerebral artery occlusion model (MCAO) and designed a fusion small peptide Tat-CX3CL1 (357-395aa) to inhibit PSD-93 and CX3CL1 interaction. The combination peaks of PSD-93 and CX3CL1 at 6 hr after I/R were observed. The binding sites were located at the 420-535 amino acid sequence of PSD-93 and 357-395 amino acid sequence of CX3CL1. Tat-CX3CL1 (357-395aa) could inhibit the interaction of PSD-93 and CX3CL1 and inhibited the pro-inflammatory cytokine IL-1β and TNF-α expression and provided neuroprotection following reperfusion. Together, these data suggest that PSD-93 binds CX3CL1 to activate microglia and initiate neuroinflammation. Specific blockade of PSD-93-CX3CL1 interaction reduces I/R induced neuronal cell death, and provides a new therapeutic target for ischemic stroke. Show less
no PDF DOI: 10.1111/jnc.15324
DLG2
Yuxin Cui, Zhilei Li, Junxia Cao +5 more · 2021 · Frontiers in oncology · Frontiers · added 2026-04-24
Lung cancer is one of the most prevalent cancers in both men and women worldwide. The nucleic acid G4 structures have been implicated in the transcriptional programmes of cancer-related genes in some Show more
Lung cancer is one of the most prevalent cancers in both men and women worldwide. The nucleic acid G4 structures have been implicated in the transcriptional programmes of cancer-related genes in some cancers such as lung cancer. However, the role of the dominant G4 resolvase DHX36 in the progression of lung cancer remains unknown. In this study, by bioinformatic analysis of public datasets (TCGA and GEO), we find DHX36 is an independent prognosis indicator in non-small-cell lung carcinoma (NSCLC) with subtype dependence. The stable lentiviral knockdown of the DHX36 results in accelerated migration and aggregation of the S-phase subpopulation in lung cancer cells. The reduction of DHX36 level de-sensitises the proliferation response of lung cancer cells to chemotherapeutic drugs such as paclitaxel with cell dependence. The knockdown of this helicase leads to promoted tumour growth, demonstrated by a 3D fluorescence spheroid lung cancer model, and the stimulation of cell colony formation as shown by single-cell cultivation. High throughput proteomic array indicates that DHX36 functions in lung cancer cells through regulating multiple signalling pathways including activation of protein activity, protein autophosphorylation, Fc-receptor signalling pathway, response to peptide hormone and stress-activated protein kinase signalling cascade. A causal transcriptomic analysis suggests that DHX36 is significantly associated with mRNA surveillance, RNA degradation, DNA replication and Myc targets. Therefore, we unveil that DHX36 presents clinical significance and plays a role in tumour suppression in lung cancer, and propose a potentially new concept for an anti-cancer therapy based on helicase-specific targeting. Show less
📄 PDF DOI: 10.3389/fonc.2021.655757
DHX36

Decreased

Qianli Ma, Jin Zhang, Jingjing Huang +11 more · 2021 · Translational lung cancer research · added 2026-04-24
Early-stage female lung adenocarcinoma is the most common type of lung cancer encountered in thoracic surgery departments. Tumor-node-metastasis (TNM) staging does not adequately explain a significant Show more
Early-stage female lung adenocarcinoma is the most common type of lung cancer encountered in thoracic surgery departments. Tumor-node-metastasis (TNM) staging does not adequately explain a significant stratification phenomenon in the prognosis of patients with stage I lung adenocarcinoma. We aimed to investigate the contributory role of We analyzed the microRNA (miRNA) expression level in tumor tissues (high-risk group In all, 24 miRNAs were found to be significantly different between the high-risk group and low-risk group. The expression level of The present study showed that Show less
no PDF DOI: 10.21037/tlcr-21-906
SNAI1
Yi-Zhang Liu, Chi Zhang, Jie-Feng Jiang +5 more · 2021 · Clinica chimica acta; international journal of clinical chemistry · Elsevier · added 2026-04-24
Atherosclerosis, as a chronic inflammatory disease within the arterial wall, is a leading cause of morbidity and mortality worldwide due to its role in myocardial infarction, stroke and peripheral art Show more
Atherosclerosis, as a chronic inflammatory disease within the arterial wall, is a leading cause of morbidity and mortality worldwide due to its role in myocardial infarction, stroke and peripheral artery disease. Additional evidence is emerging that the angiopoietin-like (ANGPTL) family of proteins participate in the pathology of this disease process via endothelial dysfunction, inflammation, dyslipidemia, calcification, foam cell formation and platelet activation. This review summarizes current knowledge on the ANGPTL family of proteins in atherosclerosis related pathological processes. Moreover, the potential value of ANGPTL family proteins as predictive biomarkers in atherosclerosis is discussed. Given the attractive role of ANGPTL3, ANGPTL4, ANGPTL8 in atherosclerotic dyslipidemia via regulation of lipoprotein lipase (LPL), antisense oligonucleotide or/and monoclonal antibody-based inactivation of these proteins represent potential atherosclerotic therapies. Show less
no PDF DOI: 10.1016/j.cca.2021.06.024
ANGPTL4
Qiguo Zhang, Wenyu Gong, Hongyan Wu +11 more · 2021 · Carcinogenesis · Oxford University Press · added 2026-04-24
Bortezomib-based chemotherapy represents the most prevalent regimens for multiple myeloma (MM), whereas acquired drug resistance remains a major obstacle. Myeloma cells often produce excessive amount Show more
Bortezomib-based chemotherapy represents the most prevalent regimens for multiple myeloma (MM), whereas acquired drug resistance remains a major obstacle. Myeloma cells often produce excessive amount of dickkopf-1 (DKK1), giving rise to myeloma bone disease. However, it remains obscure about the effects and mechanisms of DKK1 in the progression and bortezomib responsiveness of MM cells. In the current study, we found WWP2, an E3 ubiquitin-protein ligase, was downregulated in the bortezomib-resistant cells along with high expression of DKK1. Further investigation revealed that WWP2 was a direct target of Wnt/β-catenin signaling pathway, and DKK1 suppressed the expression of WWP2 via canonical Wnt signaling. We further identified that WWP2 mediated the ubiquitination and degradation of GLI2, a main transcriptional factor of the Hedgehog (Hh) pathway. Therefore, DKK1-induced WWP2 downregulation improved GLI2 stability and activation of Hh signaling pathway, contributing to the resistance to bortezomib of MM cells. Clinical data also validated that WWP2 expression was associated with the treatment response and clinic outcomes of MM patients. WWP2 overexpression restricted MM progression and enhanced cell sensitivity to bortezomib treatment in vitro and in vivo. Taken together, our findings demonstrate that DKK1 facilitates the generation of bortezomib resistance in MM via downregulating WWP2 and activating Hh pathway. Thus, the manipulation of DKK1-WWP2-GLI2 axis might sensitize myeloma cells to proteasome inhibitors. Show less
no PDF DOI: 10.1093/carcin/bgab086
WWP2
Cong Xiang, Yannan Zhang, Qiaoli Chen +11 more · 2021 · Journal of cellular and molecular medicine · Blackwell Publishing · added 2026-04-24
Insulin-independent glucose metabolism, including anaerobic glycolysis that is promoted in resistance training, plays critical roles in glucose disposal and systemic metabolic regulation. However, the Show more
Insulin-independent glucose metabolism, including anaerobic glycolysis that is promoted in resistance training, plays critical roles in glucose disposal and systemic metabolic regulation. However, the underlying mechanisms are not completely understood. In this study, through genetically manipulating the glycolytic process by overexpressing human glucose transporter 1 (GLUT1), hexokinase 2 (HK2) and 6-phosphofructo-2-kinase-fructose-2,6-biphosphatase 3 (PFKFB3) in mouse skeletal muscle, we examined the impact of enhanced glycolysis in metabolic homeostasis. Enhanced glycolysis in skeletal muscle promoted accelerated glucose disposal, a lean phenotype and a high metabolic rate in mice despite attenuated lipid metabolism in muscle, even under High-Fat diet (HFD). Further study revealed that the glucose metabolite sensor carbohydrate-response element-binding protein (ChREBP) was activated in the highly glycolytic muscle and stimulated the elevation of plasma fibroblast growth factor 21 (FGF21), possibly mediating enhanced lipid oxidation in adipose tissue and contributing to a systemic effect. PFKFB3 was critically involved in promoting the glucose-sensing mechanism in myocytes. Thus, a high level of glycolysis in skeletal muscle may be intrinsically coupled to distal lipid metabolism through intracellular glucose sensing. This study provides novel insights for the benefit of resistance training and for manipulating insulin-independent glucose metabolism. Show less
📄 PDF DOI: 10.1111/jcmm.16698
MLXIPL
Jia Zheng, Ling Zhang, Jiayi Liu +2 more · 2021 · Frontiers in nutrition · Frontiers · added 2026-04-24
Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain Show more
Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet ( Show less
📄 PDF DOI: 10.3389/fnut.2021.657848
MC4R
Yu Zhang, Jiapeng Xu, Hongbing Fu +3 more · 2021 · Carcinogenesis · Oxford University Press · added 2026-04-24
Gastric cancer (GC) remains one of the most frequent cancers worldwide. Previous studies have shown that E3 ubiquitin ligase E3C (UBE3C) promotes the progression of multiple types of cancer. However, Show more
Gastric cancer (GC) remains one of the most frequent cancers worldwide. Previous studies have shown that E3 ubiquitin ligase E3C (UBE3C) promotes the progression of multiple types of cancer. However, little is known about the expression and molecular mechanism of UBE3C in GC. In this study, UBE3C is upregulated in clinical GC samples and RNA-seq data from The Cancer Genome Atlas, and the UBE3C upregulation is correlated with poor clinical outcomes in patients with GC. In vitro, knockdown of UBE3C suppresses proliferation and enhances apoptosis in GC cells by inhibiting β-catenin signaling pathway. In contrast, in vitro overexpression of UBE3C promotes GC cell proliferation and inhibits apoptosis through the upregulation of β-catenin signaling by promoting ubiquitination of AXIN1. In vivo, knockdown of UBE3C inhibits tumor growth in a nude mouse model. Concurrently, the UBE3C knockdown resulted in an increase of AXIN1 and a reduction of β-catenin in the nucleus and cytoplasm in the xenograft tumor tissues. Our results demonstrate that UBE3C promotes GC progression through activating the β-catenin signaling via degradation of AXIN1. Our data suggest that UBE3C exerts oncogenic effects in GC and thus provides a promising prognostic biomarker and a potential therapeutic target for GC therapy. Show less
no PDF DOI: 10.1093/carcin/bgaa098
AXIN1
Hui Yang, Melody Zhang, Xuan-Yu Mao +3 more · 2021 · Cells · MDPI · added 2026-04-24
Secreted angiopoietin/angiopoietin-like (
📄 PDF DOI: 10.3390/cells10102590
ANGPTL4
H-Y Piao, S Guo, Y Wang +1 more · 2021 · Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · Springer · added 2026-04-24
Clinically, hypoxia is associated with increased distant metastasis and poor survival in gastric cancer (GC). In this study, we set out from the cellular interaction to further explain the molecular m Show more
Clinically, hypoxia is associated with increased distant metastasis and poor survival in gastric cancer (GC). In this study, we set out from the cellular interaction to further explain the molecular mechanism of invasion in GC cells under hypoxic conditions. Gastric cancer cells were cultured under 1% O HGC-medium induced NGC dissociated. Long non-coding RNA (lncRNA) prostate cancer gene expression marker 1 (PCGEM1) was specifically expressed in HGC exosomes. HGC-derived PCGEM1-riched exosomes could promote the invasion and migration of NGC. On the mechanism, PCGEM1 maintained stability and reduced the degradation of SNAI1, which could induce the epithelial-mesenchymal transition of GC. LncRNA PCGEM1 was overexpressed in GC cells. And part of the PCGEM1 can be encapsulated into exosomes. These exosomes promoted invasion and migration of other GC cells. We considered PCGEM1 might act as a "scaffold" combined with SNAI1 and prompt the invasion and migration of GC. Show less
no PDF DOI: 10.1007/s12094-020-02412-9
SNAI1
Weimin Wang, Ke Min, Gaoyang Chen +5 more · 2021 · Journal of Cancer · added 2026-04-24
📄 PDF DOI: 10.7150/jca.58768
CETP
Chenshen Huang, Na Zhang, Hao Xiong +8 more · 2021 · Frontiers in immunology · Frontiers · added 2026-04-24
Currently, a comprehensive method for exploration of transcriptional regulation has not been well established. We explored a novel pipeline to analyze transcriptional regulation using co-analysis of R Show more
Currently, a comprehensive method for exploration of transcriptional regulation has not been well established. We explored a novel pipeline to analyze transcriptional regulation using co-analysis of RNA sequencing (RNA-seq), assay for transposase-accessible chromatin using sequencing (ATAC-seq), and chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq). The G protein-coupled receptors (GPCRs) possibly associated with macrophages were further filtered using a reduced-Cox regression model. ATAC-seq profiles were used to map the chromatin accessibility of the GPRC5B promoter region. Pearson analysis was performed to identify the transcription factor (TF) whose expression was correlated with open chromatin regions of GPRC5B promoter. ChIP-seq profiles were obtained to confirm the physical binding of GATA4 and its predicted binding regions. For verification, quantitative polymerase chain reaction (qPCR) and multidimensional database validations were performed. The reduced-Cox regression model revealed the prognostic value of GPRC5B. A novel pipeline for TF exploration was proposed. With our novel pipeline, we first identified chr16:19884686-19885185 as a reproducible open chromatin region in the GPRC5B promoter. Thereafter, we confirmed the correlation between GATA4 expression and the accessibility of this region, confirmed its physical binding, and proved GPRC5B, correlated with macrophages, was a key GPCR affecting COAD prognosis. Further, with our novel pipeline, TF GATA4 was identified as a direct upstream of GPRC5B. This study proposed a novel pipeline for TF exploration and provided a theoretical basis for COAD therapy. Show less
📄 PDF DOI: 10.3389/fimmu.2021.741634
GPRC5B
Tian Hua, Rui-Min Wang, Xiao-Chong Zhang +4 more · 2021 · Bioscience reports · added 2026-04-24
Ovarian cancer (OV) is the most lethal gynecologic malignancy. One major reason of the high mortality of the disease is due to platinum-based chemotherapy resistance. Increasing evidence reveal the im Show more
Ovarian cancer (OV) is the most lethal gynecologic malignancy. One major reason of the high mortality of the disease is due to platinum-based chemotherapy resistance. Increasing evidence reveal the important biological functions and clinical significance of zinc finger proteins (ZNFs) in OV. In the present study, the relationship between the zinc finger protein 76 (ZNF76) and clinical outcome and platinum resistance in patients with OV was explored. We further analyzed ZNF76 expression via multiple gene expression databases and identified its functional networks using cBioPortal. RT-qPCR and IHC assay shown that the ZNF76 mRNA and protein expression were significantly lower in OV tumor than that in normal ovary tissues. A strong relationship between ZNF76 expression and platinum resistance was determined in patients with OV. The low expression of ZNF76 was associated with worse survival in OV. Multivariable analysis showed that the low expression of ZNF76 was an independent factor predicting poor outcome in OV. The prognosis value of ZNF76 in pan-cancer was validated from multiple cohorts using the PrognoScan database and GEPIA 2. A gene-clinical nomogram was constructed by multivariate cox regression analysis, combined with clinical characterization and ZNF76 expression in TCGA. Functional network analysis suggested that ZNF76 was involved in several biology progressions which associated with OV. Ten hub genes (CDC5L, DHX16, SNRPC, LSM2, CUL7, PFDN6, VARS, HSD17B8, PPIL1, and RGL2) were identified as positively associated with the expression of ZNF76 in OV. In conclusion, ZNF76 may serve as a promising prognostic-related biomarker and predict the response to platinum in OV patients. Show less
no PDF DOI: 10.1042/BSR20212026
SNRPC
Libin Wen, Jiaping Zhu, Fengxi Zhang +3 more · 2021 · BMC veterinary research · BioMed Central · added 2026-04-24
Porcine circovirus-like virus P1 is a relatively new kind of virus that is closely related to the post-weaning multisystemic wasting syndrome, congenital tremors, and abortions in swine. The molecular Show more
Porcine circovirus-like virus P1 is a relatively new kind of virus that is closely related to the post-weaning multisystemic wasting syndrome, congenital tremors, and abortions in swine. The molecular mechanisms of P1 virus infection and pathogenesis are fully unknown. To analyze P1 and its host interactions, we used a yeast two-hybrid (Y2H) assay to identify cellular proteins interacting with the Cap of the P1 virus. In this study, the Cap of the P1 virus exhibited no self-activation and toxicity to yeast cells and was used as bait to screen the Y2H library prepared from the pancreas tissue. Five cellular proteins (EEP, Ral GDS, Bcl-2-L-12, CPS1, and one not identified) were found to interact with P1 Cap. The interaction between Cap and Ral GDS was confirmed by co-immunoprecipitation. Our data are likely to support the future investigation of the underlying mechanism of P1 infection and pathogenesis. Show less
📄 PDF DOI: 10.1186/s12917-021-02926-6
CPS1
Sally Yepes, Nirav N Shah, Jiwei Bai +20 more · 2021 · Cancers · MDPI · added 2026-04-24
Chordoma is a rare bone cancer with an unknown etiology. TBXT is the only chordoma susceptibility gene identified to date; germline single nucleotide variants and copy number variants in TBXT have bee Show more
Chordoma is a rare bone cancer with an unknown etiology. TBXT is the only chordoma susceptibility gene identified to date; germline single nucleotide variants and copy number variants in TBXT have been associated with chordoma susceptibility in familial and sporadic chordoma. However, the genetic susceptibility of chordoma remains largely unknown. In this study, we investigated rare germline genetic variants in genes involved in TBXT/chordoma-related signaling pathways and other biological processes in chordoma patients from North America and China. We identified variants that were very rare in general population and internal control datasets and showed evidence for pathogenicity in 265 genes in a whole exome sequencing (WES) dataset of 138 chordoma patients of European ancestry and in a whole genome sequencing (WGS) dataset of 80 Chinese patients with skull base chordoma. Rare and likely pathogenic variants were identified in 32 of 138 European ancestry patients (23%), including genes that are part of notochord development, PI3K/AKT/mTOR, Sonic Hedgehog, SWI/SNF complex and mesoderm development pathways. Rare pathogenic variants in COL2A1, EXT1, PDK1, LRP2, TBXT and TSC2, among others, were also observed in Chinese patients. We identified several rare loss-of-function and predicted deleterious missense variants in germline DNA from patients with chordoma, which may influence chordoma predisposition and reflect a complex susceptibility, warranting further investigation in large studies. Show less
📄 PDF DOI: 10.3390/cancers13112704
EXT1
Jiaojiao Zhu, Cuizhe Wang, Xueting Zhang +9 more · 2021 · Journal of diabetes investigation · Blackwell Publishing · added 2026-04-24
Microribonucleic acid-155 (microRNA155) and microRNA29 are reported to inhibit glucose metabolism in some cell and animal models, but no evidence from susceptible populations that examines the relatio Show more
Microribonucleic acid-155 (microRNA155) and microRNA29 are reported to inhibit glucose metabolism in some cell and animal models, but no evidence from susceptible populations that examines the relationship between microRNA155 or microRNA29 and type 2 diabetes mellitus currently exists. Furthermore, target genes regulated by microRNA155 and microRNA29 that affect glucose and lipid metabolism remain unknown. Human participants were divided into normal weight (n = 72), obesity (n = 120) and type 2 diabetes (n = 59) groups. The contents of microRNA155 and microRNA29 abundance in serum were measured, and candidate genes potentially related to glucose and lipid metabolism targeted by either microRNA155 or microRNA29 were screened. Overexpression of microRNA155 and microRNA29 in HepG2 cells was used to verify candidate gene expression, and measure the effects on glucose and lipid metabolism. Serum levels of microRNA155 and microRNA29 show a significant increase in individuals with obesity and type 2 diabetes compared with normal weight individuals. Identified target genes for microRNA155 were MAPK14, MAP3K10, DUSP14 and PRKAR2B. Identified target genes for microRNA29 were PEX11A and FADS1. Overexpression of microRNA155 or microRNA29 in HepG2 cells was found to downregulate the expression of identified target genes, and result in inhibition of triglyceride synthesis and glucose incorporation. MicroRNA155 and microRNA29 were significantly higher in type 2 diabetes patients compared with the control patients, their levels were also positively correlated with fasting plasma glucose levels, and over-expression of microRNA155 or microRNA29 were found to downregulate glucose and lipid metabolism target genes, and reduce lipid synthesis and glucose incorporation in HepG2 cells. Show less
📄 PDF DOI: 10.1111/jdi.13334
FADS1
XiaoYan Guo, Qinqin Zheng, Mingrui Lin +2 more · 2021 · Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics · added 2026-04-24
To explore the genetic basis for a pedigree affected with hereditary multiple osteochondroma (HMO). Peripheral blood samples were collected from the proband and members of his pedigree with informed c Show more
To explore the genetic basis for a pedigree affected with hereditary multiple osteochondroma (HMO). Peripheral blood samples were collected from the proband and members of his pedigree with informed consent. Following extraction of genomic DNA, all coding exons and flanking intronic sequences (-10 bp) of the EXT1 and EXT2 genes were subjected to targeted capture and next generation sequencing (NGS). Suspected variant was verified by Sanger sequencing. A heterozygous nonsense variant (c.1911C>A) was found in exon 10 of the EXT1 gene in the proband and his affected father but not in a healthy sister and normal controls. The variant was classified as a pathogenic based on the guidelines of the American College of Medical Genetics and Genomics (PVS1+PM2+PP1). Bioinformatic analysis predicted that the c.1911C>A variant may be disease-causing via nonsense-mediated mRNA decay and anomalous splicing. The c.1911C>A variant probably underlay the disease in this pedigree. Discovery of this variant enriched the variant spectrum of HMO. Show less
no PDF DOI: 10.3760/cma.j.cn511374-20200415-00272
EXT1
Qian ZHANG, Challa Tenagne Delessa, Robert Augustin +33 more · 2021 · Cell metabolism · Elsevier · added 2026-04-24
Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypot Show more
Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism. Show less
📄 PDF DOI: 10.1016/j.cmet.2021.01.015
GIPR
Ming Gao, Guijie Guo, Jinzhou Huang +17 more · 2021 · Nucleic acids research · Oxford University Press · added 2026-04-24
RPA is a critical factor for DNA replication and replication stress response. Surprisingly, we found that chromatin RPA stability is tightly regulated. We report that the GDP/GTP exchange factor DOCK7 Show more
RPA is a critical factor for DNA replication and replication stress response. Surprisingly, we found that chromatin RPA stability is tightly regulated. We report that the GDP/GTP exchange factor DOCK7 acts as a critical replication stress regulator to promote RPA stability on chromatin. DOCK7 is phosphorylated by ATR and then recruited by MDC1 to the chromatin and replication fork during replication stress. DOCK7-mediated Rac1/Cdc42 activation leads to the activation of PAK1, which subsequently phosphorylates RPA1 at S135 and T180 to stabilize chromatin-loaded RPA1 and ensure proper replication stress response. Moreover, DOCK7 is overexpressed in ovarian cancer and depleting DOCK7 sensitizes cancer cells to camptothecin. Taken together, our results highlight a novel role for DOCK7 in regulation of the replication stress response and highlight potential therapeutic targets to overcome chemoresistance in cancer. Show less
📄 PDF DOI: 10.1093/nar/gkab134
DOCK7
Yang Yang, Mingyang Feng, LiangLiang Bai +10 more · 2021 · Journal of translational medicine · BioMed Central · added 2026-04-24
EMT is an important biological process in the mechanism of tumor invasion and metastasis. However, there are still many unknowns about the specific mechanism of EMT in tumor. At present, a comprehensi Show more
EMT is an important biological process in the mechanism of tumor invasion and metastasis. However, there are still many unknowns about the specific mechanism of EMT in tumor. At present, a comprehensive analysis of EMT-related genes in colorectal cancer (CRC) is still lacking. All the data were downloaded from public databases including TCGA database (488 tumor samples and 52 normal samples) as the training set and the GEO database (GSE40967 including 566 tumor samples and 19 normal samples, GSE12945 including 62 tumor samples, GSE17536 including 177 tumor samples, GSE17537 including 55 tumor samples) as the validation sets. One hundred and sixty-six EMT-related genes (EMT-RDGs) were selected from the Molecular Signatures Database. Bioinformatics methods were used to analyze the correlation between EMT-RDGs and CRC prognosis, metastasis, drug efficacy, and immunity. We finally obtained nine prognostic-related EMT-RDGs (FGF8, NOG, PHLDB2, SIX2, SNAI1, TBX5, TIAM1, TWIST1, TCF15) through differential expression analysis, Unicox and Lasso regression analysis, and then constructed a risk prognosis model. There were significant differences in clinical characteristics, 22 immune cells, and immune functions between the high-risk and low-risk groups and the different states of the nine prognostic-related EMT-RDGs. The methylation level and mutation status of nine prognostic-related EMT-RDGs all affect their regulation of EMT. The Cox proportional hazards regression model was also constructed by the methylation sites of nine prognostic-related EMT-RDGs. In addition, the expression of FGF8, PHLDB2, SIX2, and SNAIL was higher and the expression level of NOG and TWIST1 was lower in the non-metastasis CRC group. Nine prognostic-related EMT-RDGs also affected the drug treatment response of CRC. Targeting these nine prognostic-related EMT-RDGs can regulate CRC metastasis and immune, which is beneficial for the prognosis of CRC patients, improve drug sensitivity in CRC patients. Show less
no PDF DOI: 10.1186/s12967-021-03065-0
SNAI1
Yongyun Zhang, Xinyang Fan, Lihua Qiu +3 more · 2021 · Journal of dairy science · added 2026-04-24
Liver X receptor α (LXRα; NR1H3) is an important transcription factor that can facilitate milk fat synthesis by regulating the transcription of FASN in mice and goats. Nevertheless, the lipid synthesi Show more
Liver X receptor α (LXRα; NR1H3) is an important transcription factor that can facilitate milk fat synthesis by regulating the transcription of FASN in mice and goats. Nevertheless, the lipid synthesis related to LXRα and its regulation on FASN in the buffalo mammary gland remain elusive. Here, we demonstrated that the mRNA and protein expression of LXRα in buffalo mammary tissue increased in lactation compared with that in the dry-off period. Overexpression of NR1H3 enhanced the lipid droplet formation and triacylglycerol concentration in buffalo mammary epithelial cells (BuMEC), whereas the knockdown of NR1H3 resulted in a decrease in the number of lipid droplets. At the same time, NR1H3 also affected the expression of regulatory factors (INSIG1, INSIG2, SREBF1, and PPARG) related to milk fat synthesis and that of genes involved in de novo synthesis (FASN, ACACA, and SCD), and uptake and transport (LPL, CD36, and FABP3) of fatty acids as well as triacylglycerol synthesis (GPAM, APGAT6, and DGAT1). Luciferase reporter assays indicated that overexpression of NR1H3 resulted in an increase in the activity of FASN promoter, whereas the knockdown of NR1H3 had an opposite effect. When NR1H3 was overexpressed, mutations in LXRE or SRE could decrease the promoter activity of FASN. Furthermore, mutagenesis of both LXRE and SRE within the FASN promoter completely eliminated the induced activity of LXRα. Our results reveal that buffalo LXRα promotes milk fat synthesis through regulating the expression of FASN by directly interacting with FASN promoter and affecting the SREBF1 expression. This study underscores a crucial role of LXRα in regulating lipid synthesis of the buffalo mammary gland. Show less
no PDF DOI: 10.3168/jds.2021-20596
NR1H3
Yingshu Cao, Xin Di, Qinghua Zhang +2 more · 2021 · Frontiers in oncology · Frontiers · added 2026-04-24
The RNA-binding motif protein 10 (RBM10) is involved in alternative splicing and modifies mRNA post-transcriptionally. RBM10 is abnormally expressed in the lung, breast, and colorectal cancer, female Show more
The RNA-binding motif protein 10 (RBM10) is involved in alternative splicing and modifies mRNA post-transcriptionally. RBM10 is abnormally expressed in the lung, breast, and colorectal cancer, female genital tumors, osteosarcoma, and other malignant tumors. It can inhibit proliferation, promote apoptosis, and inhibit invasion and metastasis. RBM10 has long been considered a tumor suppressor because it promotes apoptosis through the regulation of the MDM2-p53 negative feedback loop, Bcl-2, Bax, and other apoptotic proteins and inhibits proliferation through the Notch signaling and rap1a/Akt/CREB pathways. However, it has been recently demonstrated that RBM10 can also promote cancer. Given these different views, it is necessary to summarize the research progress of RBM10 in various fields to reasonably analyze the underlying molecular mechanisms, and provide new ideas and directions for the clinical research of RBM10 in various cancer types. In this review, we provide a new perspective on the reasons for these opposing effects on cancer biology, molecular mechanisms, research progress, and clinical value of RBM10. Show less
no PDF DOI: 10.3389/fonc.2021.603932
RBM6
Yunpeng Li, Xiaozhu Wang, Liumei Lu +11 more · 2021 · Molecular metabolism · Elsevier · added 2026-04-24
Homo- or heterodimerization of G protein-coupled receptors (GPCRs) generally alters the normal functioning of these receptors and mediates their responses to a variety of physiological stimuli in vivo Show more
Homo- or heterodimerization of G protein-coupled receptors (GPCRs) generally alters the normal functioning of these receptors and mediates their responses to a variety of physiological stimuli in vivo. It is well known that melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R) are key regulators of appetite and energy homeostasis in the central nervous system (CNS). However, the GPCR partners of MC3R and MC4R are not well understood. Our objective is to analyze single cell RNA-seq datasets of the hypothalamus to explore and identify novel GPCR partners of MC3R and MC4R and examine the pharmacological effect on the downstream signal transduction and membrane translocation of melanocortin receptors. We conducted an integrative analysis of multiple single cell RNA-seq datasets to reveal the expression pattern and correlation of GPCR families in the mouse hypothalamus. The emerging GPCRs with important metabolic functions were selected for cloning and co-immunoprecipitation validation. The positive GPCR partners were then tested for the pharmacological activation, competitive binding assay and surface translocation ELISA experiments. Based on the expression pattern of GPCRs and their function enrichment results, we narrowed down the range of potential GPCR interaction with MC3R and MC4R for further confirmation. Co-immunoprecipitation assay verified 23 and 32 novel GPCR partners that interacted with MC3R and MC4R in vitro. The presence of these GPCR partners exhibited different effects in the physiological regulation and signal transduction of MC3R and MC4R. This work represented the first large-scale screen for the functional GPCR complex of central melanocortin receptors and defined a composite metabolic regulatory GPCR network of the hypothalamic nucleuses. Show less
📄 PDF DOI: 10.1016/j.molmet.2021.101317
MC4R
Xitong Zhao, Huatao Liu, Yongjie Pan +6 more · 2021 · Frontiers in genetics · Frontiers · added 2026-04-24
Preadipocyte differentiation plays an important role in lipid deposition and affects fattening efficiency in pigs. In the present study, preadipocytes isolated from the subcutaneous adipose tissue of Show more
Preadipocyte differentiation plays an important role in lipid deposition and affects fattening efficiency in pigs. In the present study, preadipocytes isolated from the subcutaneous adipose tissue of three Landrace piglets were induced into mature adipocytes Show less
📄 PDF DOI: 10.3389/fgene.2021.753725
ANGPTL4
Yingxue Wang, Zhe Yin, Ni Zhang +4 more · 2021 · Journal of musculoskeletal & neuronal interactions · added 2026-04-24
To explore the role and mechanism of miR-125a-3p in rheumatoid arthritis (RA) progression. The RA-tissues and fibroblast-like synovial cells in rheumatoid arthritis (RA-FLS) were used in this study. q Show more
To explore the role and mechanism of miR-125a-3p in rheumatoid arthritis (RA) progression. The RA-tissues and fibroblast-like synovial cells in rheumatoid arthritis (RA-FLS) were used in this study. qRT-PCR, western blot and ELISA assay were performed to detect the expression levels of IL-6, IL-β and ΤΝF-α. Dual-luciferase reporter gene assay was used to observe the binding effect of miR-125a-3p and MAST3, and CCK-8 was used to observe the effect of miR-125a-3p on the proliferation of RA-FLS. miR-125a-3p was significantly downregulated in the RA-tissues and RA-FLS, and miR-125a-3p could inhibit the proliferation and reduce the inflammation response of RA-FLS. Besides, MAST3 was found as a target of miR-125a-3p, and increased MAST3 could reverse the effects of miR-125a-3p on RA-FLS including decreased proliferation, reduced inflammation level and the inactivation of Wnt/β-catenin and NF-κB pathways. This study suggests that miR-125a-3p could inactivate the Wnt/β-catenin and NF-κB pathways to reduce the proliferation and inflammation response of RA-FLS via targeting MAST3. Show less
MAST3