👤 Shuai Xu

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Also published as: Ting-Xin Xu, Shuang Xu, Renyuan Xu, Cheng Xu, Xiao Xu, Jia-Chen Xu, Yanyong Xu, Shengjie Xu, Nong Xu, D-J Xu, Hongfa Xu, Shiyi Xu, Yunjian Xu, Maochang Xu, Lingyan Xu, Guoheng Xu, Zaibin Xu, Yuexuan Xu, Jinhe Xu, Yitong Xu, Yaping Xu, Miao Xu, Hongming Xu, Jiang Xu, Feng-Qin Xu, Zaihua Xu, Yaru Xu, Yuanzhong Xu, Qiuyu Xu, Mingcong Xu, Mai Xu, Biao Xu, Jingjun Xu, Shuwan Xu, Ya-Ru Xu, Zhilong Xu, Jun-Chao Xu, Shutao Xu, TianBo Xu, Jinyu Xu, Peng Xu, Guo-Xing Xu, Jie-Hua Xu, Yushan Xu, Yongsong Xu, Xin-Rong Xu, Xiang-Min Xu, Bilin Xu, Xiaolong Xu, Jinchao Xu, Han Xu, Xuting Xu, Yu Xu, Yingqianxi Xu, Yanyang Xu, Aili Xu, Weizhi Xu, Peidi Xu, Tongyang Xu, Tieshan Xu, Jianping Xu, Wen-Juan Xu, Bing Xu, Chengyun Xu, Xiaofeng Xu, Zhengang Xu, Guang-Hong Xu, Fangui Xu, Shan-Shan Xu, Hailiang Xu, Song-Song Xu, Quanzhong Xu, Mengqi Xu, Gezhi Xu, Dawei Xu, Linyan Xu, Yidan Xu, Tonghong Xu, Meishu Xu, Panpan Xu, Keli Xu, Xiufeng Xu, Hongwen Xu, Hanyuan Xu, Liang Xu, Zaoyi Xu, Fengqin Xu, Run-Xiang Xu, Xiaoyan Xu, Ruxiang Xu, Huiming Xu, Daqian Xu, Qin-Zhi Xu, Jiancheng Xu, Boming Xu, Zihao Xu, Jinghong Xu, Aimin Xu, Renfang Xu, Ran Xu, Di-Mei Xu, Xiang-liang Xu, Yana Xu, Richard H Xu, Yanchang Xu, Danyi Xu, Xiaocheng Xu, Chengqi Xu, Lingli Xu, Xiaoshuang Xu, H X Xu, Min Xu, Ya'nan Xu, Zhi Ping Xu, Zihe Xu, Hongle Xu, Xuan Xu, Jielin Xu, Yuping Xu, Yinli Xu, Limin Xu, Renshi Xu, Da Xu, C C Xu, Yongqing Xu, Heping Xu, Yiquan Xu, Weilan Xu, Jingjing Xu, Yangxian Xu, Yifan Xu, Congjian Xu, Wentao Xu, Binqiang Xu, Yuerong Xu, Jiaqi Xu, Shang-Fu Xu, Jiachi Xu, Zhi-Qing David Xu, Yuejuan Xu, Chao Xu, Yi-Xian Xu, Longfei Xu, Ziwei Xu, Mengyue Xu, Jingying Xu, Wenhui Xu, Zi-Xiang Xu, Caixia Xu, Chenjie Xu, Xiaoting Xu, Jiacheng Xu, Chunhui Xu, Chengxun Xu, Hengyi Xu, Songsong Xu, Lingyao Xu, Qingqiu Xu, Gangchun Xu, Yanjun Xu, Zifan Xu, Qiong Xu, Wenxuan Xu, Jiayunzhu Xu, Yifeng Xu, DongZhu Xu, Lingna Xu, Qianzhu Xu, Bocheng Xu, Qingjia Xu, Yanni Xu, Li-Yan Xu, Benhong Xu, Fang Xu, Xingsheng Xu, Geyang Xu, Anqi Xu, Zeao Xu, Mengsi Xu, Jun Xu, Ning'an Xu, Qiuhong Xu, H F Xu, Lian-Wei Xu, Hua Xu, Danping Xu, Xiaofang Xu, Shanshan Xu, Sheng-Qian Xu, Bingxin Xu, Ke Xu, Shiqing Xu, Cunshuan Xu, Guangwei Xu, Beibei Xu, Changwu Xu, Zhuangzhuang Xu, Chong-Feng Xu, Yunyi Xu, Yunxuan Xu, Zeya Xu, Jinshu Xu, Laizhi Xu, Xinyu Xu, Meiyu Xu, Bi-Yun Xu, Mingliang Xu, Weixia Xu, Bingfang Xu, Suling Xu, W W Xu, Lidan Xu, Chengkai Xu, Feng Xu, Yunhe Xu, Zesheng Xu, Li Xu, Song Xu, Yungen Xu, Yaobo Xu, Qinli Xu, Yi-Liang Xu, Dong Xu, Tan Xu, Ruiling Xu, Wanqi Xu, Ziyang Xu, Xiaohong Ruby Xu, Guangyu Xu, Xiao-Shan Xu, Wenxin Xu, Yongsheng Xu, Jingya Xu, Zhong-Hua Xu, Jiajie Xu, Dan Xu, Youjia Xu, Longsheng Xu, Mengjie Xu, Guo-Tong Xu, Ting Xu, Chunwei Xu, Tianmin Xu, Xianghong Xu, Nenggui Xu, Hongxia Xu, Meixi Xu, Rongying Xu, Guoliang Xu, Lisi Xu, Leisheng Xu, Yurui Xu, Xianli Xu, Honglin Xu, Yunfang Xu, Guo Xu, Shengyu Xu, Kelin Xu, Xiaoqin Xu, Zheng Xu, Junchang Xu, Jiaying Xu, Beisi Xu, Chunyu Xu, Zhen-Guo Xu, Haonan Xu, Tianyi Xu, Haiman Xu, Lili Xu, Yi Xu, Dongju Xu, Qihang Xu, Zhongwei Xu, Zihua Xu, Qikui Xu, Zhijie Xu, Li-Jun Xu, Qi-Qi Xu, Hanchen Xu, Yaqi Xu, Daohua Xu, Shaonian Xu, Xihui Xu, Ziqi Xu, D Xu, Tian-Ying Xu, Xiangbin Xu, Chen-Run Xu, Bin Xu, Jianjuan Xu, Zhanyu Xu, Lingjuan Xu, Wenjie Xu, Shuwen Xu, Cian Xu, Qiulin Xu, Yu-Ming Xu, Zeyu Xu, Jia Xu, Zengliang Xu, Yujie Xu, Yuting Xu, Jing-Yi Xu, Jiajia Xu, Xiqi Xu, Leiyu Xu, Shi-Na Xu, Ruonan Xu, Wenhuan Xu, Bai-Hui Xu, Jishu Xu, Xiangyu Xu, Lu-Lu Xu, Shiyun Xu, Huaxiang Xu, Lei Xu, Yuli Xu, Chan Xu, Tengfei Xu, Yong Xu, Xuejun Xu, Hang Xu, Jinjie Xu, Junjie Xu, Haoda Xu, Rui-Ming Xu, Yunxi Xu, Jinghua Xu, Ye Xu, Jiyi Xu, Mei-Jun Xu, Jianyong Xu, Yingzheng Xu, Kaiyue Xu, Yeqiu Xu, Songli Xu, Chenqi Xu, Cheng-Jian Xu, Qiaoshi Xu, YanFeng Xu, Rongrong Xu, Jin Xu, Huimian Xu, Zaikun Xu, Aixiao Xu, Yanfei Xu, Chunlin Xu, Huiqiong Xu, Dapeng Xu, Fengxia Xu, Yongmei Xu, Yubin Xu, Xiaojing Xu, Pu Xu, Xiaoli Xu, Wenming Xu, Wenjing Xu, Wenjuan Xu, Haijin Xu, Yawei Xu, Chuanrui Xu, Wenping Xu, Tongtong Xu, Zhigang Xu, Yinfeng Xu, Zi-Hua Xu, Jiean Xu, Ming Xu, Keshu Xu, Weili Xu, Guofeng Xu, Ai-Guo Xu, Xingyu Xu, Shujing Xu, Weiqun Xu, Wen-Hao Xu, Hong-wei Xu, Jianfeng Xu, Y Xu, Steven Jing-Liang Xu, Fangfang Xu, Xiao-Dan Xu, Keyun Xu, Yetao Xu, Qianhui Xu, Chaoqun Xu, Fenghuang Xu, Yuzhi Xu, Tengxiao Xu, Zelin Xu, Xueni Xu, Jing-Ying Xu, Yichi Xu, Ruifeng Xu, Kewei Xu, Jiapeng Xu, Fang-Fang Xu, Sifan Xu, Pengli Xu, Jiaqin Xu, Xiaotao Xu, Chunming Xu, X Xu, Xinyin Xu, Gang Xu, Wei Xu, Yuzhen Xu, Wancheng Xu, Qiming Xu, Hailey Xu, Yuanyuan Xu, Yimeng Xu, Xiaoming Xu, Shihao Xu, Zhipeng Xu, Minxuan Xu, Dilin Xu, Haowen Xu, Rui Xu, Jingzhou Xu, Qiongying Xu, Jinyi Xu, Zhengshui Xu, Q P Xu, Yongjian Xu, Qiushi Xu, Hui Ming Xu, Junfei Xu, Mengjun Xu, Yanzhe Xu, Xiaolei Xu, Qin Xu, Zichuan Xu, Xinyun Xu, Xiaoge Xu, Tianyu Xu, Yigang Xu, Hongyan Xu, Lanjin Xu, Guowang Xu, Jingjie Xu, Yangyang Xu, Yi-Huan Xu, Guanhua Xu, Hongrong Xu, Fen Xu, Jian Xu, Pin-Xian Xu, Tiantian Xu, Zhonghui Xu, Changfu Xu, Dong-Hui Xu, Jialu Xu, Yi-Ni Xu, Yuzhong Xu, Hongli Xu, Mingyuan Xu, Minghao Xu, Qinghua Xu, C F Xu, Yiting Xu, Qian Xu, Jiahong Xu, Haixiang Xu, Xizheng Xu, Kun Xu, Yunfei Xu, Xiaoyang Xu, Xiaojun Xu, Xinyuan Xu, Chen Xu, Guogang Xu, Lingyi Xu, Jinguo Xu, Guiyun Xu, Chunjie Xu, Wenbin Xu, Manman Xu, Cheng-Bin Xu, Dongke Xu, Jia-Mei Xu, Bing-E Xu, Lijiao Xu, You-Song Xu, Mengmeng Xu, Yu-Xin Xu, Jianwei Xu, Kuanfeng Xu, Chun Xu, Shiliyang Xu, Waner Xu, Zhiyao Xu, Gu-Feng Xu, Wenyuan Xu, J T Xu, Ling Xu, Chaohua Xu, Haifeng Xu, Lisha Xu, Huaisha Xu, Xiayun Xu, Qian-Fei Xu, Jinying Xu, Tengyun Xu, Chaoguang Xu, Fuyi Xu, Shihui Xu, Yingna Xu, Aishi Xu, Yanyan Xu, Qiuhui Xu, Bilian Xu, Jinsheng Xu, Qinwen Xu, Tianfeng Xu, Liyi Xu, Lihui Xu, Guanyi Xu, Wenyan Xu, Ru-xiang Xu, Zongzhen Xu, Nan Xu, Rui-Xia Xu, Zhiting Xu, Jinxian Xu, Jiaming Xu, Shan-Rong Xu, Yi-Tong Xu, Xiaojuan Xu, Guifa Xu, Xia-Jing Xu, Libin Xu, Dequan Xu, Guoxu Xu, Lubin Xu, Cai Xu, Hong Xu, Mengying Xu, Tian-Le Xu, J Xu, Weidong Xu, Chengbi Xu, Yibin Xu, Cong-jian Xu, Qianlan Xu, Tingting Xu, Caiqiu Xu, Hong-Yan Xu, Hanqian Xu, Xiao Le Xu, Bei Xu, Ming-Zhu Xu, Guanlan Xu, Jianxin Xu, Long Xu, Xiaopeng Xu, Yinjie Xu, Shufen Xu, Zhihua Xu, Di Xu, Ming-Jiang Xu, Qingwen Xu, Jiake Xu, Tingxuan Xu, Peng-Ju Xu, Ping Xu, Li-Zhi Xu, Shang-Rong Xu, Baoping Xu, Huan Xu, Wenwu Xu, Zhenyu Xu, Chong Xu, Sihua Xu, Anlong Xu, Lu Xu, Chen-Yang Xu, Xiaoyu Xu, Zhe Xu, Qiuyue Xu, Guangquan Xu, Peiyu Xu, Huihui Xu, Ding Xu, Yuchen Xu, Jianguo Xu, Xuegong Xu, Lingyang Xu, Jia-Yue Xu, Liping Xu, Yiyi Xu, Yuling Xu, Jianqiu Xu, Lichi Xu, Xiaojiang Xu, Xiao-Hui Xu, Mao Xu, Zhaofa Xu, Yuyang Xu, Qingchan Xu, Yanli Xu, Julie Xu, Minglan Xu, G Xu, Yao Xu, Miaomiao Xu, Yali Xu, Yanqi Xu, Tian Xu, Xiaowen Xu, Xiaojin Xu, Qing-Yang Xu, Lingxiang Xu, Jianguang Xu, Zhanchi Xu, Shiwen Xu, Haikun Xu, Hongbei Xu, Yixin Xu, Zhan Xu, Xingshun Xu, Wenzhuo Xu, Fangmin Xu, Fu Xu, Haimin Xu, Jiahui Xu, Shengtao Xu, Zhiwei Xu, Peiwei Xu, Daichao Xu, Wen-Hui Xu, Xingyan Xu, H Eric Xu, Zhi-Feng Xu, Mingming Xu, Hongtao Xu, Daiqi Xu, Keman Xu, Yinying Xu, Yuexin Xu, Yuanwei Xu, Xuanqi Xu, L Xu, Jinfeng Xu, Chunyan Xu, Hanting Xu, Chaoyu Xu, Shendong Xu, Tiancheng Xu, Guangsen Xu, Chentong Xu, Yaozeng Xu, Banglao Xu, Tao Xu, Danyan Xu, Ren-He Xu, Haiyan Xu, Jian-Guang Xu, Yu-Fen Xu, Youzhi Xu, Hui Xu, Enwei Xu, F F Xu, Ningda Xu, Zejun Xu, Li-Wei Xu, N Y Xu, Xiaoya Xu, Ren Xu, Ze-Jun Xu, Yanan Xu, Jiapei Xu, Peigang Xu, Tianxiang Xu, Haiqi Xu, Qing-Wen Xu, Junnv Xu, Tian-Rui Xu, Wang-Hong Xu, Wanfu Xu, Maotian Xu, Suoyu Xu, Mingli Xu, Liwen Xu, Qingqing Xu, Zhenming Xu, Jingyi Xu, Yihua Xu, Dong-Juan Xu, Mu Xu, Meifeng Xu, Li-Ling Xu, Dongmei Xu, Jianliang Xu, Xinjie Xu, Pengfei Xu, Changlin Xu, Yingli Xu, Fang-Yuan Xu, Ying Xu, Guo-Liang Xu, Zhiqiang Xu, Xirui Xu, Haiying Xu, Wen Xu, Xiaoyin Xu, Wenwen Xu, Mengping Xu, Jing-Yu Xu, Chunlan Xu, Danfeng Xu, Yuan Xu, Wenchun Xu, Zekuan Xu, Nuo Xu, Shuxiang Xu, Min Jie Xu, Zixuan Xu, Bingqi Xu, Penghui Xu, Hongen Xu, Zongli Xu, Tianli Xu, Bo Xu, Qingyuan Xu, Zhaojun Xu, Shuhua Xu, Min-Xuan Xu, Xu Xu, Runhao Xu, M Xu, Xiongfei Xu, Zhaoyao Xu, Yingju Xu, Yayun Xu, Kaixiang Xu, Guang-Qing Xu, Lingling Xu, Jiyu Xu, Anton Xu, Jason Xu, Donghang Xu, Xiaowu Xu, Fengzhe Xu, Xia Xu, Xiangshan Xu, Wan-Ting Xu, Fengyan Xu, Qingheng Xu, Changlu Xu, Huaiyuan Xu, Jinsong Xu, Dongchen Xu, Rang Xu, Peng-Yuan Xu, Jinyuan Xu, Weihong Xu, Wanxue Xu, Xinyi Xu, Jie Xu, Danning Xu, Haiming Xu, Junfeng Xu, Shan Xu, Sutong Xu, Meng Xu, Yueyue Xu, Jixuan Xu, Hongjian Xu, Zhidong Xu, Jinjin Xu, Xiaobo Xu, Hongmei Xu, Shu-Xian Xu, Chuang Xu, Shuaili Xu, Yun Xu, Zhixian Xu, Yue Xu, George X Xu, Man Xu, Jiaai Xu, Zeqing Xu, Baijie Xu, Zheng-Fan Xu, Bojie Xu, Mengru Xu, H Y Xu, Yinhe Xu, Linna Xu, Liqun Xu, Zhi-Zhen Xu, Xiaohui Xu, Xingmeng Xu, Yinxia Xu, Pan Xu, Pengjie Xu, Kai Xu, Kexin Xu, Xiaolin Xu, Cun Xu, Yuxiang Xu, Tong Xu, Jingyu Xu, Li-Li Xu, Yancheng Xu, Chunxiao Xu, Yan Xu, Huajun Xu, Hongjiang Xu, Shuiyang Xu, Kaihao Xu, Suo-Wen Xu, Heng Xu, Zebang Xu, Hongbo Xu, Chenhao Xu, Fanghua Xu, Yaowen Xu, Jing Xu, Qianqian Xu, Andrew Z Xu, Flora Mengyang Xu, Yuanzhi Xu, Leilei Xu, Leyuan Xu, M-Y Xu, Hongzhi Xu, Zongren Xu, Xinyue Xu, Qingxia Xu, Cineng Xu, Xiao-Hua Xu, Nannan Xu, Guoshuai Xu, Mingzhu Xu, X S Xu, Guang Xu, Zhiyang Xu, Song-Hui Xu, Wang-Dong Xu, De-Xiang Xu, Yi Ran Xu, Shengen Xu, Jianzhong Xu, F Xu, Dexiang Xu, Rui-Hua Xu, Tongxin Xu, Wanting Xu, Bingqian Xu, Jiaqian Xu, Yang Xu, Yu-Ping Xu, Zhanqiong Xu, Haixia Xu, Hao Xu, HuiTing Xu, Hanfei Xu, Shu-Zhen Xu, Zhong Xu, Xun Xu, Xiaolu Xu, S Xu, Ning Xu, Guangyan Xu, Chengye Xu, Xizhan Xu, Ya-Peng Xu, Jianming Xu, Wenhao Xu, Minghong Xu, Mingqian Xu, Yaqin Xu, Chang-Qing Xu, Weiyong Xu, Huixuan Xu, Jialin Xu, Z Xu, Fei Xu, Pao Xu, Youping Xu, Keke Xu, Jia-Li Xu, Shunjiang Xu, Feilai Xu, Yucheng Xu, Qi Xu, Jinhua Xu, Chunli Xu, Zhiliang Xu, Jinxin Xu, Lianjun Xu, Bingqing Xu, Weihai Xu, Lifen Xu, Wenqi Xu, Zheng-Hong Xu, Lin Xu, Zuojun Xu, Yanquan Xu, Yanwu Xu, Mingjie Xu, Hui-Lian Xu, Dongjun Xu, Maodou Xu, Cong Xu, Rong Xu, Haoyang Xu, Shanhai Xu, Yinglin Xu, Haoyu Xu, Wenqing Xu, Jiali Xu, Changliu Xu, Xiaoke Xu, Feng-Xia Xu, Carrie Xu, Yuheng Xu, Shimeng Xu, Wanwan Xu, Weiming Xu, Gui-Ping Xu, Zhenzhou Xu, Yangbin Xu, Aohong Xu, Wenlong Xu, Jia-Xin Xu, Luyi Xu, Changde Xu, Manyi Xu, De Xu, Xinxuan Xu, Gaosi Xu, Baofeng Xu, Chang Xu, Wanhai Xu, Qing Xu, Zuyuan Xu, Pingwen Xu, Feng-Yuan Xu, Aoling Xu, Erping Xu, Shaoqi Xu, Zhicheng Xu, Lun-Shan Xu, Jianing Xu, Shiyao Sherrie Xu, Boqing Xu, Janfeng Xu, Yin Xu, Weijie Xu, Yu-Peng Xu, Ya-Nan Xu, Gaoyuan Xu, Iris M J Xu, Zhi Xu, Xiaomeng Xu, Mengyi Xu, Meifang Xu, Houxi Xu, Yuanfeng Xu, Shuqia Xu, Da-Peng Xu, Hong-tao Xu, Yaling Xu, Mei Xu, Xiaojiao Xu, Zhiru Xu, Dandan Xu, Weide Xu, W Xu, Shun Xu, Jianhua Xu, Tongda Xu, Lijun Xu, Cynthia M Xu, Yechun Xu, Xiao-Lin Xu, Ziye Xu, Xiaohan Xu, Guozheng Xu, Rongbin Xu, Nathan Xu, Wangdong Xu, Kailian Xu, Yongfeng Xu, Zhunan Xu, Jiawei Xu, Yuhan Xu, Ruohong Xu, Shanqi Xu, Shoujia Xu, T Xu, Weifeng Xu, Qiuyun Xu, Hu Xu, Yanming Xu, Hongwei Xu, Ziyu Xu, Kaishou Xu, Jian Hua Xu, Xin Xu, Liu Xu, Zetan Xu, Leiting Xu, Yong-Nan Xu, Houguo Xu, Zhizhen Xu, Ya-lin Xu, Xiang Xu, Suowen Xu, Xuejin Xu, Yiming Xu, Shude Xu, Genxing Xu, Yun-Teng Xu, Yanling Xu, Yuanhong Xu, Lijuan Xu, Xingzhi Xu, Guanghao Xu, Qiu-Han Xu, Siqun Xu, Wen-Xiong Xu, Qianghua Xu, Shuangbing Xu, Wenjun Xu, Jiangang Xu, Yangliu Xu, Jinjian Xu, W M Xu, Shanqiang Xu, Zefeng Xu
articles

Visfatin facilitates gastric cancer malignancy by targeting snai1 via the NF-κB signaling.

D Cao, L Chu, Z Xu +4 more · 2021 · Human & experimental toxicology · SAGE Publications · added 2026-04-24
Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a we Show more
Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a well-known regulator of EMT process in cancers. However, the relationship between visfatin and snai1 in GC remains unclear. The current study aimed to explore the role of visfatin in GC. The RT-qPCR and western blot analysis were used to measure RNA and protein levels, respectively. The cell migration and invasion were tested by Trans-well assays and western blot analysis. Visfatin showed upregulation in GC cells. Additionally, Visfatin with increasing concentration facilitated epithelial-mesenchymal transition (EMT) process by increasing E-cadherin and reducing N-cadherin and Vimentin protein levels in GC cells. Moreover, endogenous overexpression and knockdown of visfatin promoted and inhibited migratory and invasive abilities of GC cells, respectively. Then, we found that snai1 protein level was positively regulated by visfatin in GC cells. In addition, visfatin activated the NF-κB signaling to modulate snai1 protein expression. Furthermore, the silencing of snai1 counteracted the promotive impact of visfatin on cell migration, invasion and EMT process in GC. Visfatin facilitates cell migration, invasion and EMT process by targeting snai1 via the NF-κB signaling, which provides a potential insight for the treatment of GC. Show less
no PDF DOI: 10.1177/09603271211006168
SNAI1

The SWI/SNF-Related, Matrix Associated, Actin-Dependent Regulator of Chromatin A4 Core Complex Represses Respiratory Syncytial Virus-Induced Syncytia Formation and Subepithelial Myofibroblast Transition.

Xiaofang Xu, Dianhua Qiao, Chenyang Dong +4 more · 2021 · Frontiers in immunology · Frontiers · added 2026-04-24
Epigenetics plays an important role in the priming the dynamic response of airway epithelial cells to infectious and environmental stressors. Here, we examine the epigenetic role of the SWI/SNF Relate Show more
Epigenetics plays an important role in the priming the dynamic response of airway epithelial cells to infectious and environmental stressors. Here, we examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Depletion of SMARCA4 destabilized the abundance of the SMARCE1/ARID1A SWI/SNF subunits, disrupting the innate response and triggering a hybrid epithelial/mesenchymal (E/M) state. Assaying SMARCA4 complex-regulated open chromatin domains by transposase cleavage -next generation sequencing (ATAC-Seq), we observed that the majority of cleavage sites in uninfected cells have reduced chromatin accessibility. Paradoxically, SMARCA4 complex-depleted cells showed enhanced RSV-inducible chromatin opening and gene expression in the EMT pathway genes, Show less
no PDF DOI: 10.3389/fimmu.2021.633654
SNAI1

Dimeric guaianes from leaves of Xylopia vielana as snail inhibitors identified by high content screening.

Qi-Qi Xu, Chao Zhang, Ya-Long Zhang +3 more · 2021 · Bioorganic chemistry · Elsevier · added 2026-04-24
The transcriptional repressor Snail trriggers epithelial-mesenchymal transition (EMT), the process allowing cancer cells with invasive and metastasis properties. In this study, we screened medicinal p Show more
The transcriptional repressor Snail trriggers epithelial-mesenchymal transition (EMT), the process allowing cancer cells with invasive and metastasis properties. In this study, we screened medicinal plants for the Snail inhibitory active components by high content screen (HCS) and found that the crude extract of Xylopia vielana leaves showed potential activity. Subsequently, bioassay-guided isolation of the extract of Xylopia vielana was performed to obtain twenty-four dimeric guaianes (1-24), including 16 new analogues (1-5, 8-11, 13-15, 17, 18, 21, and 22). Their structures were elucidated by the comprehensive application of multiple spectroscopic methods. Compounds 1, 11, 12, and 16 were initially identified as the active compounds. Wound healing assay, transwell migration assay and western blot experiments verified that compounds 1 and 12 inhibited the expression of Snail in a concentration-dependent manner, and compound 12 was verified as a potent tumor migration inhibitory agent. This work showed a practical strategy for the discovery of new Snail inhibitors from natural products and provided potential insights for dimeric guaianes as anticancer lead compounds specifically targeting Snail protein. Show less
no PDF DOI: 10.1016/j.bioorg.2021.104646
SNAI1

Histone Demethylase

Yun Feng, Xin Zhao, Zhengda Li +8 more · 2021 · Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada · added 2026-04-24
Somatic cell nuclear transfer (SCNT) holds vast potential in agriculture. However, its applications are still limited by its low efficiency. Histone 3 lysine 9 trimethylation (H3K9me3) was identified Show more
Somatic cell nuclear transfer (SCNT) holds vast potential in agriculture. However, its applications are still limited by its low efficiency. Histone 3 lysine 9 trimethylation (H3K9me3) was identified as an epigenetic barrier for this. Histone demethylase KDM4D could regulate the level of H3K9me3. However, its effects on buffalo SCNT embryos are still unclear. Thus, we performed this study to explore the effects and underlying mechanism of KDM4D on buffalo SCNT embryos. The results revealed that compared with the IVF embryos, the expression level of KDM4D in SCNT embryos was significantly lower at 8- and 16-cell stage, while the level of H3K9me3 in SCNT embryos was significantly higher at 2-cell, 8-cell, and blastocyst stage. Microinjection of KDM4D mRNA could promote the developmental ability of buffalo SCNT embryos. Furthermore, the expression level of ZGA-related genes such as ZSCAN5B, SNAI1, eIF-3a, and TRC at the 8-cell stage was significantly increased. Meanwhile, the pluripotency-related genes like POU5F1, SOX2, and NANOG were also significantly promoted at the blastocyst stage. The results were reversed after KDM4D was inhibited. Altogether, these results revealed that KDM4D could correct the H3K9me3 level, increase the expression level of ZGA and pluripotency-related genes, and finally, promote the developmental competence of buffalo SCNT embryos. Show less
no PDF DOI: 10.1017/S1431927620024964
SNAI1

Aberrant Activation of Notch1 Signaling in Glomerular Endothelium Induces Albuminuria.

Liqun Li, Qiang Liu, Tongyao Shang +7 more · 2021 · Circulation research · added 2026-04-24
Glomerular capillaries are lined with a highly specialized fenestrated endothelium and contribute to the glomerular filtration barrier. The Notch signaling pathway is involved in regulation of glomeru Show more
Glomerular capillaries are lined with a highly specialized fenestrated endothelium and contribute to the glomerular filtration barrier. The Notch signaling pathway is involved in regulation of glomerular filtration barrier, but its role in glomerular endothelium has not been investigated due to the embryonic lethality of animal models with genetic modification of Notch pathway components in the endothelium. To determine the effects of aberrant activation of the Notch signaling in glomerular endothelium and the underlying molecular mechanisms. We established the Our results reveal novel regulatory mechanisms whereby endothelial Notch1 signaling dictates the level of VE-cadherin through the transcription factors SNAI1 and ERG, leading to dysfunction of glomerular filtration barrier and induction of albuminuria. Graphic Abstract: A graphic abstract is available for this article. Show less
no PDF DOI: 10.1161/CIRCRESAHA.120.316970
SNAI1

Snai1-induced partial epithelial-mesenchymal transition orchestrates p53-p21-mediated G2/M arrest in the progression of renal fibrosis via NF-κB-mediated inflammation.

Ruochen Qi, Jiyan Wang, Yamei Jiang +4 more · 2021 · Cell death & disease · Nature · added 2026-04-24
Renal fibrosis is the common feature of all progressive kidney diseases and exerts great burden on public health worldwide. The maladaptive repair mechanism of tubular epithelial cells, an important m Show more
Renal fibrosis is the common feature of all progressive kidney diseases and exerts great burden on public health worldwide. The maladaptive repair mechanism of tubular epithelial cells, an important mediator of renal fibrogenesis, manifests with partial epithelial-mesenchymal transition (EMT) and cell cycle arrest. The aim of this study is to investigate the possible correlation between partial EMT and cell cycle arrest, and elucidate the underlying mechanism. We examined human kidney allograft samples with interstitial fibrosis and three mice renal fibrosis models, unilateral ureter obstruction (UUO), ischemia-reperfusion injury, and Adriamycin nephropathy. The partial EMT process and p53-p21 axis were elevated in both human allograft with interstitial fibrosis, as well as three mice renal fibrosis models, and showed a time-dependent increase as fibrosis progressed in the UUO model. Snai1 controlled the partial EMT process, and led to parallel changes in renal fibrosis, G2/M arrest, and inflammation. p53-p21 axis arrested cell cycle at G2/M, and prompted partial EMT and fibrosis together with inflammation. NF-κB inhibitor Bay11-7082 disrupted the reciprocal loop between Snai1-induced partial EMT and p53-p21-mediated G2/M arrest. We demonstrated the reciprocal loop between partial EMT and G2/M arrest of TECs during renal fibrogenesis and revealed NF-κB-mediated inflammatory response as the underlying mechanism. This study suggests that targeting NF-κB might be a plausible therapeutic strategy to disrupt the reciprocal loop between partial EMT and G2/M arrest, therefore alleviating renal fibrosis. Show less
no PDF DOI: 10.1038/s41419-020-03322-y
SNAI1

The RNA helicase DDX3 induces neural crest by promoting AKT activity.

Mark Perfetto, Xiaolu Xu, Congyu Lu +5 more · 2021 · Development (Cambridge, England) · added 2026-04-24
Mutations in the RNA helicase DDX3 have emerged as a frequent cause of intellectual disability in humans. Because many individuals carrying DDX3 mutations have additional defects in craniofacial struc Show more
Mutations in the RNA helicase DDX3 have emerged as a frequent cause of intellectual disability in humans. Because many individuals carrying DDX3 mutations have additional defects in craniofacial structures and other tissues containing neural crest (NC)-derived cells, we hypothesized that DDX3 is also important for NC development. Using Show less
no PDF DOI: 10.1242/dev.184341
SNAI1

CDX2 inhibits epithelial-mesenchymal transition in colorectal cancer by modulation of Snail expression and β-catenin stabilisation via transactivation of PTEN expression.

Junhui Yu, Shan Li, Zhengshui Xu +5 more · 2021 · British journal of cancer · Nature · added 2026-04-24
Emerging evidence suggests the involvement of caudal-related homoeobox transcription factor 2 (CDX2) in tumorigenesis of various cancers. Although CDX2 functions in cancer invasion and metastasis, few Show more
Emerging evidence suggests the involvement of caudal-related homoeobox transcription factor 2 (CDX2) in tumorigenesis of various cancers. Although CDX2 functions in cancer invasion and metastasis, fewer studies focus on the role of CDX2 during the induction of epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC). Immunohistochemical analysis of CDX2 was performed. A series of in vitro and in vivo experiments were conducted to reveal the role of CDX2 in the invasion and metastasis of CRC. CDX2 was downregulated in CRC tissues and reduced CDX2 correlated with poor prognosis. Knockdown of CDX2 promoted colon cancer cell invasion in vitro and facilitated liver metastasis in vivo with inducing EMT phenotypes. Further investigation indicated that CDX2 retarded Akt and GSK-3β phosphorylation, and thereby diminished Snail expression, β-catenin stabilisation and nuclear translocation. The depletion of β-catenin neutralised the regulation of Slug and ZEB1 by CDX2 knockdown. Mechanistically, CDX2 antagonised PI3K/Akt activity in CRC by modulating PTEN expression. CDX2 directly bound to the promoter of PTEN and transactivated its expression. Our study first uncovered that CDX2 inhibits EMT and metastasis of CRC by regulation of Snail expression and β-catenin stabilisation via transactivation of PTEN expression. Show less
no PDF DOI: 10.1038/s41416-020-01148-1
SNAI1

Evaluating the biological functions of the prognostic genes identified by the Pathology Atlas in bladder cancer.

Yuanbin Chen, Ting Xu, Fei Xie +8 more · 2021 · Oncology reports · added 2026-04-24
The prognosis‑associated genes of urinary bladder cancer have been systematically investigated in the Pathology Atlas project based on The Cancer Genome Atlas data. However, the biological functions o Show more
The prognosis‑associated genes of urinary bladder cancer have been systematically investigated in the Pathology Atlas project based on The Cancer Genome Atlas data. However, the biological functions of most genes in bladder cancer remain unknown. The present study investigated the biological function of 12 of the most significant survival‑associated genes (ABRACL, MITD1, ZNF524, EMP1, HSPB6, CXorf38, TRIM38, ZNF182, ZNF195, SPRN, PTPN6 and LIPT1) in urothelial cancer reported by the Pathology Atlas project, with respect to cell proliferation and migration. In vitro, proliferation and migration analyses of T24 cells were performed following the transfection of the 12 prognostic genes. The results were validated with a small interfering (si)RNA library. Immunohistochemistry (IHC) analysis of clinical samples was performed to determine the association between gene expression and tumor metastasis. Furthermore, RNA sequencing was used to investigate the downstream signals. Among the 12 prognostic genes, MIT‑domain containing protein 1 (MITD1) transfection was demonstrated to inhibit T24 cell migration to a certain degree. Experiments performed with a 7‑gene siRNA library demonstrated that MITD1 knockdown markedly upregulated cell migratory abilities. Mechanistically, the influence of MITD1 on cell signal transduction was assessed via RNA sequencing. Cell migration‑associated genes, including KISS1, SPANXB1, SPINT1, PIWIL2, SNAI1, APLN and CTHRC1 were dysregulated. IHC analysis demonstrated that MITD1 protein expression was notably lower in metastatic lymph nodes compared with the primary tumors. Taken together, the results of the present study suggest that the prognostic gene, MITD1 may serve as a migration inhibitor, and be developed as a potential therapeutic target for improving the prognosis of bladder cancer. Show less
no PDF DOI: 10.3892/or.2020.7853
SNAI1

CBP-mediated Slug acetylation stabilizes Slug and promotes EMT and migration of breast cancer cells.

Xiaoyan Dai, Yanli Xin, Weizhi Xu +3 more · 2021 · Science China. Life sciences · Springer · added 2026-04-24
Slug, a member of the Snail family of transcriptional repressors, plays a key role in cancer progression, cellular plasticity, and epithelial to mesenchymal transition (EMT). Slug is a fast-turnover p Show more
Slug, a member of the Snail family of transcriptional repressors, plays a key role in cancer progression, cellular plasticity, and epithelial to mesenchymal transition (EMT). Slug is a fast-turnover protein and its stability is controlled by post-translational modifications. Here, we identified that Slug is acetylated by acetyltransferase CREB-binding protein (CBP) in breast cancer cells. CBP directly interacts with the C-terminal domain of Slug through its catalytic histone acetyltransferase (HAT) domain, leading to acetylation of Slug at lysines 166 and 211. Analysis with acetylation-specific antibodies revealed that Slug is highly acetylated in metastatic breast cancer cells. Notably, Slug acetylation, mediated by CBP at lysines 166 and 211, doubles its half-life and increases its stability. Further, acetylated Slug downregulates the expression of E-cadherin, the epithelial marker, and upregulates the expression of N-cadherin and vimentin, thereby promoting breast cancer cell migration. In conclusion, the present study demonstrates that CBP-mediated Slug acetylation increases its stability, promoting EMT and migration of breast cancer cells. Show less
no PDF DOI: 10.1007/s11427-020-1736-5
SNAI1

N6-methyladenosine (m6A) RNA methylation regulator SNRPC is a prognostic biomarker and is correlated with immunotherapy in hepatocellular carcinoma.

Jihao Cai, Minglei Zhou, Jianxin Xu · 2021 · World journal of surgical oncology · BioMed Central · added 2026-04-24
Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world, and due to its complex pathogenic factors, its prognosis is poor. N6-methyladenosine (m The HCC RNA-seq profiles in Show more
Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world, and due to its complex pathogenic factors, its prognosis is poor. N6-methyladenosine (m The HCC RNA-seq profiles in The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) databases, including 421 LIHC and 440 LIRI-JP samples, respectively, were used in this study. Both the expression of SNRPC in HCC was upregulated in the TCGA and ICGC databases compared to normal tissues. Next, the expression of SNRPC was validated as a risk factor for prognosis by Kaplan-Meier analysis and employed to establish a nomogram with T pathologic stage. By gene set variation (GSVA) analysis and gene set enrichment (GSEA) analysis, we found that SNRPC was mainly related to protein metabolism and the immune process. Furthermore, the estimation of stromal and immune cells in malignant tumor tissues using expression (ESTIMATE), microenvironment cell population counter (MCP-counter), and single sample GSEA (ssGSEA) algorithms revealed that the high-SNRPC group had a lower stromal score, lower abundance of endothelial cells and fibroblasts, and lower immune infiltration. Ultimately, a tumor immune dysfunction and exclusion (TIDE) analysis revealed that patients in the low-SNRPC group may be more sensitive to immune checkpoint inhibitor therapy. SNRPC could serve as a promising prognostic and immunotherapeutic marker in HCC and might contribute to new directions and strategies for HCC treatment. Show less
no PDF DOI: 10.1186/s12957-021-02354-8
SNRPC

Deacetylation-dependent regulation of PARP1 by SIRT2 dictates ubiquitination of PARP1 in oxidative stress-induced vascular injury.

Naijin Zhang, Ying Zhang, Boquan Wu +8 more · 2021 · Redox biology · Elsevier · added 2026-04-24
Poly(ADP-ribose) polymerase 1 (PARP1) has a major regulatory role in cardiovascular disease. However, inhibiting PARP1 activity does not significantly improve clinical outcomes of cardiovascular disea Show more
Poly(ADP-ribose) polymerase 1 (PARP1) has a major regulatory role in cardiovascular disease. However, inhibiting PARP1 activity does not significantly improve clinical outcomes of cardiovascular disease, which suggests that the regulatory mechanism of PARP1 in cardiovascular disease is unclear. Here, we focused on deacetylation regulatory mechanisms of PARP1 and crosstalk of PARP1 post-translational modifications. We uncovered the crucial molecular interactions and protein modifications of deacetylase Sirtuin 2 (SIRT2) and PARP1 in vascular damage. The results showed that SIRT2 was involved in this process and oxidative stress damage factor PARP1 was a novel physiological substrate of SIRT2. SIRT2 interacted with PARP1 at the PARP-A-helical domain and deacetylated the K249 residue of PARP1. Furthermore, SIRT2 promoted ubiquitination of the K249 residue of PARP1 via mobilization of the E3 ubiquitin ligase WW domain-containing protein 2 (WWP2), which led to proteasome-mediated degradation of PARP1. Knockout of SIRT2 in mice and cells increased PARP1 acetylation and decreased PARP1 ubiquitination, which in turn aggravated oxidative stress-induced vascular injury and remodeling. Conversely, overexpression of SIRT2 in mice and cells decreased PARP1 acetylation, increased PARP1 ubiquitination, and relieved oxidative stress-induced vascular injury and remodeling. Overall, this study revealed a previously unrecognized mechanistic link between SIRT2 and PARP1 in the regulation of oxidative stress-induced vascular injury. Show less
no PDF DOI: 10.1016/j.redox.2021.102141
WWP2

DKK1 suppresses WWP2 to enhance bortezomib resistance in multiple myeloma via regulating GLI2 ubiquitination.

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

Gut Hormone GIP Induces Inflammation and Insulin Resistance in the Hypothalamus.

Yukiko Fu, Kentaro Kaneko, Hsiao-Yun Lin +5 more · 2020 · Endocrinology · added 2026-04-24
The hypothalamus plays a critical role in controlling energy balance. High-fat diet (HFD) feeding increases the gene expression of proinflammatory mediators and decreases insulin actions in the hypoth Show more
The hypothalamus plays a critical role in controlling energy balance. High-fat diet (HFD) feeding increases the gene expression of proinflammatory mediators and decreases insulin actions in the hypothalamus. Here, we show that a gut-derived hormone, glucose-dependent insulinotropic polypeptide (GIP), whose levels are elevated during diet-induced obesity, promotes and mediates hypothalamic inflammation and insulin resistance during HFD-induced obesity. Unbiased ribonucleic acid sequencing of GIP-stimulated hypothalami revealed that hypothalamic pathways most affected by intracerebroventricular (ICV) GIP stimulation were related to inflammatory-related responses. Subsequent analysis demonstrated that GIP administered either peripherally or centrally, increased proinflammatory-related factors such as Il-6 and Socs3 in the hypothalamus, but not in the cortex of C57BL/6J male mice. Consistently, hypothalamic activation of IκB kinase-β inflammatory signaling was induced by ICV GIP. Further, hypothalamic levels of proinflammatory cytokines and Socs3 were significantly reduced by an antagonistic GIP receptor (GIPR) antibody and by GIPR deficiency. Additionally, centrally administered GIP reduced anorectic actions of insulin in the brain and diminished insulin-induced phosphorylation of Protein kinase B and Glycogen synthase kinase 3β in the hypothalamus. Collectively, these findings reveal a previously unrecognized role for brain GIP signaling in diet-induced inflammation and insulin resistance in the hypothalamus. Show less
no PDF DOI: 10.1210/endocr/bqaa102
GIPR

Molecular mechanism of an antagonistic antibody against glucose-dependent insulinotropic polypeptide receptor.

Xiaoshan Min, Junming Yie, Jinghong Wang +15 more · 2020 · mAbs · Taylor & Francis · added 2026-04-24
Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone involved in regulating glucose and lipid metabolism. GIP receptor (GIPR) antagonism is believed to offer therapeutic potential Show more
Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone involved in regulating glucose and lipid metabolism. GIP receptor (GIPR) antagonism is believed to offer therapeutic potential for various metabolic diseases. Pharmacological intervention of GIPR, however, has limited success due to lack of effective antagonistic reagents. Previously we reported the discovery of two mouse anti-murine GIPR monoclonal antibodies (mAbs) with distinctive properties in rodent models. Here, we report the detailed structural and biochemical characterization of these two antibodies, mAb1 and mAb2. Show less
📄 PDF DOI: 10.1080/19420862.2019.1710047
GIPR

Future perspective: high-throughput construction of new ultrasensitive cytokine and virion liquid chips for high-throughput screening (HTS) of anti-inflammatory drugs or clinical diagnosis and treatment of inflammatory diseases.

Yingzhu Feng, Jiuhong Huang, Chuanhua Qu +6 more · 2020 · Analytical and bioanalytical chemistry · Springer · added 2026-04-24
Pathogen-host cell interactions play an important role in many human infectious and inflammatory diseases. Several pathogens, including Escherichia coli (E. coli), Mycobacterium tuberculosis (M. tb), Show more
Pathogen-host cell interactions play an important role in many human infectious and inflammatory diseases. Several pathogens, including Escherichia coli (E. coli), Mycobacterium tuberculosis (M. tb), and even the recent 2019 novel coronavirus (2019-nCoV), can cause serious breathing and brain disorders, tissue injury and inflammation, leading to high rates of mortality and resulting in great loss to human physical and mental health as well as the global economy. These infectious diseases exploit the microbial and host factors to induce serious inflammatory and immunological symptoms. Thus the development of anti-inflammatory drugs targeting bacterial/viral infection is an urgent need. In previous studies, YojI-IFNAR2, YojI-IL10RA, YojI-NRP1,YojI-SIGLEC7, and YojI-MC4R membrane-protein interactions were found to mediate E. coli invasion of the blood-brain barrier (BBB), which activated the downstream anti-inflammatory proteins NACHT, LRR and PYD domains-containing protein 2(NLRP2), using a proteomic chip conjugated with cell immunofluorescence labeling. However, the studies of pathogen (bacteria/virus)-host cell interactions mediated by membrane protein interactions did not extend their principles to broad biomedical applications such as 2019-nCoV infectious disease therapy. The first part of this feature article presents in-depth analysis of the cross-talk of cellular anti-inflammatory transduction signaling among interferon membrane protein receptor II (IFNAR2), interleukin-10 receptor subunit alpha (IL-10RA), NLRP2 and [Ca Show less
📄 PDF DOI: 10.1007/s00216-020-02894-0
MC4R

Effect of Sleeve Gastrectomy on Glycometabolism via Forkhead Box O1 (FoxO1)/Lipocalin-2 (LCN2) Pathway.

Zhi Liu, Fuyun Sun, Zitian Liu +8 more · 2020 · Medical science monitor : international medical journal of experimental and clinical research · added 2026-04-24
BACKGROUND The mechanism by which sleeve gastrectomy (SG) improves glycometabolism has remained unclear so far. Increasing evidence has demonstrated that bone is a regulator of glucose metabolism, and Show more
BACKGROUND The mechanism by which sleeve gastrectomy (SG) improves glycometabolism has remained unclear so far. Increasing evidence has demonstrated that bone is a regulator of glucose metabolism, and osteoblast-derived forkhead box O1 (FoxO1) and lipocalin-2 (LCN2) are regulators of energy metabolism. The aim of this study was to investigate whether the FOXO1/LCN2 signaling pathway is involved in the anti-diabetic effect of SG. MATERIAL AND METHODS Insulin resistance was induced in Wistar rats, which were then intraperitoneally injected with streptozotocin to induce a type 2 diabetic state. Levels of fasting blood glucose, serum insulin, HbA1c, and LCN2 were analyzed at corresponding time points after SG and sham surgeries. The expressions of FOXO1, LCN2, and the melanocortin 4 receptor (MC4R) in bone and hypothalamus were detected by immunofluorescence. FOXO1 siRNA was applied to downregulate FOXO1 expression in osteoblasts of rats. The influence of FOXO1 gene on expression of LCN2 was investigated in cultured osteoblasts by western blot and PCR. RESULTS Glucose metabolism in the SG group was significantly improved. The LCN2 expression in bone in the SG group was higher than that in the sham group, whereas FOXO1 expression in the SG group was lower than that in the sham group. The binding rate of LCN2 and MC4R in the hypothalamus was also higher in the SG group compared with that in the sham group. The downregulation of FOXO1 expression in osteoblasts was accompanied by upregulation of LCN2 expression. CONCLUSIONS These results suggest that the FOXO1/LCN2 signaling pathway participates in the anti-diabetic effect of SG. Show less
📄 PDF DOI: 10.12659/MSM.927458
MC4R

Genetic Susceptibility to Gestational Diabetes Mellitus in a Chinese Population.

Minkai Cao, Le Zhang, Ting Chen +7 more · 2020 · Frontiers in endocrinology · Frontiers · added 2026-04-24
📄 PDF DOI: 10.3389/fendo.2020.00247
MC4R

Angiopoietin-like protein 4 promotes very-low-density lipoprotein assembly and secretion in bovine hepatocytes in vitro.

Yezi Kong, Chenxu Zhao, Yan Huang +7 more · 2020 · IUBMB life · Wiley · added 2026-04-24
In dairy cows, fatty liver is one of the most common metabolic diseases that occurs during the periparturient period. Angiopoietin-like protein 4 (ANGPTL4) is a well-known downstream target of peroxis Show more
In dairy cows, fatty liver is one of the most common metabolic diseases that occurs during the periparturient period. Angiopoietin-like protein 4 (ANGPTL4) is a well-known downstream target of peroxisome proliferator-activated receptors (PPARs), which regulate the glucose and fatty acid metabolisms. The inhibition of lipoprotein lipase (LPL) activity interferes with the storage of triglycerides (TG) in adipocytes, which plays an essential role in lipid metabolism in rodents. However, it remains unclear whether ANGPTL4 is involved in the pathological process of fatty liver in dairy cows as a result of the regulation of the hepatocellular lipid transport system. This study intended to investigate the effect of ANGPTL4 on the very-low-density lipoprotein (VLDL) assembly and secretion in bovine hepatocytes. Bovine hepatocytes were isolated using a modified two-step perfusion and collagenase digestion process, and treated with different concentrations of ANGPTL4 (0, 4, 12, and 24 ng/ml) for 24 hr. The results showed that a high concentration of ANGPTL4 could significantly increase the extracellular concentration of VLDL while reducing the intracellular content of TG. Thus, it was confirmed that ANGPTL4 could promote the transport of TG in the form of VLDL by partially regulating the expression of related proteins in hepatocytes, thereby contributing to the partial adaptive regulation of lipid transport in dairy cows. Show less
no PDF DOI: 10.1002/iub.2403
ANGPTL4

Correlations between single nucleotide polymorphisms in FABP4 and meat quality and lipid metabolism gene expression in Yanbian yellow cattle.

Bao-Zhen Yin, Jia-Chen Fang, Jia-Su Zhang +5 more · 2020 · PloS one · PLOS · added 2026-04-24
FABP4 is a candidate gene for carcass and meat quality traits in livestock and poultry. However, the effects of FABP4 have not been examined in the Yanbian yellow cattle, an economically important loc Show more
FABP4 is a candidate gene for carcass and meat quality traits in livestock and poultry. However, the effects of FABP4 have not been examined in the Yanbian yellow cattle, an economically important local cattle breed in China. In this study, we characterized single nucleotide polymorphisms (SNPs) in FABP4 in this cattle breed and their associations with meat quality traits. Six SNPs (referred to as SNP1-6) were identified in FABP4 by direct sequencing and polymerase chain reaction-restriction fragment length polymorphism. The six SNPs were significantly correlated with meat quality traits. In particular, the GG and GA genotypes of SNP1 were significantly associated with water and fat contents and GG and AA genotypes of SNP1 were significantly associated with protein contents (P < 0.05). The fat content and marbling in heterozygous individuals at SNP2-6 were significantly higher than those in wild-type or mutant individuals (P < 0.05), while protein content was significantly higher in wild-type and mutant individuals than in heterozygous individuals (P < 0.05). A gene expression analysis indicated that the lipid metabolism-related genes FABP4, PPARγ, ANGPTL4, and LPL show similar expression patterns with respect to FABP4 genotypes, with the highest levels in wild-type individuals and the lowest levels in mutants. In conclusion, FABP4 SNPs can be used for marker-assisted selection in Yanbian yellow cattle breeding. Show less
📄 PDF DOI: 10.1371/journal.pone.0234328
ANGPTL4

Effects of Hypoxia and Radiation-Induced Exosomes on Migration of Lung Cancer Cells and Angiogenesis of Umbilical Vein Endothelial Cells.

Fang Mo, Yanwu Xu, Junling Zhang +7 more · 2020 · Radiation research · added 2026-04-24
Numerous studies have shown that exosomes play important roles in tumor biology development. However, the function of exosomal protein in cancer progression under different oxygen condition after irra Show more
Numerous studies have shown that exosomes play important roles in tumor biology development. However, the function of exosomal protein in cancer progression under different oxygen condition after irradiation is poorly understood. In this study, non-small cell lung cancer (NSCLC) A549 cells were γ-ray irradiated under normoxic or hypoxic conditions, then the exosomes released from the irradiated cells were collected and co-cultured with nonirradiated A549 cells or human umbilical vein endothelial cells (HUVECs). It was found that the exosomes significantly promoted the proliferation, migration and invasion of A549 cells as well as the proliferation and angiogenesis of HUVECs. Moreover, the exosomes released from hypoxic cells and/or irradiated cells had more powerful driving force in tumor progression compared to that generated from normoxia cells. Meanwhile, the proteins contained in the exosomes derived from A549 cells under different conditions were detected using tandem mass tag (TMT), and their expression profiles were analyzed. It was found that the exosome-derived protein of angiopoietin-like 4 (ANGPTL4) contributed to the migration of A549 cells as well as the angiogenesis of HUVECs, suggesting its potential as an effective diagnostic biomarker of metastasis and even a therapeutic target of lung cancer. Show less
no PDF DOI: 10.1667/RR15555.1
ANGPTL4

Alteration of Angiopoietin-Like Protein 4 Levels in Serum or Urine Correlate with Different Biochemical Markers in Hyperlipidemia-Related Proteinuria.

Xia Gao, Min Zhang, Weidong Feng +4 more · 2020 · BioMed research international · added 2026-04-24
Angiopoietin-like protein 4 (ANGPTL4) is widely known as a key regulator of lipid metabolism. We investigated the relationship between ANGPTL4 expression in serum or urine and blood lipid or urine pro Show more
Angiopoietin-like protein 4 (ANGPTL4) is widely known as a key regulator of lipid metabolism. We investigated the relationship between ANGPTL4 expression in serum or urine and blood lipid or urine protein levels of patients with hyperlipidemia- (HL-) related proteinuria. Sixty-eight patients with HL-related proteinuria (HL-Pro group), 68 patients with HL without proteinuria (HL-NPro group), 46 patients with non-HL-related proteinuria (NHL-Pro group), and 50 healthy control (Con) subjects were selected. There were no significant differences in serum ANGPTL4 levels between the Con group (36.82 ± 17.03 ng/ml) and the HL-Pro group (27.94 (18.90, 53.72) ng/ml). Additionally, the serum ANGPTL4 levels in the HL-Pro group were significantly lower than those in the HL-NPro group (53.32 ± 24.01 ng/ml) ( Show less
📄 PDF DOI: 10.1155/2020/5281251
ANGPTL4

EZH2 inhibition promotes ANGPTL4/CREB1 to suppress the progression of ulcerative colitis.

Kun Li, Jing Yang, Xiao-Fei Lei +4 more · 2020 · Life sciences · Elsevier · added 2026-04-24
Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. However, the mechanism of EZH2 in ulcerative colitis progression remains unclear. Lipopolysaccharide (LPS)-treated Show more
Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. However, the mechanism of EZH2 in ulcerative colitis progression remains unclear. Lipopolysaccharide (LPS)-treated Caco-2 cells and dextran sodium sulfate (DSS)-treated mice were used as model of ulcerative colitis. The levels of EZH2, angiopoietin-like 4 (ANGPTL4) and cyclic adenosine monophosphate response element-binding protein 1 (CREB1) were tested via quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell viability and apoptosis was measured via 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide or flow cytometry. The abundances of inflammatory cytokines were examined via qRT-PCR and enzyme-linked immunosorbent assay. The association between EZH2 and ANGPTL4 was explored via chromatin immunoprecipitation. The colon damage in DSS-treated mice was investigated by colon length, histological analysis, inflammatory response and apoptosis. LPS induced viability inhibition, inflammatory response and apoptosis in Caco-2 cells. EZH2 expression was increased but ANGPTL4 and CREB1 levels were decreased in LPS-challenged Caco-2 cells. Overexpression of ANGPTL4 or CREB1 suppressed LPS-induced damage in Caco-2 cells. EZH2 could target ANGPTL4 to mediate CREB1 expression. Inhibition of EZH2 suppressed LPS-caused injury. Moreover, knockdown of ANNGPTL4 or CREB1 attenuated the role of EZH2 inhibition. DSS caused the reduced colon length and increased inflammatory response as well as apoptosis. EZH2 expression was up-regulated but ANGPTL4 and CREB1 expression were down-regulated in DSS-treated mice. Inhibition of EZH2 declined LPS-induced injury in Caco-2 cells by mediating ANGPTL4 and CREB1, indicating the potential of EZH2 in treatment of ulcerative colitis. Show less
no PDF DOI: 10.1016/j.lfs.2020.117553
ANGPTL4

A lipoprotein lipase-GPI-anchored high-density lipoprotein-binding protein 1 fusion lowers triglycerides in mice: Implications for managing familial chylomicronemia syndrome.

Amitabh V Nimonkar, Stephen Weldon, Kevin Godbout +7 more · 2020 · The Journal of biological chemistry · American Society for Biochemistry and Molecular Biology · added 2026-04-24
Lipoprotein lipase (LPL) is central to triglyceride metabolism. Severely compromised LPL activity causes familial chylomicronemia syndrome (FCS), which is associated with very high plasma triglyceride Show more
Lipoprotein lipase (LPL) is central to triglyceride metabolism. Severely compromised LPL activity causes familial chylomicronemia syndrome (FCS), which is associated with very high plasma triglyceride levels and increased risk of life-threatening pancreatitis. Currently, no approved pharmacological intervention can acutely lower plasma triglycerides in FCS. Low yield, high aggregation, and poor stability of recombinant LPL have thus far prevented development of enzyme replacement therapy. Recently, we showed that LPL monomers form 1:1 complexes with the LPL transporter glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) and solved the structure of the complex. In the present work, we further characterized the monomeric LPL/GPIHBP1 complex and its derivative, the LPL-GPIHBP1 fusion protein, with the goal of contributing to the development of an LPL enzyme replacement therapy. Fusion of LPL to GPIHBP1 increased yields of recombinant LPL, prevented LPL aggregation, stabilized LPL against spontaneous inactivation, and made it resistant to inactivation by the LPL antagonists angiopoietin-like protein 3 (ANGPTL3) or ANGPTL4. The high stability of the fusion protein enabled us to identify LPL amino acids that interact with ANGPTL4. Additionally, the LPL-GPIHBP1 fusion protein exhibited high enzyme activity in Show less
📄 PDF DOI: 10.1074/jbc.RA119.011079
ANGPTL4

Estradiol Enhances Anorectic Effect of Apolipoprotein A-IV through ERα-PI3K Pathway in the Nucleus Tractus Solitarius.

Min Liu, Ling Shen, Meifeng Xu +2 more · 2020 · Genes · MDPI · added 2026-04-24
Estradiol (E2) enhances the anorectic action of apolipoprotein A-IV (apoA-IV), however, the intracellular mechanisms are largely unclear. Here we reported that the phosphatidylinositol 3-kinase (PI3K) Show more
Estradiol (E2) enhances the anorectic action of apolipoprotein A-IV (apoA-IV), however, the intracellular mechanisms are largely unclear. Here we reported that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway was significantly activated by E2 and apoA-IV, respectively, in primary neuronal cells isolated from rat embryonic brainstem. Importantly, the combination of E2 and apoA-IV at their subthreshold doses synergistically activated the PI3K/Akt signaling pathway. These effects, however, were significantly diminished by the pretreatment with LY294002, a selective PI3K inhibitor. E2-induced activation of the PI3K/Akt pathway was through membrane-associated ERα, because the phosphorylation of Akt was significantly increased by PPT, an ERα agonist, and by E2-BSA (E2 conjugated to bovine serum albumin) which activates estrogen receptor on the membrane. Centrally administered apoA-IV at a low dose (0.5 µg) significantly suppressed food intake and increased the phosphorylation of Akt in the nucleus tractus solitarius (NTS) of ovariectomized (OVX) rats treated with E2, but not in OVX rats treated with vehicle. These effects were blunted by pretreatment with LY294002. These results indicate that E2's regulatory role in apoA-IV's anorectic action is through the ERα-PI3K pathway in the NTS. Manipulation of the PI3K/Akt signaling activation in the NTS may provide a novel therapeutic approach for the prevention and the treatment of obesity-related disorders in females. Show less
📄 PDF DOI: 10.3390/genes11121494
APOA4

PromarkerD Predicts Renal Function Decline in Type 2 Diabetes in the Canagliflozin Cardiovascular Assessment Study (CANVAS).

Kirsten E Peters, Jialin Xu, Scott D Bringans +4 more · 2020 · Journal of clinical medicine · MDPI · added 2026-04-24
The ability of current tests to predict chronic kidney disease (CKD) complicating diabetes is limited. This study investigated the prognostic utility of a novel blood test, PromarkerD, for predicting Show more
The ability of current tests to predict chronic kidney disease (CKD) complicating diabetes is limited. This study investigated the prognostic utility of a novel blood test, PromarkerD, for predicting future renal function decline in individuals with type 2 diabetes from the CANagliflozin CardioVascular Assessment Study (CANVAS). PromarkerD scores were measured at baseline in 3568 CANVAS participants ( Show less
📄 PDF DOI: 10.3390/jcm9103212
APOA4

Influence of genetic polymorphisms in homocysteine and lipid metabolism systems on antidepressant drug response.

Baoyu Yuan, Xiaoyan Sun, Zhi Xu +3 more · 2020 · BMC psychiatry · BioMed Central · added 2026-04-24
Variation in genes implicated in homocysteine and lipid metabolism systems may influence antidepressant response for patients with major depressive disorder (MDD). This study aimed to investigate whet Show more
Variation in genes implicated in homocysteine and lipid metabolism systems may influence antidepressant response for patients with major depressive disorder (MDD). This study aimed to investigate whether association of polymorphisms on the MTHFR, ApoE and ApoA4 genes with the treatment response in MDD subjects. A total of 281 Han Chinese MDD patients received a single antidepressant drug (SSRI or SNRI) for at least 6 weeks, among whom 275 were followed up for 8 weeks. Their response to 6 weeks' treatment and remission to 8 weeks' treatment with antidepressant drugs was determined by changes in the 17-item Hamilton Depression Rating Scale (HARS-17) score. Single SNP and haplotype associations with treatment response were analyzed by UNPHASED 3.0.13. Logistic regression analysis was used to explore the interactions between genotypes and gender or drug type on treatment outcome, only those SNPs that had interactional association with gender or drug type were subjected to further stratified analysis. In total group, the haplotype (C-A) in MTHFR (rsl801133 and rs1801131) and the ApoE rs405509 AA genotype were significantly associated with better efficacy of antidepressants; In gender subgroups, only haplotype (C-A) in MTHFR (rsl801133 and rs1801131) was significantly associated with better efficacy of antidepressants in male subgroup; In drug type subgroup, the haplotype (C-A) in MTHFR (rsl801133 and rs1801131) and haplotype (G-C) in ApoE (rs7412 and rs405509) were associated with better efficacy of antidepressants in SNRI treated subgroup; The ApoA4 rs5092 G allele and GG genotype were associated with worse efficacy of antidepressants in SNRI treated subgroup. Genetic polymorphisms in homocysteine and lipid metabolism systems are associated with antidepressant response, particularly for the interactions of the certain genetic with gender or drug type. Show less
📄 PDF DOI: 10.1186/s12888-020-02798-4
APOA4

APOC3 rs2070667 Associates with Serum Triglyceride Profile and Hepatic Inflammation in Nonalcoholic Fatty Liver Disease.

Qing-Yang Xu, Han Li, Hai-Xia Cao +2 more · 2020 · BioMed research international · added 2026-04-24
Single-nucleotide polymorphisms (SNPs) of apolipoprotein C3 (
📄 PDF DOI: 10.1155/2020/8869674
APOC3

Inactivation of ApoC3 by CRISPR/Cas9 Protects Against Atherosclerosis in Hamsters.

Mengmeng Guo, Yitong Xu, Zhao Dong +7 more · 2020 · Circulation research · added 2026-04-24
no PDF DOI: 10.1161/CIRCRESAHA.120.317686
APOC3

MicroRNA-424-5p regulates aortic smooth muscle cell function in atherosclerosis by blocking APOC3-mediated nuclear factor-κB signalling pathway.

Chuanfang Li, Meng Zhang, Yuchuan Dai +1 more · 2020 · Experimental physiology · added 2026-04-24
What is the central question of this study? What is the role of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cells? How does miR-424-5p function as a suppressor of the inflammatory response? W Show more
What is the central question of this study? What is the role of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cells? How does miR-424-5p function as a suppressor of the inflammatory response? What is the main finding and its importance? Upregulation of miR-424-5p inhibits the inflammatory response in aortic smooth muscle cells. miR-424-5p inactivates the nuclear factor-κB signalling pathway through the downregulation of apolipoprotein C3. Dysregulated aortic smooth muscle cells in chronic inflammation result in plaque formation in atherosclerosis (AS), which is a systemic disease that affects the large arteries with the activation of inflammatory pathways as a key process in its pathogenesis. The aim of the study was to investigate the regulatory mechanism of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cell activities and inflammation in AS via the regulation of apolipoprotein C3 (APOC3) and the nuclear factor-κB (NF-κB) signalling pathway. The results showed that miR-424-5p was poorly expressed and APOC3 highly expressed in the peripheral blood of AS patients and rat models of AS. Molecularly, our results confirmed that miR-424-5p targeted the APOC3 gene directly and inhibited APOC3 expression, which resulted in repressed activation of the NF-κB signalling pathway. The gain- and loss-of-function approaches were used to determine the effects of miR-424-5p and APOC3 on inflammation and on the proliferation, apoptosis and migration of aortic smooth muscle cells. Upregulation of miR-424-5p or silencing of APOC3 significantly suppressed proliferation, migration and inflammation and promoted apoptosis of aortic smooth muscle cells, which was achieved through inactivation of the NF-κB signalling pathway. Taken together, our results show that miR-424-5p upregulation impedes the progression of AS by blocking the APOC3-mediated NF-κB signalling pathway, which could be used as a novel target and a potential therapeutic pathway against AS. Show less
no PDF DOI: 10.1113/EP088088
APOC3