👤 Zhengfang Lin

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Also published as: Ai-Hsuan Lin, Aifu Lin, Ailong Lin, Aiping Lin, Aizhen Lin, Alexander Lin, Alexander P Lin, Ann Lin, Bei Lin, Bencheng Lin, Bi-Yun Lin, Biaoyang Lin, Bichun Lin, Bihua Lin, Bin Lin, Binbin Lin, Bing-Biao Lin, Bing-Jin Lin, Bing-Xue Lin, Bing-Yao Lin, Bingbing Lin, Bingqi Lin, Bo Lin, Bo-Wen Lin, Bode Lin, Bonnie Lin, Boxu Lin, Brian Leei Lin, Brian Lin, Bridget M Lin, C H Lin, C T Lin, C Y Lin, Cai-Xia Lin, Caiyu Lin, Chang Lin, Chang-Ching A Lin, Changchun Lin, Changpo Lin, Chao Lin, Chao-Chieh Lin, Chao-Feng Lin, Chao-Hsiung Lin, Chaohui Lin, Charles P Lin, Chen Lin, Chen-Yong Lin, Cheng Lin, Cheng-Chieh Lin, Cheng-Li Lin, Cheng-Yen Lin, Chengping Lin, Chengqi Lin, Chengyuan Lin, Chenquan Lin, Chi-Hung Lin, Chi-Shiuan Lin, Chi-Ying Lin, Chia-Chin Lin, Chia-Hao Lin, Chia-Ho Lin, Chia-Hsin Lin, Chia-Hung Lin, Chia-Liang Lin, Chia-Yu Lin, Chiao-Huang Lin, Chiao-Mei Lin, Chien-Ju Lin, Chien-Wei Lin, Chien-Yu Lin, Chih-Chun Lin, Chih-Hsun Lin, Chih-Ming Lin, Chih-Pei Lin, Chih-Yu Lin, Chii-Mei Lin, Chin-Hsien Lin, Chin-Sheng Lin, Chin-Yu Lin, Ching-Hung Lin, Ching-Yih Lin, Ching-Yu Lin, Chingju Lin, Cho-Hao Lin, Chuan Lin, Chuan-Chao Lin, Chun Lin, Chun-Lin Lin, Chun-Mao Lin, Chung-Hsien Lin, Chung-Ming Lin, Chunhua Lin, Chunming Lin, Chyuan-Sheng Lin, Cindy Lin, Cong Lin, Cuei-Jyuan Lin, Cui-Jun Lin, Cuilan Lin, Dafeng Lin, Daiqiong Lin, Dan Lin, Dan-Yu Lin, Daniel W Lin, Danyu Lin, Dao-Chao Lin, De-Chen Lin, Ding Lin, Dong Lin, Dong-Tsamn Lin, Dongmei Lin, Dongru Lin, Dongxin Lin, Dongzi Lin, Douglas I Lin, Eugene Lin, F Lin, Fan Lin, Fan-Li Lin, Fang Lin, Fangrui Lin, Fangyu Lin, Fangzhao Lin, Fei Lin, Fen Lin, Feng Lin, Feng-Chang Lin, Feng-Ming Lin, Feng-Yen Lin, Foxiang Lin, Fu Sheng Lin, Fujun Lin, Gang Lin, Ge Lin, Grace Lin, Guan-Bo Lin, Guang-Yao Lin, Guangzheng Lin, Gufa Lin, Guihu Lin, Guimei Lin, Guo-Wang Lin, Guofu Lin, Guoqiang Lin, Guowen Lin, H G Lin, H R Lin, Hai Lin, Haibiao Lin, Haimiao Lin, Haipeng Lin, Haitong Lin, Haiyan Lin, Han Lin, Han-Huei Lin, Hang Lin, Hang-Yan Lin, Hanyu Lin, Hao Lin, Hao-Yu Lin, Haochang Lin, Haocheng Lin, Haodong Lin, Haoyi Lin, Haoyu Lin, He Lin, Heng Lin, Heng-Huei Lin, Henghui Lin, Hening Lin, Hong Lin, Hongcheng Lin, Hongchun Lin, Honghuang Lin, Hongkun Lin, Hongsheng Lin, Hongyan Lin, Hsiao-Yun Lin, Hsien-Chih Lin, Hsin-Ti Lin, Hsing-Pei Lin, Hsiu-Chu Lin, Hua Lin, Huanhuan Lin, Hui Lin, Hui-Hsuan Lin, Hui-Ju Lin, Hui-Kuan Lin, Hui-Ping Lin, Hui-Ru Lin, Hui-Yan Lin, Hui-Yi Lin, Huijuan Lin, Huilan Lin, Huimei Lin, Huisheng Lin, Hung-Chih Lin, Hung-Ju Lin, Hung-Jung Lin, I-Ching Lin, I-Jung Lin, I-Ling Lin, Jake Lin, James A Lin, Jamie S Lin, Jane-Ming Lin, Jeng-Feng Lin, Jia Lin, Jia-Bin Lin, Jia-Feng Lin, Jia-Li Lin, Jia-Qi Lin, Jiabin Lin, Jiacheng Lin, Jiaheng Lin, Jiahui Lin, Jiajing Lin, Jiali Lin, Jiamao Lin, Jiamei Lin, Jian-Yu Lin, JianMin Lin, Jiandie D Lin, Jiandie Lin, Jianfei Lin, Jiang Lin, Jianhao Lin, Jianhua Lin, Jianhui Lin, Jianjian Lin, Jiantao Lin, Jianwei Lin, Jianyin Lin, Jiaqi Lin, Jiaqian Lin, Jiaquan Lin, Jiarui Lin, Jiatong Lin, Jiayang Lin, Jiayi Lin, Jiayuh Lin, Jie Lin, Jie Ming Lin, Jieye Lin, Jieying Lin, Jijin Lin, Jim Jr-Min Lin, Jin Lin, Jin'e Lin, Jin-Ru Lin, Jinchuan Lin, Jing Lin, Jing-Ping Lin, Jing-Ying Lin, Jing-Yu Lin, Jinghan Lin, Jingmei Lin, Jingyu Lin, Jingyuan Lin, Jinlong Lin, Jinxiu Lin, Jinzhong Lin, Jiu Lin, Jiuann-Huey Ivy Lin, Jiunn-Lee Lin, Jiyan Lin, Jo-Yu Lin, Joanne Lin, Johnson Lin, Jue Lin, Juin-Han Lin, Jun-Ming Lin, Junjian Lin, Junnan Lin, Junyi Lin, Kai Lin, Kai-Hsin Lin, Kai-Min Lin, Kai-Yan Lin, Kai-Yen Lin, Kang Lin, Kashuai Lin, Katia Lin, Ke Lin, Ke-Shin Lin, Kejian Lin, Keng-Hung Lin, Kim Y Lin, Kimberly Y Lin, Kongying Lin, Kuan-Hung Lin, Kuang Lin, L Lin, L Y Lin, Lanyan Lin, Le-Hang Lin, Lei Lin, Leilei Lin, Lezhen Lin, Li An Lin, Li Lin, Li-An Lin, Li-Ching Lin, Li-E Lin, Li-Fen Lin, Li-Ling Lin, Li-Rong Lin, Li-Song Lin, Lian-Yu Lin, Liang-Chun Lin, Liang-Tzung Lin, Lihao Lin, Lijin Lin, Liling Lin, Limei Lin, Lin Lin, Ling Lin, Ling-Li Lin, Liping Lin, Lisong Lin, Liwen Lin, Lizhong Lin, Lizhu Lin, Long Lin, Long-Yau Lin, Lu Lin, Luping Lin, M Lin, Manjie Lin, Mao-Shin Lin, Mao-Tsun Lin, Mary Grace Lin, Mei-Chi Lin, Meifang Lin, Meizhen Lin, Meng-Fei Lin, Meng-Wei Lin, Mengsha Lin, Mengxin Lin, Mengyao Lin, Miao Lin, Miao-Chong Joy Lin, Min Lin, Min-Huan Lin, Min-Jie Lin, Min-Rou Lin, Ming-Der Lin, Ming-Hong Lin, Ming-Huei Lin, Ming-Tai Lin, Ming-Wei Lin, Mingkuan Lin, Mingmei Lin, Mingqun Lin, Mingrui Lin, Mingxing Lin, Mingying Lin, Monica Lin, Nan Lin, Nancy U Lin, Nianwei Lin, Ning Lin, Ning-Ning Lin, Ningning Lin, Pei Lin, Pei-Chin Lin, Pei-Lin Lin, Pei-Yi Lin, Peijia Lin, Peng Lin, Peng-Chan Lin, Pengfei Lin, Penghui Lin, Ping Lin, Pingping Lin, Po-Han Lin, Qi Lin, Qian Lin, Qianmeng Lin, Qiannan Lin, Qiao Lin, Qiao-Hong Lin, Qiaoxuan Lin, Qichang Lin, Qin Lin, Qing Lin, Qinghua Lin, Qingling Lin, Qingqing Lin, Qingxiang Lin, Qinlu Lin, Qiong Lin, Qiongfen Lin, Qitai Lin, Qiuling Lin, Qu Lin, Quan-Zhen Lin, R-I Lin, Raozhou Lin, Renjing Lin, Richard Z Lin, Rong Lin, Ronghai Lin, Rongjie Lin, Ru Lin, Rui Lin, Ruifan Lin, Ruilang Lin, Ruiyi Lin, Rutao Lin, S C Lin, S K Lin, S L Lin, S Lin, S Y Lin, S-J Lin, Sen Lin, Sen-Qing Lin, Sha Lin, Shan Lin, Shanyi Lin, Shanyun Lin, Shaowei Lin, Sharon Lin, Sheldon S Lin, Sheng Lin, Sheng-Cai Lin, Sheng-Che Lin, Sheng-Jia Lin, Sheng-Wei Lin, Sheng-Xiang Lin, Shengjie Lin, Shi Lin, Shiaw-Yih Lin, Shibo Lin, Shih-Cherng Lin, Shih-Chieh Lin, Shih-Fan Lin, Shih-Wei Lin, Shih-Yi Lin, Shihui Lin, Shijie Lin, Shin-Yu Lin, Shing-Jong Lin, Shinian Lin, Shinn-Zong Lin, Shinne-Ren Lin, Shiow J Lin, Shiow Lin, Shiping Lin, Shiru Lin, Shiya Lin, Shiyu Lin, Shu Lin, Shu-Chun Lin, Shu-Hui Lin, Shu-Rung Lin, Shu-Wha Lin, Shuai Lin, Shuaijun Lin, Shuan-Pei Lin, Shuhai Lin, Shujuan Lin, Shun-Guo Lin, Shuo Lin, Shuqian Lin, Shyr-Yi Lin, Si-Xian Lin, Simin Lin, Simon Lin, Siong-Chi Lin, Sisi Lin, Siying Lin, Song-Shu Lin, Songyi Lin, Sophia Lin, Spencer Lin, Su-Fang Lin, Sue-Jane Lin, Sufen Lin, Suyang Lin, Suzhen Lin, Ta-Hsien Lin, Tai-Chi Lin, Tao Lin, Tianfeng Lin, Tianxin Lin, Tien-Huang Lin, Tim Lin, Ting Lin, Ting-Hsu Lin, Ting-ting Lin, Tingsheng Lin, Tingting Lin, Tse-I Lin, Tsu-Kung Lin, Tsung-Hsien Lin, Tsung-Shih Lin, Tung-Yi Lin, Tzu-Chien Lin, Vicky Lin, Wan-Wan Lin, Wan-Yu Lin, Wan-Yun Lin, Wanhui Lin, Wanjun Lin, Wei Lin, Wei-De Lin, Wei-Ling Lin, Wei-Ting Lin, Wei-Tso Lin, Wei-Wen Lin, Wei-Xiong Lin, Wei-Yin Lin, Wei-Yu Lin, WeiHao Lin, Weichun Lin, Weiji Lin, Weilong Lin, Weimin Lin, Weiqiang Lin, Wen-Jun Lin, Wen-Jye Lin, Wenjian Lin, Wenming Lin, Wenxin Lin, X J Lin, X Lin, Xi Lin, Xian-Bin Lin, Xian-Zi Lin, Xianchai Lin, Xiandong Lin, Xiang-Quan Lin, Xiangquan Lin, Xiangwu Lin, Xiangyang Lin, Xianke Lin, Xianmei Lin, Xianzhi Lin, Xianzi Lin, Xiao Lin, Xiao-Chun Lin, Xiao-long Lin, Xiaodi Lin, Xiaohan Lin, Xiaohong Lin, Xiaohui Lin, Xiaojing Lin, Xiaoling Lin, Xiaolong Lin, Xiaomin Lin, Xiaoqing Lin, Xiaowei Lin, Xiaoyan Lin, Xiaoyang Lin, Xiaoyi Lin, Xiaoyu Lin, Xiaozeng Lin, Xihong Lin, Xin Lin, Xin-Mei Lin, Xin-Xiu Lin, Xinchun Lin, Xinda Lin, Xing Lin, Xingguang Lin, Xinhua Lin, Xinrong Lin, Xinshi Lin, Xinxin Lin, Xinyao Lin, Xiu-Ru Lin, Xixiao Lin, Xu Lin, Xue Lin, Xue-Jing Lin, Xuefei Lin, Xuehua Lin, Xuejing Lin, Xuelian Lin, Xuemei Lin, Xuewan Lin, Xuyao Lin, Xuyong Lin, Y C Lin, Y Lin, Y M Lin, Ya-Hui Lin, Ya-Lin Lin, Ya-Qiu Lin, Ya-Tin Lin, Yan Lin, Yan-Ling Lin, Yancheng Lin, Yang Lin, Yang-Hsiang Lin, Yani Lin, Yanjun Lin, Yanke Lin, Yanni Lin, Yanqin Lin, Yanxia Lin, Yanzhu Lin, Yao Lin, Yao-Ping Lin, Yaohui Lin, Yaqiu Lin, Ye Lin, Yen-Chun Lin, Yen-Feng Lin, Yen-Hong Lin, Yen-Kuang Lin, Yen-Lin Lin, Yen-Shu Lin, Yen-Yi Lin, Yi Lin, Yi-An Lin, Yi-Chen Lin, Yi-Haou Lin, Yi-Hsiung Lin, Yi-Hsuan Lin, Yi-Hui Lin, Yi-Jang Lin, Yi-Ling Lin, Yi-Nan Lin, Yi-Tzu Lin, Yi-Wen Lin, Yichuan Lin, Yifei Lin, Yifeng Lin, Yihui Lin, Yilong Lin, Yina Lin, Ying Lin, Ying-Chao Lin, Ying-Hsi Lin, Yingnan Lin, Yingni Lin, Yingting Lin, Yingzhong Lin, Yiqi Lin, Yone Kawe Lin, Yong Lin, Yong-Shiang Lin, Yongbin Lin, Yongyao Lin, You Bin Lin, Youcheng Lin, Youwen Lin, Yu Lin, Yu-Chen Lin, Yu-Ching Lin, Yu-Cui Lin, Yu-Fen Lin, Yu-Hsiang Lin, Yu-Hsuan Lin, Yu-Hui Lin, Yu-Lin Lin, Yu-Ling Lin, Yu-Shan Lin, Yu-Sheng Lin, Yu-Wen Lin, Yuan Lin, Yuan-Feng Lin, Yuansheng Lin, Yubi Lin, Yuchen Lin, Yue-Jun Lin, Yueh-Min Lin, Yuezhi Lin, Yuhao Lin, Yuki Lin, Yuli Lin, Yun-Chi Lin, Yun-Lu Lin, Yun-Zhi Lin, Yunfeng Lin, Yung-Chieh Lin, Yung-Ming Lin, Yuntao Lin, Yunting Lin, Yutong Lin, Yuxi Lin, Yuxiang Lin, Yuxin Lin, Yuyuan Lin, Yuzheng Lin, Z Lin, Zaihong Lin, Ze-Shiang Lin, Zebin Lin, Zesen Lin, Zesi Lin, Zexing Lin, Zhangyu Lin, Zhao Lin, Zhaohua Lin, Zhaotong Lin, Zheguang Lin, Zhekai Lin, Zhen Lin, Zheng Lin, Zhengjie Lin, Zhenhu Lin, Zhenjia Lin, Zhenming Lin, Zhenping Lin, Zhenzhen Lin, Zheshen Lin, Zhi-Heng Lin, Zhi-Hu Lin, Zhi-ming Lin, Zhibin Lin, Zhichao Lin, Zhicheng Lin, Zhien Lin, Zhijian Lin, Zhijie Lin, Zhiqi Lin, Zhixian Lin, Zhixiong Lin, Zhiyi Lin, Zhiying Lin, Zhiyong Lin, Zhong-Hua Lin, Zhongdong Lin, Zhonghua Lin, Zhongjie Lin, Zhongqiu Lin, Zhongxiao Lin, Zhoumeng Lin, Zhuojia Lin, Zi-Han Lin, Zien Lin, Zihan Lin, Ziqiang Lin, Ziwei Lin, Zixian Lin, Zongyun Lin
articles

Decidual expression and regulation of fatty acid desaturase 3 during mouse decidualization.

Shuai Lin, Yu-Yuan Zhu, Wei Hu +4 more · 2018 · Reproduction (Cambridge, England) · added 2026-04-24
Decidualization is required for the successful establishment of pregnancy in rodents and primates. Fatty acid desaturase 3 (Fads3) belongs to the fatty acid desaturase family, which is a crucial enzym Show more
Decidualization is required for the successful establishment of pregnancy in rodents and primates. Fatty acid desaturase 3 (Fads3) belongs to the fatty acid desaturase family, which is a crucial enzyme for highly unsaturated fatty acid biosynthesis. However, the expression, regulation and function of Fads3 during early pregnancy in mice are still unknown. In this study, we examined Fads3 expression, regulation and function during mouse decidualization. The expression of Fads3 is detected in the subluminal stromal cells at implantation site on day 5 of pregnancy, but not at inter-implantation site and in day 5 pseudopregnant uteri. Compared to delayed implantation, Fads3 is strongly expressed after delayed implantation is activated by estrogen treatment. From days 6 to 8, Fads3 mRNA signals are significantly detected in the decidua. In ovariectomized mice, estrogen significantly stimulates Fads3 expression. However, estrogen has no effect on Fads3 expression in ovariectomized ERα-deficient mice, suggesting that estrogen regulation on Fads3 expression is ERα dependent. When ovariectomized mice were treated with progesterone, Fads3 expression is significantly increased by progesterone. Progesterone stimulation on Fads3 expression is also detected in cultured stromal cells, which is abrogated by RU486 treatment. These data indicate that progesterone upregulation on Fads3 expression is progesterone receptor-dependent. Fads3 knockdown by siRNA reduces in vitro decidualization of mouse stromal cells. Taken together, Fads3 may play an important role during mouse decidualization. Show less
no PDF DOI: 10.1530/REP-18-0145
FADS3

LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer.

Dezhi Cheng, Chunchun Bao, Xiuxing Zhang +3 more · 2018 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · Elsevier · added 2026-04-24
It has been announced in accumulative studies that non-coding (nc)RNAs are responsible for a varieties of biological behaviors during the progression of tumors. As two subgroups of ncRNAs family, micr Show more
It has been announced in accumulative studies that non-coding (nc)RNAs are responsible for a varieties of biological behaviors during the progression of tumors. As two subgroups of ncRNAs family, micro (mi)RNAs can interact with long non-coding (lnc)RNAs, thereby forming ceRNA network. In this study, miR-448 was expressed higher in NSCLC tissues (P < 0.01) and NSCLC cell lines (P < 0.01). Moreover, low expression of miR-448 predicted poor prognosis for patients with NSCLC (P < 0.001). Functional assays revealed the anti-oncogenic function of miR-448 in NSCLC by inhibiting cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT). Mechanically, miR-448 was found to be negatively regulated by lncRNA PRNCR1 (prostate cancer non-coding RNA 1). Moreover, HEY2 (Hairy and enhancer of split-related with YRPW motif protein 2) was demonstrated to be the target mRNA of miR-448 in NSCLC cells. All mechanism experiments revealed that lncRNA PRNCR1 exerted ceRNA function in NSCLC by regulating miR-448 and HEY2. To validate the function of PRNCR1-miR-488-HEY2 network in NSCLC progression, rescue assays were conducted. Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. Show less
no PDF DOI: 10.1016/j.biopha.2018.08.105
HEY2

Ubiquitin-specific protease 22 acts as an oncoprotein to maintain glioma malignancy through deubiquitinating B cell-specific Moloney murine leukemia virus integration site 1 for stabilization.

Guan-Zhong Qiu, Xiao-Yuan Mao, Yue Ma +8 more · 2018 · Cancer science · Blackwell Publishing · added 2026-04-24
Ubiquitin-specific protease 22 (USP22) is a member of the "death-from-cancer" signature, which plays a key role in cancer progression. Previous evidence has shown that USP22 is overexpressed and corre Show more
Ubiquitin-specific protease 22 (USP22) is a member of the "death-from-cancer" signature, which plays a key role in cancer progression. Previous evidence has shown that USP22 is overexpressed and correlates with poor prognosis in glioma. The effect and mechanism of USP22 in glioma malignancy, especially cancer stemness, remain elusive. Herein, we find USP22 is more enriched in stem-like tumorspheres than differentiated glioma cells. USP22 knockdown inhibits cancer stemness in glioma cell lines. With a cell-penetrating TAT-tag protein, B cell-specific Moloney murine leukemia virus integration site 1 (BMI1), a robust glioma stem-cell marker, is found to mediate the effect of USP22 on glioma stemness. By immunofluorescence, USP22 and BMI1 are found to share similar intranuclear expression in glioma cells. By analysis with immunohistochemistry and bioinformatics, USP22 is found to positively correlate with BMI1 at the post-translational level only rather than at the transcriptional level. By immunoprecipitation and in vivo deubiquitination assay, USP22 is found to interact with and deubiquitinate BMI1 for protein stabilization. Microarray analysis shows that USP22 and BMI1 mutually regulate a series of genes involved in glioma stemness such as POSTN, HEY2, PDGFRA and ATF3. In vivo study with nude mice confirms the role of USP22 in promoting glioma tumorigenesis by regulating BMI1. All these findings indicate USP22 as a novel deubiquitinase of BMI1 in glioma. We propose a working model of the USP22-BMI1 axis, which promotes glioma stemness and tumorigenesis through oncogenic activation. Thus, targeting USP22 might be an effective strategy to treat glioma especially in those with elevated BMI1 expression. Show less
📄 PDF DOI: 10.1111/cas.13646
HEY2

Phenotypic variations in carriers of predicted protein-truncating genetic variants in MYBPC3: an autopsy-based case series.

Nori Williams, Robert Marion, Thomas V McDonald +9 more · 2018 · Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology · Elsevier · added 2026-04-24
Our aim is to characterize predicted protein-truncating variants (PTVs) in MYBPC3, the gene most commonly associated with hypertrophic cardiomyopathy (HCM), found in a series of autopsied HCM cases af Show more
Our aim is to characterize predicted protein-truncating variants (PTVs) in MYBPC3, the gene most commonly associated with hypertrophic cardiomyopathy (HCM), found in a series of autopsied HCM cases after sudden unexpected cardiac death. All cases underwent death scene investigation, gross and microscopic autopsies, toxicological testing, a review of medical records, and a molecular analysis of 95 cardiac genes. We found four pathogenic PTVs in MYBPC3 among male decedents. All variants were previously submitted to ClinVar without phenotype details. Two PTVs were located in the cardiac-specific myosin S2-binding (M) motif at the N-terminus of the MYBPC3-encoded cMyBP-C protein, and two PTVs were in the non-cardiac-specific C-terminus of the protein. The carriers of two cardiac-specific M-motif PTVs died at age 38 years; their heart weight (HW, g) and body mass index (BMI, kg/m Show less
no PDF DOI: 10.1016/j.carpath.2018.09.001
MYBPC3

Telomere shortening is a hallmark of genetic cardiomyopathies.

Alex C Y Chang, Andrew C H Chang, Anna Kirillova +15 more · 2018 · Proceedings of the National Academy of Sciences of the United States of America · National Academy of Sciences · added 2026-04-24
This study demonstrates that significantly shortened telomeres are a hallmark of cardiomyocytes (CMs) from individuals with end-stage hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM) Show more
This study demonstrates that significantly shortened telomeres are a hallmark of cardiomyocytes (CMs) from individuals with end-stage hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM) as a result of heritable defects in cardiac proteins critical to contractile function. Positioned at the ends of chromosomes, telomeres are DNA repeats that serve as protective caps that shorten with each cell division, a marker of aging. CMs are a known exception in which telomeres remain relatively stable throughout life in healthy individuals. We found that, relative to healthy controls, telomeres are significantly shorter in CMs of genetic HCM and DCM patient tissues harboring pathogenic mutations: Show less
no PDF DOI: 10.1073/pnas.1714538115
MYBPC3

Effects of antiepileptic drugs on lipogenic gene regulation and hyperlipidemia risk in Taiwan: a nationwide population-based cohort study and supporting in vitro studies.

Yi-Wen Li, Chung-Hsing Wang, Chao-Jung Chen +5 more · 2018 · Archives of toxicology · Springer · added 2026-04-24
To characterize the association between epilepsy, use of antiepileptic drugs (AEDs), and the risk of hyperlipidemia, we conducted a nationwide population-based cohort study with data obtained from the Show more
To characterize the association between epilepsy, use of antiepileptic drugs (AEDs), and the risk of hyperlipidemia, we conducted a nationwide population-based cohort study with data obtained from the National Health Insurance Research Database of Taiwan. The effects of AEDs on lipogenic gene expression were also examined in vitro. We identified 3617 cases involving patients, whose epilepsy was newly diagnosed between 2000 and 2011, and selected a comparison cohort comprising 14,468 patients without epilepsy. The Cox proportional hazards model was used to evaluate the association between epilepsy, AED use, and hyperlipidemia. The incidence rate of hyperlipidemia was higher in the epilepsy cohort than in the comparison cohort, with an adjusted hazard ratio (aHR) of 1.21 [95% confidence interval (CI): 1.06-1.38] after adjusting for comorbidities and medications. Epilepsy patients not taking AEDs had a higher risk of hyperlipidemia (aHR 1.65; 95% CI 1.35-2.03). Among AEDs, only valproate treatment showed a higher risk of hyperlipidemia (aHR 1.53; 95% CI 1.01-2.33), although the dose-dependent effect did not reach statistical significance. In vitro studies with two hepatic cell lines showed that valproate may exert its effects by activating the liver X receptor alpha (LXRα) signaling pathway, inducing the expression of lipogenesis-related genes and increasing cellular lipid contents. In silico calculations concluded that valproate can bind stably with the ligand-binding domain of LXRα. Thus, valproate-induced hepatic lipogenic gene expression may occur through LXRα activation. Predicting the 'off-target' effects of valproate may prove valuable in developing antiepileptic agents with fewer adverse reactions. Monitoring blood lipid levels throughout the course of treatment is recommended. Show less
no PDF DOI: 10.1007/s00204-018-2263-3
NR1H3

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

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

Andrographolide Inhibits Oxidized LDL-Induced Cholesterol Accumulation and Foam Cell Formation in Macrophages.

Hung-Chih Lin, Chong-Kuei Lii, Hui-Chun Chen +3 more · 2018 · The American journal of Chinese medicine · added 2026-04-24
oxLDL is involved in the pathogenesis of atherosclerotic lesions through cholesterol accumulation in macrophage foam cells. Andrographolide, the bioactive component of Andrographis paniculata, possess Show more
oxLDL is involved in the pathogenesis of atherosclerotic lesions through cholesterol accumulation in macrophage foam cells. Andrographolide, the bioactive component of Andrographis paniculata, possesses several biological activities such as anti-inflammatory, anti-oxidant, and anticancer functions. Scavenger receptors (SRs), including class A SR (SR-A) and CD36, are responsible for the internalization of oxLDL. In contrast, receptors for reverse cholesterol transport, including ABCA1 and ABCG1, mediate the efflux of cholesterol from macrophage foam cells. Transcription factor liver X receptor [Formula: see text] (LXR[Formula: see text] plays a key role in lipid metabolism and inflammation as well as in the regulation of ABCA1 and ABCG1 expression. Because of the contribution of inflammation to macrophage foam cell formation and the potent anti-inflammatory activity of andrographolide, we hypothesized that andrographolide might inhibit oxLDL-induced macrophage foam cell formation. The results showed that andrographolide reduced oxLDL-induced lipid accumulation in macrophage foam cells. Andrographolide decreased the mRNA and protein expression of CD36 by inducing the degradation of CD36 mRNA; however, andrographolide had no effect on SR-A expression. In contrast, andrographolide increased the mRNA and protein expression of ABCA1 and ABCG1, which were dependent on LXR[Formula: see text]. Andrographolide enhanced LXR[Formula: see text] nuclear translocation and DNA binding activity. Treatment with the LXR[Formula: see text] antagonist GGPP and transfection with LXR[Formula: see text] siRNA reversed the ability of andrographolide to stimulate ABCA1 and ABCG1 protein expression. In conclusion, inhibition of CD36-mediated oxLDL uptake and induction of ABCA1- and ABCG1-dependent cholesterol efflux are two working mechanisms by which andrographolide inhibits macrophage foam cell formation, which suggests that andrographolide could be a potential candidate to prevent atherosclerosis. Show less
no PDF DOI: 10.1142/S0192415X18500052
NR1H3

Circular RNA regulatory network reveals cell-cell crosstalk in acute myeloid leukemia extramedullary infiltration.

Chengfang Lv, Lili Sun, Zhibo Guo +8 more · 2018 · Journal of translational medicine · BioMed Central · added 2026-04-24
Acute myeloid leukemia can develop as myoblasts infiltrate into organs and tissues anywhere other than the bone marrow, which called extramedullary infiltration (EMI), indicating a poor prognosis. Cir Show more
Acute myeloid leukemia can develop as myoblasts infiltrate into organs and tissues anywhere other than the bone marrow, which called extramedullary infiltration (EMI), indicating a poor prognosis. Circular RNAs (circRNAs) are a novel class of non-coding RNAs that feature covalently closed continuous loops, suggesting their potential as micro RNA (miRNA) "sponges" that can participate in biological processes and pathogenesis. However, investigations on circRNAs in EMI were conducted rarely. In this study, the overall alterations of circRNAs and their regulatory network between EMI and non-EMI AML were delineated. CircRNA and whole genome microarrays derived from EMI and non-EMI AML bone marrow mononuclear cells were carried out. Functional analysis was performed via Gene Ontology and KEGG test methods. The speculated functional roles of circRNAs were based on mRNAs and predicted miRNAs that played intermediate roles. Integrated bioinformatic analysis was conducted to further characterize the circRNA/miRNA/mRNA regulatory network and identify the functions of distinct circRNAs. The Cancer Genome Atlas (TCGA) data were acquired to evaluate the poor prognosis of distinct target genes of circRNAs. Reverse transcription-quantitative polymerase chain reaction was conducted to identify the expression of has_circRNA₀₀₀₄₅₂₀. Connectivity map (CMap) analysis was further performed to predict potential therapeutic agents for EMI. 253 circRNAs and 663 genes were upregulated and 259 circRNAs and 838 genes were downregulated in EMI compared to non-EMI AML samples. GO pathways were enriched in progress including cell adhesion (GO:0030155; GO:0007155), migration (GO:0016477; GO:0030334), signal transduction (GO:0009966; GO:0007165) and cell-cell communication. Overlapping circRNAs envolved in pathways related to regulate cell-cell crosstalk, 17 circRNAs were chosen based on their putative roles. 7 target genes of 17 circRNAs (LRRK1, PLXNB2, OLFML2A, LYPD5, APOL3, ZNF511, and ASB2) indicated a poor prognosis, while overexpression of PAPLN and NRXN3 indicated a better one based on data from TCGA. LY-294002, trichostatin A and SB-202190 were identified as therapeutic candidates for EMI by the CMap analysis. Taken together, this study reveals the overall alterations of circRNA and mRNA involved in EMI and suggests potential circRNAs may act as biomarkers and targets for early diagnosis and treatment of EMI. Show less
no PDF DOI: 10.1186/s12967-018-1726-x
NRXN3

Asymmetric distribution of CRUMBS polarity complex proteins from compacted 8-cell to blastocyst stage during mouse preimplantation development.

Xinlong Jiang, Wenzhong An, Xiao Yang +4 more · 2018 · Gene expression patterns : GEP · Elsevier · added 2026-04-24
During mouse preimplantation development, blastomeres are equipotent until polarity establishment at compacted 8-cell stage. The intrinsic nature of polarity is the asymmetric distribution of polarity Show more
During mouse preimplantation development, blastomeres are equipotent until polarity establishment at compacted 8-cell stage. The intrinsic nature of polarity is the asymmetric distribution of polarity proteins between inside and outside blastomeres along the direction of apical-basal axis. This study investigated the early developmental temporal and spatial expression of the main CRUMBS polarity complex proteins in the mouse preimplantation embryo. We observed that Crb3, Pals1, Patj and Mpdz are transcribed in the mouse preimplantation embryo. However, the asymmetric distribution of these polarity proteins is not established until the compacted 8-cell stage. From compaction and thereafter, CRB3 and PALS1 are progressively enriched in the apical membrane, while PATJ and MPDZ are discretely localized at both tight junctions and the apical membrane adjacent to tight junctions. These temporal and spatial distribution patterns suggest that CRUMBS polarity complex might be involved in the cell polarity establishment in the early mouse embryo and reinforce the viewpoint that developmentally spatial asymmetries are first set up at the compaction stage. The present study provides a foundation for further investigation on the functions of CRUMBS polarity complex in trophectoderm specification and blastocyst morphogenesis. Show less
no PDF DOI: 10.1016/j.gep.2017.11.002
PATJ

Author Correction: EZH2 inhibition sensitizes BRG1 and EGFR mutant lung tumours to TopoII inhibitors.

Christine M Fillmore, Chunxiao Xu, Pooja T Desai +8 more · 2018 · Nature · Nature · added 2026-04-24
We wish to correct two mutations in Supplementary Table 4 of this Letter. The NCI-H460 cell line was annotated as being mutant for TP53. NCI-H460 has been verified to be TP53 wild type by several sour Show more
We wish to correct two mutations in Supplementary Table 4 of this Letter. The NCI-H460 cell line was annotated as being mutant for TP53. NCI-H460 has been verified to be TP53 wild type by several sources Show less
no PDF DOI: 10.1038/s41586-018-0580-6
PIK3C3

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

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

Genome-wide screening differential long non-coding RNAs expression profiles discloses its roles involved in OHSS development.

Haiyan Lin, Yu Li, Weijie Xing +3 more · 2018 · Journal of assisted reproduction and genetics · Springer · added 2026-04-24
To screen differentially expressed lncRNAs involved in OHSS. OHSS is defined as ovarian hyperstimulation syndrome. It is characterized as enlarged ovary and increased vascular permeability. Case-contr Show more
To screen differentially expressed lncRNAs involved in OHSS. OHSS is defined as ovarian hyperstimulation syndrome. It is characterized as enlarged ovary and increased vascular permeability. Case-control study. University-affiliated hospital. Patients with OHSS high risk (n = 30) and low risk (n = 30) were included in this study. None. LncRNAs from women with OHSS high risk and low risk were used for high-throughput sequencing profiling. The eight most differentially expressed lncRNAs in granulosa cells were validated by semi-quantitative reverse transcription-polymerase chain reaction analysis. A total of 23,815 lncRNAs were detected and 482 were differentially expressed (fold-change ≥2; p < 0.05, FDR value < 0.001), of which 205 were upregulated and 277 were downregulated. Lnc-SEC16B.1-6, lnc-SNURF-13, lnc-LGR6-6, and lnc-H2AFY2-2 were up-regulated, while lnc-BRD2-2, lnc-HSPA6-2, and lnc-CLIC6-5 were downregulated significantly in granulosa cells. These results were confirmed by qRT-PCR. KEGG pathways and Gene Ontology enrichment analysis revealed that several biological processes were significantly associated. Meanwhile, the lncRNA/miRNA interaction network was established according to ceRNA network model. Comprehensive expression screening identified eight novel lncRNAs associated with risk factors of OHSS process. Although it is unclear how these altered lncRNAs regulate the process of OHSS, our findings suggest these lncRNAs may be novel players in OHSS development. Show less
no PDF DOI: 10.1007/s10815-018-1199-0
SEC16B

Lysosomal acid phosphatase 2 is an unfavorable prognostic factor but is associated with better survival in stage II colorectal cancer patients receiving chemotherapy.

Yu-Chieh Lee, Chia-Yu Su, Yuan-Feng Lin +5 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
Colorectal cancer (CRC) is one of the leading cancers worldwide. Surgery is the main therapeutic modality for stage II CRC. However, the implementation of adjuvant chemotherapy remains controversial a Show more
Colorectal cancer (CRC) is one of the leading cancers worldwide. Surgery is the main therapeutic modality for stage II CRC. However, the implementation of adjuvant chemotherapy remains controversial and is not universally applied so far. In this study, we found that the protein expression of lysosomal acid phosphatase 2 (ACP2) was increased in CRC and that stage II CRC patients with high ACP2 expression showed a poorer outcome than those with low ACP2 expression (p = 0.004). To investigate this discrepancy, we analyzed the relation between ACP2 expression and several clinical cofactors.Among patients who received chemotherapy, those with an high expression of ACP2 showed better survival in both stage II and III CRC than those with low ACP2 expression. In stage II CRC patients, univariate analysis showed ACP2 expression and T stage to be cofactors significantly associated with overall survival (ACP2: p = 0.006; T stage: p = 0.034). Multivariate Cox proportion hazard model analysis also revealed ACP2 to be an independent prognostic factor for overall survival (ACP2: p = 0.006; T stage: p = 0.041). Furthermore, ACP2-knockdown CRC cells showed an increase in chemoresistance to 5-FU treatment and increased proliferation marker in the ACP2 knockdown clone.Taken together, our results suggested that ACP2 is an unfavorable prognostic factor for stage II CRC and may serve as a potential chemotherapy-sensitive marker to help identify a subset of stage II and III CRC patients for whom chemotherapy would improve survival.Highlights1. To the best of our knowledge, the study is the first report to show ACP2 overexpression in human colorectal cancer (CRC) and its association with poor outcome in stage II CRC.2. Patients with stage II and III CRCs with high expression of ACP2 were more sensitive to chemotherapy than those with a low expression.3. ACP2 expression may serve as a marker for CRC patients receiving chemotherapy and help identify the subset of CRC patients who would benefit from chemotherapy. Show less
📄 PDF DOI: 10.18632/oncotarget.14552
ACP2

Supplementation of cilostazol during in vitro maturation enhances the meiosis and developmental competence of yak oocytes by influencing cAMP content and mRNA expression.

Xian-Rong Xiong, Dao-Liang Lan, Jian Li +2 more · 2017 · Animal reproduction science · Elsevier · added 2026-04-24
The efficiency of in vitro embryo production remains low compared with that observed in vivo. Recent studies have independently shown that cyclic adenosine monophosphate (cAMP) modulation prior to in Show more
The efficiency of in vitro embryo production remains low compared with that observed in vivo. Recent studies have independently shown that cyclic adenosine monophosphate (cAMP) modulation prior to in vitro maturation (IVM) supplementation improves oocyte developmental competence. In this context, special cAMP modulators have been applied during IVM as promising alternatives to improve this biotechnology. Accordingly, this study was conducted to evaluate the effects of treatment with cilostazol, a PDE3 inhibitor, during pre-IVM culture on oocyte meiotic maturation in yak. Immature yak cumulus-oocyte complexes (COCs) were treated in vitro without (control) or with 5μM cilostazol for 0, 2, or 4h prior to IVM. Results showed that the presence of cilostazol in pre-IVM medium significantly increased the percentages of oocytes at metaphase II stage compared with that in the control groups (P<0.05). Moreover, pre-IVM with cilostazol significantly enhanced intraoocyte cAMP and glutathione (GSH) levels at the pre-IVM or IVM phase relative to the no pre-IVM groups (P<0.05). After in vitro fertilization (IVF) and parthenogenetic activation (PA), the developmental competences of oocytes and embryo quality were improved significantly after pre-IVM with cilostazol compared with the control groups (P<0.05), given that the cleavage and blastocyst formation rates and the total number of blastocyst cells were increased. The presence of cilostazol also increased the levels of mRNA expression for adenylate cyclase 3 (ADCY3) and protein kinase 1 (PKA1), as well as decreased the abundance of phosphodiesterase 3A (PDE3A) in COCs and IVF blastocysts, compared with their control counterparts (P<0.05). The results demonstrated that the meiotic progression of immature yak oocytes could be reversibly affected by cAMP modulators. By contrast, treatment with cilostazol during pre-IVM positively affected the developmental competence of yak oocytes, probably by improving intraoocyte cAMP and GSH levels and regulating mRNA expression patterns. We concluded that appropriate treatment with cilostazol during pre-IVM would be beneficial for oocyte maturation in vitro. Show less
no PDF DOI: 10.1016/j.anireprosci.2017.08.013
ADCY3

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

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

ANGPTL4 mediates the protective role of PPARγ activators in the pathogenesis of preeclampsia.

Lei Liu, Xu Zhuang, Meng Jiang +3 more · 2017 · Cell death & disease · Nature · added 2026-04-24
Peroxisome proliferator-activated receptor γ (PPARγ) has been shown to be a therapeutic target for preeclampsia (PE). Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional secretory protein invol Show more
Peroxisome proliferator-activated receptor γ (PPARγ) has been shown to be a therapeutic target for preeclampsia (PE). Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional secretory protein involved in regulating lipid metabolism and angiogenesis in various tissues. However, the expression of PPARγ and ANGPTL4 and their interaction in PE remain elusive. Here we showed that PPARγ agonist rosiglitazone upregulated the expression and secretion of ANGPTL4 in a dose-dependent manner in HTR8/SVneo cells, human umbilical vein endothelial cells (HUVECs) and placental explants. More importantly, we confirmed that the PPARγ/retinoid X receptor α heterodimer specifically binds to the ANGPTL4 promoter region and enhances its transcriptional activity. In addition, the levels of ANGPTL4 and PPARγ activators in the serum and their expression in placental tissues were significantly reduced in preeclamptic patients compared with normal pregnant subjects. Furthermore, functional studies demonstrated that ANGPTL4 mediates the facilitative effects of the PPARγ agonist on the survival, proliferation, migration and invasion of HTR8/SVneo cells, placental explants outgrowth and angiogenesis in HUVECs. Taken together, our results suggest that ANGPTL4 is a potential target gene for PPARγ and mediates the protective role of PPARγ activators in the pathogenesis of PE. Show less
📄 PDF DOI: 10.1038/cddis.2017.419
ANGPTL4

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

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

Detection of susceptibility loci on

Eugene Lin, Po-Hsiu Kuo, Yu-Li Liu +2 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
Although the association of single nucleotide polymorphisms (SNPs) with metabolic syndrome (MetS) has been reported in various populations in several genome-wide association studies (GWAS), the data i Show more
Although the association of single nucleotide polymorphisms (SNPs) with metabolic syndrome (MetS) has been reported in various populations in several genome-wide association studies (GWAS), the data is not conclusive. In this GWAS study, we assessed whether SNPs are associated with MetS and its individual components independently and/or through complex interactions in a Taiwanese population. A total of 10,300 Taiwanese subjects were assessed in this study. Metabolic traits such as waist circumference, triglyceride, high-density lipoprotein (HDL) cholesterol, systolic and diastolic blood pressure, and fasting glucose were measured. Our data showed an association of MetS at the genome-wide significance level ( Our study indicates that the Show less
📄 PDF DOI: 10.18632/oncotarget.20967
APOA5

APOA5 Gene Polymorphisms and Cardiovascular Diseases: Metaprediction in Global Populations.

Yen-Chun Lin, Veronica Nunez, Robin Johns +1 more · 2017 · Nursing research · added 2026-04-24
Apolipoprotein A5 (APOA5) 1131 is one of the most investigated gene polymorphisms in association with cardiovascular diseases (CVD) for its roles in epigenetics pathways. The major objective of this m Show more
Apolipoprotein A5 (APOA5) 1131 is one of the most investigated gene polymorphisms in association with cardiovascular diseases (CVD) for its roles in epigenetics pathways. The major objective of this metaprediction study was to comprehensively examine the association of polymorphism risk subtypes of APOA5 1131 gene and potential contributing factors of CVD risks in global populations. This study is a meta-analysis to determine APOA5 gene polymorphisms as risk factors for CVDs. Following the guidelines of meta-analyses, we applied big data analytics including the recursive partition tree, nonlinear association curve fit, and heat maps for data visualization-in addition to the conventional pooled analyses. A total of 17,692 CVD cases and 23,566 controls from 50 study groups were included. The frequency of APOA5 1131 CC and TC polymorphisms in Asian populations (22.2%-52.6%) were higher than that in other populations, including Caucasians and Eurasians (10.0%-25.0%). The homozygous CC and heterozygous TC genotypes (both p < .0001) were associated with increased risks for CVD and were higher in many Western nations, including Canada, Spain, the Czech Republic, Hungary, Turkey, Egypt, France, and Iran. The CC genotype was associated with greater risks (RR > 2.00, p < .0001) for dyslipidemia and myocardial infarction, whereas RR > 1.00 was associated with metabolic syndrome, coronary artery disease, and stroke. Air pollution was significantly associated with APOA5 1131 CC and TC polymorphisms. The findings of this study provided novel insight to further understand the associations among APOA5 1131 polymorphisms, air pollution, and the development of CVDs. Methylation studies are needed to examine epigenetic factors associated with APOA5 1131 polymorphisms and CVD and to suggest potential prevention strategies for CVD. Show less
no PDF DOI: 10.1097/NNR.0000000000000207
APOA5

Axin1 up-regulated 1 accelerates stress-induced cardiomyocytes apoptosis through activating Wnt/β-catenin signaling.

Xing Ye, Junyi Lin, Zebin Lin +6 more · 2017 · Experimental cell research · Elsevier · added 2026-04-24
Stress-induced cardiomyocyte apoptosis contributes to the pathogenesis of a variety of cardiovascular diseases, but how stress induces cardiomyocyte apoptosis remains largely unclear. The present stud Show more
Stress-induced cardiomyocyte apoptosis contributes to the pathogenesis of a variety of cardiovascular diseases, but how stress induces cardiomyocyte apoptosis remains largely unclear. The present study aims to investigate the effects of Axin1 up-regulated 1 (Axud1), a novel pro-apoptotic protein, on the cardiomyocyte survival and the underlying mechanisms. To this end, a rat model under restraint stress (RS) was established and in vitro stress-induced cardiomyocytes culture was achieved. Our data showed that Axud1 was upregulated in the rat myocardia after exposure to RS. Anti-apoptotic Bcl-2 was decreased, whereas pro-apoptotic Bax and Cleaved caspase-3 (Cc3) were increased in a time-dependent manner. The Wnt/β-catenin signaling was observed to be interestingly activated in heart undergoing RS. In addition, the treatment of norepinephrine (NE) to in vitro cardiomyocytes increased Axud1 level and induced cell apoptosis. Wnt/β-catenin signaling was consistently activated. Knockdown of Axud1 using specific siRNA blunted NE-induced cardiomyocytes apoptosis and also inactivated the Wnt/β-catenin signaling. XAV-939, an inhibitor of Wnt/β-catenin signaling, partially reversed the pro-apoptotic effect of NE. In conclusion, Axud1 accelerated stress-induced cardiomyocytes apoptosis through activation of Wnt/β-catenin signaling pathway. Our data provided novel evidence that therapeutic strategies against Axud1 or Wnt/β-catenin signaling might be promising in relation to RS-induced myocardial injury. Show less
no PDF DOI: 10.1016/j.yexcr.2017.08.027
AXIN1

Novel SUMO-Protease SENP7S Regulates β-catenin Signaling and Mammary Epithelial Cell Transformation.

Samaneh Karami, Feng-Ming Lin, Santosh Kumar +6 more · 2017 · Scientific reports · Nature · added 2026-04-24
SUMO post-translational modification of proteins or SUMOylation ensures normal cell function. Disruption of SUMO dynamics prompts various pathophysiological conditions, including cancer. The burden of Show more
SUMO post-translational modification of proteins or SUMOylation ensures normal cell function. Disruption of SUMO dynamics prompts various pathophysiological conditions, including cancer. The burden of deSUMOylating the large SUMO-proteome rests on 6 full-length mammalian SUMO-proteases or SENP. While multiple SENP isoforms exist, the function of these isoforms remains undefined. We now delineate the biological role of a novel SENP7 isoform SENP7S in mammary epithelial cells. SENP7S is the predominant SENP transcript in human mammary epithelia but is significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes. Like other SENP family members, SENP7S has SUMO isopeptidase activity but unlike full-length SENP7L, SENP7S is localized in the cytosol. In vivo, SUMOylated β-catenin and Axin1 are both SENP7S-substrates. With knockdown of SENP7S in mammary epithelial cells, Axin1-β-catenin interaction is lost and β-catenin escapes ubiquitylation-dependent proteasomal degradation. SUMOylated β-catenin accumulates at the chromatin and activates multiple oncogenes. Hence, non-tumorigenic MCF10-2A cells with reduced SENP7S exhibit greater cell proliferation and anchorage-dependent growth. SENP7S depletion directly potentiates tumorigenic properties of MCF10-2A cells with induction of anchorage-independent growth and self-renewal in 3D-spheroid conditions. Collectively, the results identify SENP7S as a novel mediator of β-catenin signaling and normal mammary epithelial cell physiology. Show less
📄 PDF DOI: 10.1038/srep46477
AXIN1

Vitamin D receptor is a novel transcriptional regulator for Axin1.

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

Prognostic values of distinct CBX family members in breast cancer.

Yuan-Ke Liang, Hao-Yu Lin, Chun-Fa Chen +1 more · 2017 · Oncotarget · Impact Journals · added 2026-04-24
Chromobox (CBX) family proteins are canonical components in polycomb repressive complexes 1 (PRC1), with epigenetic regulatory function and transcriptionally repressing target genes via chromatin modi Show more
Chromobox (CBX) family proteins are canonical components in polycomb repressive complexes 1 (PRC1), with epigenetic regulatory function and transcriptionally repressing target genes via chromatin modification. A plethora of studies have highlighted the function specifications among CBX family members in various cancer, including lung cancer, colon cancer and breast cancer. Nevertheless, the functions and prognostic roles of distinct CBX family members in breast cancer (BC) remain elusive. In this study, we reported the prognostic values of CBX family members in patients with BC through analysis of a series of databases, including Show less
📄 PDF DOI: 10.18632/oncotarget.21325
CBX1

Design, Synthesis, and Biological Evaluation of N,N-Disubstituted-4-Arylthiazole-2-Methylamine Derivatives as Cholesteryl Ester Transfer Inhibitors.

Xinran Wang, Xuehua Lin, Xuanqi Xu +5 more · 2017 · Molecules (Basel, Switzerland) · MDPI · added 2026-04-24
Cholesteryl ester transfer protein (CETP) has been identified as a potential target for cardiovascular disease (CVD) for its important role in the reverse cholesteryl transfer (RCT) process. In our pr Show more
Cholesteryl ester transfer protein (CETP) has been identified as a potential target for cardiovascular disease (CVD) for its important role in the reverse cholesteryl transfer (RCT) process. In our previous work, compound Show less
📄 PDF DOI: 10.3390/molecules22111925
CETP

Protein-Truncating Variants at the Cholesteryl Ester Transfer Protein Gene and Risk for Coronary Heart Disease.

Akihiro Nomura, Hong-Hee Won, Amit V Khera +62 more · 2017 · Circulation research · added 2026-04-24
Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the To test Show more
Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the To test whether protein-truncating variants (PTVs) at the We sequenced the exons of the Compared with noncarriers, carriers of PTV at Show less
📄 PDF DOI: 10.1161/CIRCRESAHA.117.311145
CETP

Yeast Cip1 is activated by environmental stress to inhibit Cdk1-G1 cyclins via Mcm1 and Msn2/4.

Ya-Lan Chang, Shun-Fu Tseng, Yu-Ching Huang +12 more · 2017 · Nature communications · Nature · added 2026-04-24
Upon environmental changes, proliferating cells delay cell cycle to prevent further damage accumulation. Yeast Cip1 is a Cdk1 and Cln2-associated protein. However, the function and regulation of Cip1 Show more
Upon environmental changes, proliferating cells delay cell cycle to prevent further damage accumulation. Yeast Cip1 is a Cdk1 and Cln2-associated protein. However, the function and regulation of Cip1 are still poorly understood. Here we report that Cip1 expression is co-regulated by the cell-cycle-mediated factor Mcm1 and the stress-mediated factors Msn2/4. Overexpression of Cip1 arrests cell cycle through inhibition of Cdk1-G1 cyclin complexes at G1 stage and the stress-activated protein kinase-dependent Cip1 T65, T69, and T73 phosphorylation may strengthen the Cip1and Cdk1-G1 cyclin interaction. Cip1 accumulation mainly targets Cdk1-Cln3 complex to prevent Whi5 phosphorylation and inhibit early G1 progression. Under osmotic stress, Cip1 expression triggers transient G1 delay which plays a functionally redundant role with another hyperosmolar activated CKI, Sic1. These findings indicate that Cip1 functions similarly to mammalian p21 as a stress-induced CDK inhibitor to decelerate cell cycle through G1 cyclins to cope with environmental stresses.A G1 cell cycle regulatory kinase Cip1 has been identified in budding yeast but how this is regulated is unclear. Here the authors identify cell cycle (Mcm1) and stress-mediated (Msn 2/4) transcription factors as regulating Cip1, causing stress induced CDK inhibition and delay in cell cycle progression. Show less
📄 PDF DOI: 10.1038/s41467-017-00080-y
CLN3

CPS1 maintains pyrimidine pools and DNA synthesis in KRAS/LKB1-mutant lung cancer cells.

Jiyeon Kim, Zeping Hu, Ling Cai +23 more · 2017 · Nature · Nature · added 2026-04-24
Metabolic reprogramming by oncogenic signals promotes cancer initiation and progression. The oncogene KRAS and tumour suppressor STK11, which encodes the kinase LKB1, regulate metabolism and are frequ Show more
Metabolic reprogramming by oncogenic signals promotes cancer initiation and progression. The oncogene KRAS and tumour suppressor STK11, which encodes the kinase LKB1, regulate metabolism and are frequently mutated in non-small-cell lung cancer (NSCLC). Concurrent occurrence of oncogenic KRAS and loss of LKB1 (KL) in cells specifies aggressive oncological behaviour. Here we show that human KL cells and tumours share metabolomic signatures of perturbed nitrogen handling. KL cells express the urea cycle enzyme carbamoyl phosphate synthetase-1 (CPS1), which produces carbamoyl phosphate in the mitochondria from ammonia and bicarbonate, initiating nitrogen disposal. Transcription of CPS1 is suppressed by LKB1 through AMPK, and CPS1 expression correlates inversely with LKB1 in human NSCLC. Silencing CPS1 in KL cells induces cell death and reduces tumour growth. Notably, cell death results from pyrimidine depletion rather than ammonia toxicity, as CPS1 enables an unconventional pathway of nitrogen flow from ammonia into pyrimidines. CPS1 loss reduces the pyrimidine to purine ratio, compromises S-phase progression and induces DNA-polymerase stalling and DNA damage. Exogenous pyrimidines reverse DNA damage and rescue growth. The data indicate that the KL oncological genotype imposes a metabolic vulnerability related to a dependence on a cross-compartmental pathway of pyrimidine metabolism in an aggressive subset of NSCLC. Show less
📄 PDF DOI: 10.1038/nature22359
CPS1

Neuroprotective effect of dual specificity phosphatase 6 against glutamate-induced cytotoxicity in mouse hippocampal neurons.

Xiaoyun Huang, Wang Liao, Yihong Huang +6 more · 2017 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · Elsevier · added 2026-04-24
Dual specificity phosphatase 6 (DUSP6), a member of the dual specificity protein phosphatase subfamily, can inactivate ERK1/2. However, its possible role in glutamate-induced oxidative cytotoxicity ef Show more
Dual specificity phosphatase 6 (DUSP6), a member of the dual specificity protein phosphatase subfamily, can inactivate ERK1/2. However, its possible role in glutamate-induced oxidative cytotoxicity effects is not clear.Here, we aimed to investigate whether DUSP6 was neuroprotective against glutamate-induced cytotoxicity in HT22 mouse hippocampal cells and primary cultured hippocampal neurons (pc-HNeu). HT22 and pc-HNeu cells were treated with varying concentrations of glutamate (from 0.05mM to 5.0mM) and DUSP6 protein expression were detected by western blotting. DUSP6-overexpressing HT22 and pc-HNeu cells were generated by transfection with DUSP6-overexpressing plasmid. The effects of DUSP6 overexpression on glutamate-induced cytotoxicity, cell death, cell apoptosis, and cell autophagy were determined by cell proliferation assays, flow cytometry, transmission electron microscopy, and western blotting. Glutamate treatment from 0.5mM to 5.0mM downregulated DUSP6 protein expression in both HT22 and pc-HNeu cells. DUSP6 overexpression ameliorated glutamate-induced cell death, apoptosis, and autophagy in both HT22 and pc-HNeu cells. Furthermore, ERK1/2 phosphorylation was decreased by DUSP6 overexpression. In conclusion, DUSP6 has neuroprotective effects against glutamate-induced cytotoxicity in HT22 and pc-HNeu cells. Targeting DUSP6 may be a useful strategy to prevent neuronal death in neurodegenerative diseases including AD. Show less
no PDF DOI: 10.1016/j.biopha.2017.04.096
DUSP6

Epithelial heparan sulfate regulates Sonic Hedgehog signaling in lung development.

Hua He, Meina Huang, Shenfei Sun +2 more · 2017 · PLoS genetics · PLOS · added 2026-04-24
The tree-like structure of the mammalian lung is generated from branching morphogenesis, a reiterative process that is precisely regulated by numerous factors. How the cell surface and extra cellular Show more
The tree-like structure of the mammalian lung is generated from branching morphogenesis, a reiterative process that is precisely regulated by numerous factors. How the cell surface and extra cellular matrix (ECM) molecules regulate this process is still poorly understood. Herein, we show that epithelial deletion of Heparan Sulfate (HS) synthetase Ext1 resulted in expanded branching tips and reduced branching number, associated with several mesenchymal developmental defects. We further demonstrate an expanded Fgf10 expression and increased FGF signaling activity in Ext1 mutant lungs, suggesting a cell non-autonomous mechanism. Consistent with this, we observed reduced levels of SHH signaling which is responsible for suppressing Fgf10 expression. Moreover, reactivating SHH signaling in mutant lungs rescued the tip dilation phenotype and attenuated FGF signaling. Importantly, the reduced SHH signaling activity did not appear to be caused by decreased Shh expression or protein stability; instead, biologically active form of SHH proteins were reduced in both the Ext1 mutant epithelium and surrounding wild type mesenchymal cells. Together, our study highlights the epithelial HS as a key player for dictating SHH signaling critical for lung morphogenesis. Show less
📄 PDF DOI: 10.1371/journal.pgen.1006992
EXT1