👤 Shu-Chun 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-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, 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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

Activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network in human hepatocellular carcinoma by systems-theoretic analysis.

Lin Wang, Juxiang Huang, Minghu Jiang +3 more · 2012 · TheScientificWorldJournal · added 2026-04-24
Studies were done on analysis of biological processes in the same high expression (fold change ≥2) activated PTHLH feedback-mediated cell adhesion gene ontology (GO) network of human hepatocellular ca Show more
Studies were done on analysis of biological processes in the same high expression (fold change ≥2) activated PTHLH feedback-mediated cell adhesion gene ontology (GO) network of human hepatocellular carcinoma (HCC) compared with the corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). Activated PTHLH feedback-mediated cell adhesion network consisted of anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, cell adhesion, cell differentiation, cell-cell signaling, G-protein-coupled receptor protein signaling pathway, intracellular transport, metabolism, phosphoinositide-mediated signaling, positive regulation of transcription, regulation of cyclin-dependent protein kinase activity, regulation of transcription, signal transduction, transcription, and transport in HCC. We proposed activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network. Our hypothesis was verified by the different activated PTHLH feedback-mediated cell adhesion GO network of HCC compared with the corresponding inhibited GO network of no-tumor hepatitis/cirrhotic tissues, or the same compared with the corresponding inhibited GO network of HCC. Activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network included BUB1B, GNG10, PTHR2, GNAZ, RFC4, UBE2C, NRXN3, BAP1, PVRL2, TROAP, and VCAN in HCC from GEO dataset using gene regulatory network inference method and our programming. Show less
no PDF DOI: 10.1100/2012/428979
NRXN3

Genome-wide association study of prognosis in advanced non-small cell lung cancer patients receiving platinum-based chemotherapy.

Lingmin Hu, Chen Wu, Xueying Zhao +26 more · 2012 · Clinical cancer research : an official journal of the American Association for Cancer Research · added 2026-04-24
Genetic variation may influence chemotherapy response and overall survival in cancer patients. We conducted a genome-wide scan in 535 advanced-stage non-small cell lung cancer (NSCLC) patients from tw Show more
Genetic variation may influence chemotherapy response and overall survival in cancer patients. We conducted a genome-wide scan in 535 advanced-stage non-small cell lung cancer (NSCLC) patients from two independent cohorts (307 from Nanjing and 228 from Beijing). A replication was carried out on an independent cohort of 340 patients from Southeastern China followed by a second validation on 409 patients from the Massachusetts General Hospital (Boston, MA). Consistent associations with NSCLC survival were identified for five single-nucleotide polymorphisms (SNP) in Chinese populations with P values ranging from 3.63 × 10(-5) to 4.19 × 10(-7) in the additive genetic model. The minor allele of three SNPs (rs7629386 at 3p22.1, rs969088 at 5p14.1, and rs3850370 at 14q24.3) were associated with worse NSCLC survival while 2 (rs41997 at 7q31.31 and rs12000445 at 9p21.3) were associated with better NSCLC survival. In addition, rs7629386 at 3p22.1 (CTNNB1) and rs3850370 at 14q24.3 (SNW1-ALKBH1-NRXN3) were further replicated in the Caucasian population. In this three-stage genome-wide association studies, we identified five SNPs as markers for survival of advanced-stage NSCLC patients treated with first-line platinum-based chemotherapy in Chinese Han populations. Two of these SNPs, rs7629386 and rs3850370, could also be markers for survival among Caucasian patients. Show less
no PDF DOI: 10.1158/1078-0432.CCR-12-1202
NRXN3

Mammalian PIK3C3/VPS34: the key to autophagic processing in liver and heart.

Nadia Jaber, Zhixun Dou, Richard Z Lin +2 more · 2012 · Autophagy · added 2026-04-24
PIK3C3/Vps34 is the class III PtdIns3K that is evolutionarily conserved from yeast to mammals. Its central role in mammalian autophagy has been suggested through the use of pharmacological inhibitors Show more
PIK3C3/Vps34 is the class III PtdIns3K that is evolutionarily conserved from yeast to mammals. Its central role in mammalian autophagy has been suggested through the use of pharmacological inhibitors and the study of its binding partners. However, the precise role of PIK3C3 in mammals is not clear. Using mouse strains that allow tissue-specific deletion of PIK3C3, we have described an essential role of PIK3C3 in regulating autophagy, and liver and heart function. Show less
no PDF DOI: 10.4161/auto.19627
PIK3C3

Class III PI3K Vps34 plays an essential role in autophagy and in heart and liver function.

Nadia Jaber, Zhixun Dou, Juei-Suei Chen +8 more · 2012 · Proceedings of the National Academy of Sciences of the United States of America · National Academy of Sciences · added 2026-04-24
A critical regulator of autophagy is the Class III PI3K Vps34 (also called PIK3C3). Although Vps34 is known to play an essential role in autophagy in yeast, its role in mammals remains elusive. To elu Show more
A critical regulator of autophagy is the Class III PI3K Vps34 (also called PIK3C3). Although Vps34 is known to play an essential role in autophagy in yeast, its role in mammals remains elusive. To elucidate the physiological function of Vps34 and to determine its precise role in autophagy, we have generated Vps34(f/f) mice, in which expression of Cre recombinase results in a deletion of exon 4 of Vps34 and a frame shift causing a deletion of 755 of the 887 amino acids of Vps34. Acute ablation of Vps34 in MEFs upon adenoviral Cre infection results in a diminishment of localized generation of phosphatidylinositol 3-phosphate and blockade of both endocytic and autophagic degradation. Starvation-induced autophagosome formation is blocked in both Vps34-null MEFs and liver. Liver-specific Albumin-Cre;Vps34(f/f) mice developed hepatomegaly and hepatic steatosis, and impaired protein turnover. Ablation of Vps34 in the heart of muscle creatine kinase-Cre;Vps34(f/f) mice led to cardiomegaly and decreased contractility. In addition, while amino acid-stimulated mTOR activation was suppressed in the absence of Vps34, the steady-state level of mTOR signaling was not affected in Vps34-null MEFs, liver, or cardiomyocytes. Taken together, our results indicate that Vps34 plays an essential role in regulating functional autophagy and is indispensable for normal liver and heart function. Show less
no PDF DOI: 10.1073/pnas.1112848109
PIK3C3

Glucose-dependent insulinotropic peptide receptor expression in the hippocampus and neocortex of mesial temporal lobe epilepsy patients and rats undergoing pilocarpine induced status epilepticus.

Cláudia P Figueiredo, Victor L S Antunes, Eduardo L G Moreira +9 more · 2011 · Peptides · Elsevier · added 2026-04-24
The glucose-dependent insulinotropic peptide receptor (GIPR) has been implicated with neuroplasticity and may be related to epilepsy. GIPR expression was analyzed by immunohistochemistry in the hippoc Show more
The glucose-dependent insulinotropic peptide receptor (GIPR) has been implicated with neuroplasticity and may be related to epilepsy. GIPR expression was analyzed by immunohistochemistry in the hippocampus (HIP) and neocortex (Cx) of rats undergoing pilocarpine induced status epilepticus (Pilo-SE), and in three young male patients with left mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS) treated surgically. A combined GIPR immunohistochemistry and Fluoro-Jade staining was carried out to investigate the association between the GIPR expression and neuronal degeneration induced by Pilo-SE. GIPR was expressed in the cytoplasm of neurons from the HIP CA subfields, dentate gyrus (DG) and Cx of animals and human samples. The GIPR expression after the Pilo-SE induction increases significantly in the HIP after 1h and 5 days, but not after 12h or 50 days. In the Cx, the GIPR expression increases after 1h, 12h and 5 days, but not 50 days after the Pilo-SE. The expression of GIPR 12h after Pilo-SE was inversely proportional to the Fluoro-Jade staining intensity. In the human tissue, GIPR expression patterns were similar to those observed in chronic Pilo-SE animals. No Fluoro-Jade stained cells were observed in the human sample. GIPR is expressed in human HIP and Cx. There was a time and region dependent increase of GIPR expression in the HIP and Cx after Pilo-SE that was inversely associated to neuronal degeneration. Show less
no PDF DOI: 10.1016/j.peptides.2010.12.010
GIPR

Optimizing human synovial fluid preparation for two-dimensional gel electrophoresis.

Carl Pc Chen, Chih-Chin Hsu, Wen-Lin Yeh +6 more · 2011 · Proteome science · BioMed Central · added 2026-04-24
Proteome analysis is frequently applied in identifying the proteins or biomarkers in knee synovial fluids (SF) that are associated with osteoarthritis and other arthritic disorders. The 2-dimensional Show more
Proteome analysis is frequently applied in identifying the proteins or biomarkers in knee synovial fluids (SF) that are associated with osteoarthritis and other arthritic disorders. The 2-dimensional gel electrophoresis (2-DE) is the technique of choice in these studies. Disease biomarkers usually appear in low concentrations and may be masked by high abundant proteins. Therefore, the main aim of this study was to find the most suitable sample preparation method that can optimize the expression of proteins on 2-DE gels that can be used to develop a reference proteome picture for non-osteoarthritic knee synovial fluid samples. Proteome pictures obtained from osteoarthritic knee synovial fluids can then be compared with the reference proteome pictures obtained in this study to assist us in identifying the disease biomarkers more correctly. The proteomic tool of 2-DE with immobilized pH gradients was applied in this study. A total of 12 2-DE gel images were constructed from SF samples that were free of osteoarthritis. In these samples, 3 were not treated with any sample preparation methods, 3 were treated with acetone, 3 were treated with 2-DE Clean-Up Kit, and 3 were treated with the combination of acetone and 2-D Clean-Up Kit prior to 2-DE analysis. Gel images were analyzed using the PDQuest Basic 8.0.1 Analytical software. Protein spots that were of interest were excised from the gels and sent for identification by mass spectrometry. Total SF total protein concentration was calculated to be 21.98 ± 0.86 mg/mL. The untreated SF samples were detected to have 456 ± 33 protein spots on 2-DE gel images. Acetone treated SF samples were detected to have 320 ± 28 protein spots, 2-D Clean-Up Kit treated SF samples were detected to have 413 ± 31 protein spots, and the combined treatment method of acetone and 2-D Clean-Up Kit was detected to have 278 ± 26 protein spots 2-DE gel images. SF samples treated with 2-D Clean-Up Kit revealed clearer presentation of the isoforms and increased intensities of the less abundant proteins of haptoglobin, apolipoprotein A-IV, prostaglandin-D synthase, alpha-1B-glycoprotein, and alpha-2-HS-glycoprotein on 2-DE gel images as compared with untreated SF samples and SF samples treated with acetone. The acetone precipitation method and the combined treatment effect of acetone and 2-DE Clean-Up Kit are not preferred in preparing SF samples for 2-DE analysis as both protein intensities and numbers decrease significantly. On the other hand, 2-D Clean-Up Kit treated SF samples revealed clearer isoforms and higher intensities for the less abundant proteins of haptoglobin, apolipoprotein A-IV, prostaglandin-D synthase, alpha-1B-glycoprotein, and alpha-2-HS-glycoprotein on 2-DE gels. As a result, it is recommended that SF samples should be treated with protein clean up products such as 2-D Clean-Up Kit first before conducting proteomic research in searching for the relevant biomarkers associated with knee osteoarthritis. Show less
📄 PDF DOI: 10.1186/1477-5956-9-65
APOA4

Elevated levels of triglyceride and triglyceride-rich lipoprotein triglyceride induced by a high-carbohydrate diet is associated with polymorphisms of APOA5-1131T>C and APOC3-482C>T in Chinese healthy young adults.

Jia Lin, Ding Zhi Fang, Juan Du +4 more · 2011 · Annals of nutrition & metabolism · added 2026-04-24
Changes in lipid profiles have been shown to be associated with diet and apolipoprotein (APO) polymorphisms. Therefore, 2 polymorphisms, i.e. APOA5-1131T>C and APOC3-482C>T, and serum lipids were exam Show more
Changes in lipid profiles have been shown to be associated with diet and apolipoprotein (APO) polymorphisms. Therefore, 2 polymorphisms, i.e. APOA5-1131T>C and APOC3-482C>T, and serum lipids were examined in a Chinese healthy young population with high-carbohydrate/low-fat (HC/LF) diet intervention. After a wash-out diet for 7 days, 56 young adults (22.89 ± 1.80 years) received the HC/LF diet for 6 days. Body mass index (BMI) and fasting serum lipid profiles at baseline, after the wash-out diet, and after the HC/LF diet were measured. APOA5-1131C carriers had higher triglyceride (TG) and TG-rich lipoprotein TG (TRL-TG) levels at baseline and after the HC/LF diet, though this mainly corresponded to the female cohort. APOC3-482T carriers had higher TRL-TG levels following the wash-out and HC/LF diets, but these were not directly attributable to a single gender. Both polymorphisms may play an important role in the elevated TG and TRL-TG levels induced by the HC/LF diet, especially in females, thus indicating a potential dietary prevention of coronary heart disease in this Chinese cohort. Show less
no PDF DOI: 10.1159/000327913
APOA5

Association of a genetic variant in the apolipoprotein A5 gene with the metabolic syndrome in Chinese.

Kwok Leung Ong, Chao Qiang Jiang, Bin Liu +11 more · 2011 · Clinical endocrinology · Blackwell Publishing · added 2026-04-24
Single nucleotide polymorphisms (SNPs) in the apolipoprotein A5 gene (APOA5) are associated with hypertriglyceridaemia in our population. We studied the associations of SNPs in APOA5 with the metaboli Show more
Single nucleotide polymorphisms (SNPs) in the apolipoprotein A5 gene (APOA5) are associated with hypertriglyceridaemia in our population. We studied the associations of SNPs in APOA5 with the metabolic syndrome (MetS) in the Hong Kong and Guangzhou Chinese. We genotyped five tagging SNPs in 1330 unrelated subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study cohort with follow-up after a median interval of 6·4 years; 1952 subjects from the Guangzhou Biobank Cohort Study-Cardiovascular Disease Subcohort were used to replicate the findings. The MetS was defined according to the consensus criteria proposed jointly by several organizations in 2009. The SNP rs662799 (-1131T>C) was associated with the MetS (odds ratio = 1·47, P = 0·00082) and the number of its components present (regression coefficient = 0·204, P = 4·6 × 10(-5) ) after adjusting for age, sex, smoking, drinking and education in Hong Kong subjects at baseline. Similar association of this SNP was found in Hong Kong subjects at follow-up (P = 0·010 and 0·00021, respectively) and in Guangzhou subjects (P = 0·0041 and 0·017, respectively). The association of rs662799 with the number of the MetS components was significant regardless of age, sex, obesity and alcohol drinking, but almost disappeared after further adjusting for plasma triglycerides. Our results showed that the -1131T>C polymorphism in APOA5 was associated with the MetS because of its strong effect on plasma triglycerides. This may partly explain the higher cardiovascular risk in people with this polymorphism. Show less
no PDF DOI: 10.1111/j.1365-2265.2010.03899.x
APOA5

Interactions of MCP1 with components of the replication machinery in mammalian cells.

Elsa Bronze-da-Rocha, Chii-Mei Lin, Tsutomu Shimura +1 more · 2011 · International journal of biological sciences · added 2026-04-24
Eukaryotic DNA replication starts with the assembly of a pre-replication complex (pre-RC) at replication origins. We have previously demonstrated that Metaphase Chromosome Protein 1 (MCP1) is involved Show more
Eukaryotic DNA replication starts with the assembly of a pre-replication complex (pre-RC) at replication origins. We have previously demonstrated that Metaphase Chromosome Protein 1 (MCP1) is involved in the early events of DNA replication. Here we show that MCP1 associates with proteins that are required for the establishment of the pre-replication complex. Reciprocal immunoprecipitation analysis showed that MCP1 interacted with Cdc6, ORC2, ORC4, MCM2, MCM3 and MCM7, with Cdc45 and PCNA. Immunofluorescence studies demonstrated the co-localization of MCP1 with some of those proteins. Moreover, biochemical studies utilizing chromatin-immunoprecipitation (ChIP) revealed that MCP1 preferentially binds replication initiation sites in human cells. Interestingly, although members of the pre-RC are known to interact with some hallmarks of heterochromatin, our co-immunoprecipitation and immunofluorescence analyses showed that MCP1 did not interact and did not co-localize with heterochromatic proteins including HP1β and MetH3K9. These observations suggest that MCP1 is associated with replication factors required for the initiation of DNA replication and binds to the initiation sites in loci that replicate early in S-phase. In addition, immunological assays revealed the association of MCP1 forms with histone H1 variants and mass spectrometry analysis confirmed that MCP1 peptides share common sequences with H1.2 and H1.5 subtypes. Show less
📄 PDF DOI: 10.7150/ijbs.7.193
CBX1

Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma.

John C Chambers, Weihua Zhang, Joban Sehmi +140 more · 2011 · Nature genetics · Nature · added 2026-04-24
John C Chambers, Weihua Zhang, Joban Sehmi, Xinzhong Li, Mark N Wass, Pim Van der Harst, Hilma Holm, Serena Sanna, Maryam Kavousi, Sebastian E Baumeister, Lachlan J Coin, Guohong Deng, Christian Gieger, Nancy L Heard-Costa, Jouke-Jan Hottenga, Brigitte Kühnel, Vinod Kumar, Vasiliki Lagou, Liming Liang, Jian'an Luan, Pedro Marques Vidal, Irene Mateo Leach, Paul F O'Reilly, John F Peden, Nilufer Rahmioglu, Pasi Soininen, Elizabeth K Speliotes, Xin Yuan, Gudmar Thorleifsson, Behrooz Z Alizadeh, Larry D Atwood, Ingrid B Borecki, Morris J Brown, Pimphen Charoen, Francesco Cucca, Debashish Das, Eco J C de Geus, Anna L Dixon, Angela Döring, Georg Ehret, Gudmundur I Eyjolfsson, Martin Farrall, Nita G Forouhi, Nele Friedrich, Wolfram Goessling, Daniel F Gudbjartsson, Tamara B Harris, Anna-Liisa Hartikainen, Simon Heath, Gideon M Hirschfield, Albert Hofman, Georg Homuth, Elina Hyppönen, Harry L A Janssen, Toby Johnson, Antti J Kangas, Ido P Kema, Jens P Kühn, Sandra Lai, Mark Lathrop, Markus M Lerch, Yun Li, T Jake Liang, Jing-Ping Lin, Ruth J F Loos, Nicholas G Martin, Miriam F Moffatt, Grant W Montgomery, Patricia B Munroe, Kiran Musunuru, Yusuke Nakamura, Christopher J O'Donnell, Isleifur Olafsson, Brenda W Penninx, Anneli Pouta, Bram P Prins, Inga Prokopenko, Ralf Puls, Aimo Ruokonen, Markku J Savolainen, David Schlessinger, Jeoffrey N L Schouten, Udo Seedorf, Srijita Sen-Chowdhry, Katherine A Siminovitch, Johannes H Smit, Timothy D Spector, Wenting Tan, Tanya M Teslovich, Taru Tukiainen, Andre G Uitterlinden, Melanie M Van der Klauw, Ramachandran S Vasan, Chris Wallace, Henri Wallaschofski, H-Erich Wichmann, Gonneke Willemsen, Peter Würtz, Chun Xu, Laura M Yerges-Armstrong, Alcohol Genome-wide Association (AlcGen) Consortium, Diabetes Genetics Replication and Meta-analyses (DIAGRAM+) Study, Genetic Investigation of ANthropometric Traits (GIANT) Consortium, Global Lipids Genetics Consortium, Genetics of Liver Disease (GOLD) Consortium, International Consortium for Blood Pressure (ICBP-GWAS), Meta-analyses of Glucose and Insulin-Related Traits Consortium (MAGIC), Goncalo R Abecasis, Kourosh R Ahmadi, Dorret I Boomsma, Mark Caulfield, William O Cookson, Cornelia M Van Duijn, Philippe Froguel, Koichi Matsuda, Mark I McCarthy, Christa Meisinger, Vincent Mooser, Kirsi H Pietiläinen, Gunter Schumann, Harold Snieder, Michael J E Sternberg, Ronald P Stolk, Howard C Thomas, Unnur Thorsteinsdottir, Manuela Uda, Gérard Waeber, Nicholas J Wareham, Dawn M Waterworth, Hugh Watkins, John B Whitfield, Jacqueline C M Witteman, Bruce H R Wolffenbuttel, Caroline S Fox, Mika Ala-Korpela, Kari Stefansson, Peter Vollenweider, Henry Völzke, Eric E Schadt, James Scott, Marjo-Riitta Järvelin, Paul Elliott, Jaspal S Kooner Show less
Concentrations of liver enzymes in plasma are widely used as indicators of liver disease. We carried out a genome-wide association study in 61,089 individuals, identifying 42 loci associated with conc Show more
Concentrations of liver enzymes in plasma are widely used as indicators of liver disease. We carried out a genome-wide association study in 61,089 individuals, identifying 42 loci associated with concentrations of liver enzymes in plasma, of which 32 are new associations (P = 10(-8) to P = 10(-190)). We used functional genomic approaches including metabonomic profiling and gene expression analyses to identify probable candidate genes at these regions. We identified 69 candidate genes, including genes involved in biliary transport (ATP8B1 and ABCB11), glucose, carbohydrate and lipid metabolism (FADS1, FADS2, GCKR, JMJD1C, HNF1A, MLXIPL, PNPLA3, PPP1R3B, SLC2A2 and TRIB1), glycoprotein biosynthesis and cell surface glycobiology (ABO, ASGR1, FUT2, GPLD1 and ST3GAL4), inflammation and immunity (CD276, CDH6, GCKR, HNF1A, HPR, ITGA1, RORA and STAT4) and glutathione metabolism (GSTT1, GSTT2 and GGT), as well as several genes of uncertain or unknown function (including ABHD12, EFHD1, EFNA1, EPHA2, MICAL3 and ZNF827). Our results provide new insight into genetic mechanisms and pathways influencing markers of liver function. Show less
📄 PDF DOI: 10.1038/ng.970
FADS1

Variants in GLIS3 and CRY2 are associated with type 2 diabetes and impaired fasting glucose in Chinese Hans.

Chen Liu, Huaixing Li, Lu Qi +5 more · 2011 · PloS one · PLOS · added 2026-04-24
Recent genome-wide association studies have identified a number of common variants associated with fasting glucose homeostasis and type 2 diabetes in populations of European origin. This is a replicat Show more
Recent genome-wide association studies have identified a number of common variants associated with fasting glucose homeostasis and type 2 diabetes in populations of European origin. This is a replication study to examine whether such associations are also observed in Chinese Hans. We genotyped nine variants in or near MADD, ADRA2A, CRY2, GLIS3, PROX1, FADS1, C2CD4B, IGF1 and IRS1 in a population-based cohort including 3,210 unrelated Chinese Hans from Beijing and Shanghai. We confirmed the associations of GLIS3-rs7034200 with fasting glucose (beta = 0.07 mmol/l, P = 0.03), beta cell function (HOMA-B) (beta = -3.03%, P = 0.009), and type 2 diabetes (OR [95%CI]  = 1.27 [1.09-1.49], P = 0.003) after adjustment for age, sex, region and BMI. The association for type 2 diabetes remained significant after adjusting for other diabetes related risk factors including family history of diabetes, lipid profile, medication information, hypertension and life style factors, while further adjustment for HOMA-B abolished the association. The A-allele of CRY2-rs11605924 was moderately associated with increased risk of combined IFG/type 2 diabetes (OR [95%CI]  = 1.15[1.01-1.30], P = 0.04). SNPs in or near MADD, ADRA2A, PROX1, FADS1, C2CD4B, IGF1, and IRS1 did not exhibit significant associations with type 2 diabetes or related glycemic traits (P≥0.10). In conclusion, our results indicate the associations of GLIS3 locus with type 2 diabetes and impaired fasting glucose in Chinese Hans, partially mediated through impaired beta-cell function. In addition, we also found modest evidence for the association of CRY2-rs11605924 with combined IFG/type 2 diabetes. Show less
📄 PDF DOI: 10.1371/journal.pone.0021464
FADS1

Dietary arachidonate differentially alters desaturase-elongase pathway flux and gene expression in liver and intestine of suckling pigs.

Sheila K Jacobi, Xi Lin, Benjamin A Corl +3 more · 2011 · The Journal of nutrition · added 2026-04-24
Because dietary arachidonate (ARA) and its eicosanoid derivatives are major regulators of intestinal homeostasis and repair following injury, we evaluated the effects of dietary ARA on desaturation an Show more
Because dietary arachidonate (ARA) and its eicosanoid derivatives are major regulators of intestinal homeostasis and repair following injury, we evaluated the effects of dietary ARA on desaturation and elongation of (13)C-18:2(n-6) and mRNA abundance of Δ-6-desaturase (FADS2), elongase (ELOVL5), and Δ-5-desaturase (FADS1) in liver and intestine. Day-old pigs (n = 96) were fed milk-based formula containing 0, 0.5, 2.5, or 5% ARA or 5% eicosapentaenoic acid of total fatty acids for 4, 8, and 16 d. In liver, the desaturation rate [nmol/(g tissue⋅h)] of (13)C-18:2(n-6) to (13)C-18:3(n-6) decreased 56% between 4 and 16 d but was not affected by diet. Whereas accumulation in (13)C-20:3(n-6) also decreased with age by 67%, it increased linearly with increasing dietary ARA (P < 0.06). In comparison, intestinal flux was ~50% less than liver flux and was unaffected by age, but desaturation to (13)C-18:3(n-6) increased linearly (by 57%) in pigs fed ARA diets (P < 0.001), equaling the rate observed in sow-fed controls. In both liver and intestine, alternate elongation to (13)C-20:2(n-6) (via Δ-8-desaturase) was markedly elevated in pigs fed the 0% ARA diet compared with all other dietary treatments (P < 0.01). Transcript abundance of FADS2, ELOVL5, and FADS1 was not affected in liver by diet (P > 0.05) but decreased precipitously between birth and d 4 (~70%; P < 0.05). In contrast, intestinal abundance of FADS2 and FADS1 increased 60% from d 4 to 16. In conclusion, dietary ARA regulated the desaturase-elongase pathway in a tissue-specific manner. In liver, ARA had modest effects on (n-6) fatty acid flux, and intestinal FADS2 activity and mRNA increased. Additionally, hepatic flux decreased with postnatal age, whereas intestinal flux did not change. Show less
no PDF DOI: 10.3945/jn.110.127118
FADS1

The clathrin-binding domain of CALM and the OM-LZ domain of AF10 are sufficient to induce acute myeloid leukemia in mice.

A J Deshpande, A Rouhi, Y Lin +13 more · 2011 · Leukemia · Nature · added 2026-04-24
The t(10;11)(p13-14;q14-21) translocation, giving rise to the CALM-AF10 fusion gene, is a recurrent chromosomal rearrangement observed in patients with poor prognosis acute myeloid leukemia (AML). Alt Show more
The t(10;11)(p13-14;q14-21) translocation, giving rise to the CALM-AF10 fusion gene, is a recurrent chromosomal rearrangement observed in patients with poor prognosis acute myeloid leukemia (AML). Although splicing of the CALM-AF10 fusion transcripts has been described in AML patients, the contribution of different CALM and AF10 domains to in vivo leukemogenesis remains to be defined. We therefore performed detailed structure-function studies of the CALM-AF10 fusion protein. We demonstrate that fusion of the C-terminal 248 amino acids of CALM, which include the clathrin-binding domain, to the octapeptide motif-leucine-zipper (OM-LZ) domain of AF10 generated a fusion protein (termed CALM-AF10 minimal fusion (MF)), with strikingly enhanced transformation capabilities in colony assays, providing an efficient system for the expeditious assessment of CALM-AF10-mediated transformation. Leukemias induced by the CALM-AF10 (MF) mutant recapitulated multiple aspects of full-length CALM-AF10-induced leukemia, including aberrant Hoxa cluster upregulation, a characteristic molecular lesion of CALM-AF10 leukemias. In summary, this study indicates that collaboration of the clathrin-binding and the OM-LZ domains of CALM-AF10 is sufficient to induce AML. These findings further suggest that future approaches to antagonize CALM-AF10-induced transformation should incorporate strategies, which aim at blocking these key domains. Show less
no PDF DOI: 10.1038/leu.2011.153
MLLT10

LXRβ is required for glucocorticoid-induced hyperglycemia and hepatosteatosis in mice.

Rucha Patel, Monika Patel, Ricky Tsai +9 more · 2011 · The Journal of clinical investigation · added 2026-04-24
Although widely prescribed for their potent antiinflammatory actions, glucocorticoid drugs (e.g., dexamethasone) cause undesirable side effects that are features of the metabolic syndrome, including h Show more
Although widely prescribed for their potent antiinflammatory actions, glucocorticoid drugs (e.g., dexamethasone) cause undesirable side effects that are features of the metabolic syndrome, including hyperglycemia, fatty liver, insulin resistance, and type II diabetes. Liver x receptors (LXRs) are nuclear receptors that respond to cholesterol metabolites and regulate the expression of a subset of glucocorticoid target genes. Here, we show LXRβ is required to mediate many of the negative side effects of glucocorticoids. Mice lacking LXRβ (but not LXRα) were resistant to dexamethasone-induced hyperglycemia, hyperinsulinemia, and hepatic steatosis, but remained sensitive to dexamethasone-dependent repression of the immune system. In vivo, LXRα/β knockout mice demonstrated reduced dexamethasone-induced expression of the key hepatic gluconeogenic gene, phosphoenolpyruvate carboxykinase (PEPCK). In perfused liver and primary mouse hepatocytes, LXRβ was required for glucocorticoid-induced recruitment of the glucocorticoid receptor to the PEPCK promoter. These findings suggest a new avenue for the design of safer glucocorticoid drugs through a mechanism of selective glucocorticoid receptor transactivation. Show less
no PDF DOI: 10.1172/JCI41681
NR1H3

Gene expression changes in retinal Müller (glial) cells exposed to elevated pressure.

Wei Xue, Pan Du, Simon Lin +3 more · 2011 · Current eye research · added 2026-04-24
Retinal Müller (glial) cells undergo "reactive gliosis", a stress response that is accompanied by changes in their morphology and upregulation of various cellular markers. Reactive gliosis is seen in Show more
Retinal Müller (glial) cells undergo "reactive gliosis", a stress response that is accompanied by changes in their morphology and upregulation of various cellular markers. Reactive gliosis is seen in many retinal diseases and conditions; however, it is not known whether it is a common, stereotypic response or the nature of the response varies with the type of retinal stress. To address this question, we have examined gene expression changes in Müller cells exposed to elevated pressure. Rat Müller cells (rMC-1) were exposed to elevated pressure, and RNA was extracted and analyzed using Affymetrix GeneChip microarrays to identify pressure-responsive genes. Analysis of microarray data showed that at 6 h, 186 genes had > 1.5-fold change with FDR < 0.01. Of these, 62 genes were up-regulated while 124 genes were down-regulated. At 24 h, 73 genes changed > 1.5-fold. Of these, 37 genes were up-regulated while 36 genes were down-regulated. Ingenuity canonical pathway analysis showed that several signaling and metabolic pathways were significantly changed in Müller cells under high pressure. In addition, among up- and down-regulated genes, we identified eight genes-areg, bmp4, cyp1b1, gpnmb, herc2, msh2, heph, and selenbp1, that have been directly or indirectly associated with elevated intraocular pressure. Two genes, areg and gpnmb, further showed time-dependent changes in mRNA and protein expression. The results show that Müller cells in vitro respond to elevated pressure by differential regulation of expressed genes. The transcriptional profile is different from that seen with hypoxia, which indicates that Müller cells respond differentially to different microenvironmental changes in the retina. Show less
no PDF DOI: 10.3109/02713683.2011.585417
RMC1

ZNF668 functions as a tumor suppressor by regulating p53 stability and function in breast cancer.

Ruozhen Hu, Guang Peng, Hui Dai +6 more · 2011 · Cancer research · added 2026-04-24
Genome-wide sequencing studies in breast cancer have recently identified frequent mutations in the zinc finger protein 668 (ZNF668), the function of which is undefined. Here, we report that ZNF668 is Show more
Genome-wide sequencing studies in breast cancer have recently identified frequent mutations in the zinc finger protein 668 (ZNF668), the function of which is undefined. Here, we report that ZNF668 is a nucleolar protein that physically interacts with and regulates p53 and its negative regulator MDM2. Through MDM2 binding, ZNF668 regulated autoubiquitination of MDM2 and its ability to mediate p53 ubiquitination and degradation. ZNF668 deficiency also impaired DNA damage-induced stabilization of p53. RNA interference-mediated knockdown of ZNF668 was sufficient to transform normal mammary epithelial cells. ZNF668 effectively suppressed breast cancer cell proliferation in vitro and tumorigenicity in vivo. Taken together, our studies identify ZNF668 as a novel breast tumor suppressor gene that functions in regulating p53 stability. Show less
no PDF DOI: 10.1158/0008-5472.CAN-11-0853
ZNF668

Screening disease-associated proteins from sera of patients with rheumatoid arthritis: a comparative proteomic study.

Tian-wang Li, Ben-rong Zheng, Zhi-xiang Huang +6 more · 2010 · Chinese medical journal · added 2026-04-24
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation at the synovial membrane. Although great progress has been made recently in exploring the etiology and pathogen Show more
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation at the synovial membrane. Although great progress has been made recently in exploring the etiology and pathogenesis of RA, its molecular pathological mechanism remains to be further defined and it is still a great challenge in determining the diagnosis and in choosing the appropriate therapy in early patients. This study was performed to screen candidate RA-associated serum proteins by comparative proteomics to provide research clues to early diagnosis and treatment of RA. Sera isolated from 6 RA patients and 6 healthy volunteers were pooled respectively and high-abundance proteins were depleted by Plasma 7 Multiple Affinity Removal System. The protein expression profiles between the two groups were then compared by two-dimensional gel electrophoresis (2-DE) and the proteins over/under-expressed by more than 3-fold were identified by mass spectrometry analysis. To validate the differential expression levels of the identified proteins between the two groups, ELISA was performed in two of the identified proteins in individual sera from 32 RA patients and 32 volunteers. Eight proteins which over/under-expressed in sera of RA patients were identified. Among them, chain A of transthyretin (TTR) was under-expressed, while serum amyloid A protein, apolipoprotein A (ApoA)-IV, ApoA-IV precursor, haptoglobin 2, ceruloplasmin (Cp), immunoglobulin superfamily 22 and HT016 were over-expressed. ELISA test confirmed that Cp expressed remarkably higher while TTR obviously lower in RA group compared with volunteer group. There were 8 identified proteins differentially expressed between RA group and volunteer group, which might be candidate RA-associated proteins and might be promising diagnostic indicators or therapeutic targets for RA. Show less
no PDF
APOA4

A single nucleotide polymorphism in APOA5 determines triglyceride levels in Hong Kong and Guangzhou Chinese.

Chao Qiang Jiang, Bin Liu, Bernard M Y Cheung +10 more · 2010 · European journal of human genetics : EJHG · Nature · added 2026-04-24
Single nucleotide polymorphisms (SNPs) in the apolipoprotein A5 (APOA5) gene have been associated with hypertriglyceridaemia. We investigated which SNPs in the APOA5 gene were associated with triglyce Show more
Single nucleotide polymorphisms (SNPs) in the apolipoprotein A5 (APOA5) gene have been associated with hypertriglyceridaemia. We investigated which SNPs in the APOA5 gene were associated with triglyceride levels in two independent Chinese populations. In all, 1375 subjects in the Hong Kong Cardiovascular Risk Factor Prevalence Study were genotyped for five tagging SNPs chosen from HapMap. Replication was sought in 1996 subjects from the Guangzhou Biobank Cohort Study. Among the five SNPs, rs662799 (-1131T>C) was strongly related to log-transformed triglyceride levels among Hong Kong subjects (β=0.192, P=2.6 × 10(-13)). Plasma triglyceride level was 36.1% higher in CC compared to TT genotype. This association was confirmed in Guangzhou subjects (β=0.159, P=1.3 × 10(-12)), and was significantly irrespective of sex, age group, obesity, metabolic syndrome, hypertension, diabetes, smoking and alcohol drinking. The odds ratios and 95% confidence interval for plasma triglycerides ≥1.7 mmol/l associated with TC and CC genotypes were, respectively, 1.81 (1.37-2.39) and 2.22 (1.44-3.43) in Hong Kong and 1.27 (1.05-1.54) and 1.97 (1.42-2.73) in Guangzhou. Haplotype analysis suggested the association was due to rs662799 only. The corroborative findings in two independent populations indicate that the APOA5-1131T>C polymorphism is an important and clinically relevant determinant of plasma triglyceride levels in the Chinese population. Show less
no PDF DOI: 10.1038/ejhg.2010.93
APOA5

Regulation of hepatic ApoC3 expression by PGC-1β mediates hypolipidemic effect of nicotinic acid.

Carlos Hernandez, Matthew Molusky, Yaqiang Li +2 more · 2010 · Cell metabolism · Elsevier · added 2026-04-24
Peroxisome proliferator-activated receptor (PPAR) γ coactivator-1β (PGC-1β) is a transcriptional coactivator that induces hypertriglyceridemia in response to dietary fats through activating hepatic li Show more
Peroxisome proliferator-activated receptor (PPAR) γ coactivator-1β (PGC-1β) is a transcriptional coactivator that induces hypertriglyceridemia in response to dietary fats through activating hepatic lipogenesis and lipoprotein secretion. The expression of PGC-1β is regulated by free fatty acids. Here we show that PGC-1β regulates plasma triglyceride metabolism through stimulating apolipoprotein C3 (APOC3) expression and elevating APOC3 levels in circulation. Remarkably, liver-specific knockdown of APOC3 significantly ameliorates PGC-1β-induced hypertriglyceridemia in mice. Hepatic expression of PGC-1β and APOC3 is reduced in response to acute and chronic treatments with nicotinic acid, a widely prescribed drug for lowering plasma triglycerides. Adenoviral-mediated knockdown of PGC-1β or APOC3 in the liver recapitulates the hypolipidemic effect of nicotinic acid. Proteomic analysis of hepatic PGC-1β transcriptional complex indicates that it stimulates APOC3 expression through coactivating orphan nuclear receptor ERRα and recruiting chromatin-remodeling cofactors. Together, these studies identify PGC-1β as an important regulator of the APOC3 gene cluster and reveal a mechanism through which nicotinic acid achieves its therapeutic effects. Show less
📄 PDF DOI: 10.1016/j.cmet.2010.09.001
APOC3

Recent patents and advances in genomic biomarker discovery for colorectal cancers.

Chen Quyun, Zhiyun Ye, Sheng-Cai Lin +1 more · 2010 · Recent patents on DNA & gene sequences · Bentham Science · added 2026-04-24
Colorectal cancer (CRC) is the third most common cancer in the world. Early diagnosis of colorectal cancer is the key to reducing the death rate of CRC patients. Predicting the response to current the Show more
Colorectal cancer (CRC) is the third most common cancer in the world. Early diagnosis of colorectal cancer is the key to reducing the death rate of CRC patients. Predicting the response to current therapeutic modalities of CRC will also have a great impact on patient care. This review summarizes recent advances and patents in biomarker discovery in CRC under five major categories; including genomic changes, expression changes, mutations, epigenetic changes and microRNAs. The interesting patents include: 1) a patent for a method to differentiate normal exfoliated cells from cancer cells based on whether they were subjected to apoptosis and DNA degradation; 2) A model (PM-33 multiple molecular marker model) based on expression changes of up-regulation of the MDM2, DUSP6, and NFl genes down-regulation of the RNF4, MMD and EIF2S3 genes, which achieved an 88% sensitivity, and an 82% specificity for CRC diagnosis; 3) gene mutations in PTEN, KRAS, PIK3CA for predicting the response to anti-EGFR therapies, a common drug used for CRC treatment; 4) patents on epigenetic changes of ITGA4, SEPT9, ALX4, TFAP2E FOXL2, SARM1, ID4 etc. and many key miRNAs. Finally, future directions in the fields were commented on or suggested, including the combination of multiple categories of biomarkers and pathway central or network-based biomarker panels. Show less
no PDF DOI: 10.2174/187221510793205764
DUSP6

Novel human pathological mutations. Gene symbol: EXT1. Disease: multiple exostoses.

Wei-De Lin, Fuu-Jer Tsai · 2010 · Human genetics · added 2026-04-24
no PDF
EXT1

Curcumin derivatives inhibit testicular 17beta-hydroxysteroid dehydrogenase 3.

Guo-Xin Hu, Guang Liang, Yanhui Chu +7 more · 2010 · Bioorganic & medicinal chemistry letters · Elsevier · added 2026-04-24
Non-steroidal compounds that inhibit 17beta-hydroxysteroid dehydrogenase isoform 3 (17beta-HSD3), an enzyme catalyzing the final step in testosterone biosynthesis in Leydig cells, are under developmen Show more
Non-steroidal compounds that inhibit 17beta-hydroxysteroid dehydrogenase isoform 3 (17beta-HSD3), an enzyme catalyzing the final step in testosterone biosynthesis in Leydig cells, are under development for male contraceptive or treatment of androgen dependent diseases including prostate cancer. A series of curcumin analogues with more stable chemical structures were compared to curcumin as inhibitors of 17beta-HSD3 in rat intact Leydig cells as well as rat and human testis microsomes. Show less
no PDF DOI: 10.1016/j.bmcl.2010.02.089
HSD17B12

Genome-wide meta-analyses identifies seven loci associated with platelet aggregation in response to agonists.

Andrew D Johnson, Lisa R Yanek, Ming-Huei Chen +10 more · 2010 · Nature genetics · Nature · added 2026-04-24
Platelet function mediates both beneficial and harmful effects on human health, but few genes are known to contribute to variability in this process. We tested association of 2.5 million SNPs with pla Show more
Platelet function mediates both beneficial and harmful effects on human health, but few genes are known to contribute to variability in this process. We tested association of 2.5 million SNPs with platelet aggregation responses to three agonists (ADP, epinephrine and collagen) in two cohorts of European ancestry (NShow less
📄 PDF DOI: 10.1038/ng.604
JMJD1C

Nervous-tissue-specific elimination of microtubule-actin crosslinking factor 1a results in multiple developmental defects in the mouse brain.

Dmitry Goryunov, Cui-Zhen He, Chyuan-Sheng Lin +2 more · 2010 · Molecular and cellular neurosciences · Elsevier · added 2026-04-24
The microtubule-actin crosslinking factor 1 (MACF1) is a ubiquitous cytoskeletal linker protein with multiple spliced isoforms expressed in different tissues. The MACF1a isoform contains microtubule a Show more
The microtubule-actin crosslinking factor 1 (MACF1) is a ubiquitous cytoskeletal linker protein with multiple spliced isoforms expressed in different tissues. The MACF1a isoform contains microtubule and actin-binding regions and is expressed at high levels in the nervous system. Macf1-/- mice are early embryonic lethal and hence the role of MACF1 in the nervous system could not be determined. We have specifically knocked out MACF1a in the developing mouse nervous system using Cre/loxP technology. Mutant mice died within 24-36h after birth of apparent respiratory distress. Their brains displayed a disorganized cerebral cortex with a mixed layer structure, heterotopia in the pyramidal layer of the hippocampus, disorganized thalamocortical and corticofugal fibers, and aplastic anterior and hippocampal commissures. Embryonic neurons showed a defect in traversing the cortical plate. Our data suggest a critical role for MACF1 in neuronal migration that is dependent on its ability to interact with both microfilaments and microtubules. Show less
📄 PDF DOI: 10.1016/j.mcn.2010.01.010
MACF1

Linking H3K79 trimethylation to Wnt signaling through a novel Dot1-containing complex (DotCom).

Man Mohan, Hans-Martin Herz, Yoh-Hei Takahashi +6 more · 2010 · Genes & development · Cold Spring Harbor Laboratory · added 2026-04-24
Epigenetic modifications of chromatin play an important role in the regulation of gene expression. KMT4/Dot1 is a conserved histone methyltransferase capable of methylating chromatin on Lys79 of histo Show more
Epigenetic modifications of chromatin play an important role in the regulation of gene expression. KMT4/Dot1 is a conserved histone methyltransferase capable of methylating chromatin on Lys79 of histone H3 (H3K79). Here we report the identification of a multisubunit Dot1 complex (DotCom), which includes several of the mixed lineage leukemia (MLL) partners in leukemia such as ENL, AF9/MLLT3, AF17/MLLT6, and AF10/MLLT10, as well as the known Wnt pathway modifiers TRRAP, Skp1, and beta-catenin. We demonstrated that the human DotCom is indeed capable of trimethylating H3K79 and, given the association of beta-catenin, Skp1, and TRRAP, we investigated, and found, a role for Dot1 in Wnt/Wingless signaling in an in vivo model system. Knockdown of Dot1 in Drosophila results in decreased expression of a subset of Wingless target genes. Furthermore, the loss of expression for the Drosophila homologs of the Dot1-associated proteins involved in the regulation of H3K79 shows a similar reduction in expression of these Wingless targets. From yeast to human, specific trimethylation of H3K79 by Dot1 requires the monoubiquitination of histone H2B by the Rad6/Bre1 complex. Here, we demonstrate that depletion of Bre1, the E3 ligase required for H2B monoubiquitination, leads specifically to reduced bulk H3K79 trimethylation levels and a reduction in expression of many Wingless targets. Overall, our study describes for the first time the components of DotCom and links the specific regulation of H3K79 trimethylation by Dot1 and its associated factors to the Wnt/Wingless signaling pathway. Show less
no PDF DOI: 10.1101/gad.1898410
MLLT10

Two novel mutations of the MYBPC3 gene identified in Chinese families with hypertrophic cardiomyopathy.

Jia Lin, Dong-Dong Zheng, Qin Tao +6 more · 2010 · The Canadian journal of cardiology · Elsevier · added 2026-04-24
Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiovascular disorders. Mutations in the MYBPC3 gene are one of the most frequent genetic causes of HCM. To screen MYBPC3 gene mut Show more
Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiovascular disorders. Mutations in the MYBPC3 gene are one of the most frequent genetic causes of HCM. To screen MYBPC3 gene mutations in Chinese patients with HCM, and analyze the correlation between the genotype and the phenotype. The 35 exons of the MYBPC3 gene were amplified by polymerase chain reaction in the 11 consecutive unrelated Chinese pedigrees. The sequences of the products were analyzed and the mutation sites were determined. The clinical data of genotype-positive families were collected, and the correlation between genotype and phenotype was analyzed. Two mutations of the MYBPC3 gene were confirmed among 11 pedigrees. A frameshift mutation (Pro459fs) was identified in exon 17 in family H8, and a splice mutation (IVS5+5G−>C) was identified in intron 5 in family H3. These two mutations were first identified in Chinese patients with familial HCM and were absent in 110 chromosomes of healthy controls. Seven known polymorphisms were found in the cohort. Compared with what was reported abroad, the MYBPC3 gene is a common pathogenic gene responsible for HCM in Chinese patients, and the phenotypes of these two mutations in their respective families may have their own clinical characteristics. Show less
no PDF DOI: 10.1016/s0828-282x(10)70464-5
MYBPC3

Antiproliferative effect of LXR agonists T0901317 and 22(R)-hydroxycholesterol on multiple human cancer cell lines.

Chih-Pin Chuu, Hui-Ping Lin · 2010 · Anticancer research · added 2026-04-24
Previously, we and other groups reported that liver X receptor (LXR) agonists T0901317, 22(R)-hydroxycholesterol, and 24(S)-hydroxycholesterol suppressed the proliferation of prostate and breast cance Show more
Previously, we and other groups reported that liver X receptor (LXR) agonists T0901317, 22(R)-hydroxycholesterol, and 24(S)-hydroxycholesterol suppressed the proliferation of prostate and breast cancer cells. In this study, we report that T0901317 and 22(R)-hydroxycholesterol treatment inhibited the proliferation of different progression stages of LNCaP human prostate cancer cells, as well as different commonly used human cancer cell lines. Cancer cell lines with higher LXRα mRNA expression were more sensitive to 22(R)-hydroxycholesterol-induced inhibition. T0901317 treatment decreased the percentage of the cell population in S-phase and caused G(1) cell cycle arrest. Overexpression of S-phase kinase-associated protein 2 (Skp2) partially blocked the suppressive effect of T0901317 treatment. Modulating LXR signaling is therefore a potential adjuvant therapy for advanced prostate cancer and other types of cancer. Show less
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NR1H3

Thirty new loci for age at menarche identified by a meta-analysis of genome-wide association studies.

Cathy E Elks, John R B Perry, Patrick Sulem +172 more · 2010 · Nature genetics · Nature · added 2026-04-24
Cathy E Elks, John R B Perry, Patrick Sulem, Daniel I Chasman, Nora Franceschini, Chunyan He, Kathryn L Lunetta, Jenny A Visser, Enda M Byrne, Diana L Cousminer, Daniel F Gudbjartsson, Tõnu Esko, Bjarke Feenstra, Jouke-Jan Hottenga, Daniel L Koller, Zoltán Kutalik, Peng Lin, Massimo Mangino, Mara Marongiu, Patrick F McArdle, Albert V Smith, Lisette Stolk, Sophie H van Wingerden, Jing Hua Zhao, Eva Albrecht, Tanguy Corre, Erik Ingelsson, Caroline Hayward, Patrik K E Magnusson, Erin N Smith, Shelia Ulivi, Nicole M Warrington, Lina Zgaga, Helen Alavere, Najaf Amin, Thor Aspelund, Stefania Bandinelli, Inês Barroso, Gerald S Berenson, Sven Bergmann, Hannah Blackburn, Eric Boerwinkle, Julie E Buring, Fabio Busonero, Harry Campbell, Stephen J Chanock, Wei Chen, Marilyn C Cornelis, David Couper, Andrea D Coviello, Pio d'Adamo, Ulf de Faire, Eco J C de Geus, Panos Deloukas, Angela Döring, George Davey Smith, Douglas F Easton, Gudny Eiriksdottir, Valur Emilsson, Johan Eriksson, Luigi Ferrucci, Aaron R Folsom, Tatiana Foroud, Melissa Garcia, Paolo Gasparini, Frank Geller, Christian Gieger, GIANT Consortium, Vilmundur Gudnason, Per Hall, Susan E Hankinson, Liana Ferreli, Andrew C Heath, Dena G Hernandez, Albert Hofman, Frank B Hu, Thomas Illig, Marjo-Riitta Järvelin, Andrew D Johnson, David Karasik, Kay-Tee Khaw, Douglas P Kiel, Tuomas O Kilpeläinen, Ivana Kolcic, Peter Kraft, Lenore J Launer, Joop S E Laven, Shengxu Li, Jianjun Liu, Daniel Levy, Nicholas G Martin, Wendy L McArdle, Mads Melbye, Vincent Mooser, Jeffrey C Murray, Sarah S Murray, Michael A Nalls, Pau Navarro, Mari Nelis, Andrew R Ness, Kate Northstone, Ben A Oostra, Munro Peacock, Lyle J Palmer, Aarno Palotie, Guillaume Paré, Alex N Parker, Nancy L Pedersen, Leena Peltonen, Craig E Pennell, Paul Pharoah, Ozren Polasek, Andrew S Plump, Anneli Pouta, Eleonora Porcu, Thorunn Rafnar, John P Rice, Susan M Ring, Fernando Rivadeneira, Igor Rudan, Cinzia Sala, Veikko Salomaa, Serena Sanna, David Schlessinger, Nicholas J Schork, Angelo Scuteri, Ayellet V Segrè, Alan R Shuldiner, Nicole Soranzo, Ulla Sovio, Sathanur R Srinivasan, David P Strachan, Mar-Liis Tammesoo, Emmi Tikkanen, Daniela Toniolo, Kim Tsui, Laufey Tryggvadottir, Jonathon Tyrer, Manuela Uda, Rob M Van Dam, Joyce B J van Meurs, Peter Vollenweider, Gerard Waeber, Nicholas J Wareham, Dawn M Waterworth, Michael N Weedon, H Erich Wichmann, Gonneke Willemsen, James F Wilson, Alan F Wright, Lauren Young, Guangju Zhai, Wei Vivian Zhuang, Laura J Bierut, Dorret I Boomsma, Heather A Boyd, Laura Crisponi, Ellen W Demerath, Cornelia M Van Duijn, Michael J Econs, Tamara B Harris, David J Hunter, Ruth J F Loos, Andres Metspalu, Grant W Montgomery, Paul M Ridker, Tim D Spector, Elizabeth A Streeten, Kari Stefansson, Unnur Thorsteinsdottir, André G Uitterlinden, Elisabeth Widen, Joanne M Murabito, Ken K Ong, Anna Murray Show less
To identify loci for age at menarche, we performed a meta-analysis of 32 genome-wide association studies in 87,802 women of European descent, with replication in up to 14,731 women. In addition to the Show more
To identify loci for age at menarche, we performed a meta-analysis of 32 genome-wide association studies in 87,802 women of European descent, with replication in up to 14,731 women. In addition to the known loci at LIN28B (P = 5.4 × 10⁻⁶⁰) and 9q31.2 (P = 2.2 × 10⁻³³), we identified 30 new menarche loci (all P < 5 × 10⁻⁸) and found suggestive evidence for a further 10 loci (P < 1.9 × 10⁻⁶). The new loci included four previously associated with body mass index (in or near FTO, SEC16B, TRA2B and TMEM18), three in or near other genes implicated in energy homeostasis (BSX, CRTC1 and MCHR2) and three in or near genes implicated in hormonal regulation (INHBA, PCSK2 and RXRG). Ingenuity and gene-set enrichment pathway analyses identified coenzyme A and fatty acid biosynthesis as biological processes related to menarche timing. Show less
no PDF DOI: 10.1038/ng.714
SEC16B

Characterization of acute renal allograft rejection by human serum proteomic analysis.

Ying Gao, Ke Wu, Yi Xu +9 more · 2009 · Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · Springer · added 2026-04-24
To identify acute renal allograft rejection biomarkers in human serum, two-dimensional differential in-gel electrophoresis (2-D DIGE) and reversed phase high-performance liquid chromatography (RP-HPLC Show more
To identify acute renal allograft rejection biomarkers in human serum, two-dimensional differential in-gel electrophoresis (2-D DIGE) and reversed phase high-performance liquid chromatography (RP-HPLC) followed by electrospray ionization mass spectrometry (ESI-MS) were used. Serum samples from renal allograft patients and normal volunteers were divided into three groups: acute rejection (AR), stable renal function (SRF) and normal volunteer (N). Serum samples were firstly processed using Multiple Affinity Removal Column to selectively remove the highest abundance proteins. Differentially expressed proteins were analyzed using 2-D DIGE. These differential protein spots were excised, digested by trypsin, and identified by RP-HPLC-ESI/MS. Twenty-two differentially expressed proteins were identified in serum from AR group. These proteins included complement C9 precursor, apolipoprotein A-IV precursor, vitamin D-binding protein precursor, beta-2-glycoprotein 1 precursor, etc. Vitamin D-binding protein, one of these proteins, was confirmed by ELISA in the independent set of serum samples. In conclusion, the differentially expressed proteins as serum biomarker candidates may provide the basis of acute rejection noninvasive diagnosis. Confirmed vitamin D-binding protein may be one of serum biomarkers of acute rejection. Furthermore, it may provide great insights into understanding the mechanisms and potential treatment strategy of acute rejection. Show less
no PDF DOI: 10.1007/s11596-009-0511-8
APOA4

[Linkage analysis of a family with familial hypertriglyceridemia].

Xin Tang, Ying Lin, Bing Liu +3 more · 2009 · Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics · added 2026-04-24
To perform linkage analysis and mutation screening in a Chinese family with familial hpertriglyceridemia (FHTG). Thirty-two family members including 12 hypertriglyceridemia patients participated in th Show more
To perform linkage analysis and mutation screening in a Chinese family with familial hpertriglyceridemia (FHTG). Thirty-two family members including 12 hypertriglyceridemia patients participated in the study. Genotyping and haplotype analysis for 22 subjects were performed using short tandem repeat (STR) microsatellite polymorphism markers on 16 candidate genes and/or loci related to lipid metabolism. Two of the sixteen known candidate genes, APOA2 and USF1 were screened for mutation by direct DNA sequencing. No linkage was found between the candidate genes/loci of APOA5, LIPI, RP1, APOC2, ABC1, LMF1, APOA1-APOC3-APOA4, LPL, APOB, CETP, LCAT, LDLR, APOE and the phenotype in this family. The two-point Lod scores (theta =0) were all less than-1.0 for all the markers tested. Linkage analysis suggested linkage to chromosome 1q23.3-24.2 between the disease phenotype and STR marker D1S194 with a two-point maximum Lod score of 2.44 at theta =0. Fine mapping indicated that the disease gene was localized to a 5.87 cM interval between D1S104 and D1S196. No disease-causing mutation was detected in the APOA2 and USF1 genes. The above mentioned candidate genes were excluded as the disease causing genes for this family. The results implied that there might be a novel gene/locus for FHTG on chromosome 1q23.3-1q24.2. Show less
no PDF DOI: 10.3760/cma.j.issn.1003-9406.2009.05.004
APOA4