👤 Zexing 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, Zhangyu Lin, Zhao Lin, Zhaohua Lin, Zhaotong Lin, Zheguang Lin, Zhekai Lin, Zhen Lin, Zheng Lin, Zhengfang 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

[miR-23b-3p regulates the differentiation of goat intramuscular preadipocytes by targeting the

Liyi Zhang, Xin Li, Qing Xu +5 more · 2023 · Sheng wu gong cheng xue bao = Chinese journal of biotechnology · added 2026-04-24
This study aimed to explore the effect of miR-23b-3p on the differentiation of goat intramuscular preadipocytes, and to confirm whether miR-23b-3p plays its roles
no PDF DOI: 10.13345/j.cjb.230156
LPL

Methylation of lncSHGL promotes adipocyte differentiation by regulating miR-149/Mospd3 axis.

Xianwei Huang, Xiong Liu, Jiyan Lin · 2023 · Cell cycle (Georgetown, Tex.) · Taylor & Francis · added 2026-04-24
Obesity poses significant health risks and can negatively impact an individual's quality of life. The human obesity phenotype results from the differentiation of pre-adipocytes into adipocytes, which Show more
Obesity poses significant health risks and can negatively impact an individual's quality of life. The human obesity phenotype results from the differentiation of pre-adipocytes into adipocytes, which leads to hypertrophy and hyperplasia in adipose tissue. The molecular mechanisms by which long non-coding RNAs (lncRNAs) modulate adipocyte differentiation, a process implicated in obesity development, remain poorly characterized. A lncRNA which suppressed the hepatic gluconeogenesis and lipogenesis (lncSHGL) was newly identified. Our research aims to elucidate the functional role and mechanistic underpinnings of suppressor of lncSHGL in adipocyte differentiation. We observed that lncSHGL expression progressively diminished during 3T3-L1 differentiation and was downregulated in the liver and perirenal adipose tissue of ob/ob mice. lncSHGL acts as a molecular sponge for miR-149, with Mospd3 identified as a target of miR-149.Overexpression of lncSHGL and inhibition of miR-149 led to suppressed 3T3-L1 proliferation, decreased lipid droplet accumulation, and attenuated promoter activity of PPARγ2 and C/EBPα. These changes consequently resulted in reduced expression of Cyclin D1, LPL, PPARγ2, AP2, and C/EBPα, as well as inhibited the PI3K/AKT/mTOR signaling pathway. In contrast, lncSHGL suppression yielded opposing outcomes. Moreover, the effects of lncSHGL overexpression and miR-149 inhibition on reduced expression of Cyclin D1, LPL, PPARγ2, AP2, and C/EBPα were reversible upon miR-149 overexpression and Mospd3 suppression. These findings were further validated Show less
no PDF DOI: 10.1080/15384101.2023.2287367
LPL

Aerobic exercise-induced decrease of chemerin improved glucose and lipid metabolism and fatty liver of diabetes mice through key metabolism enzymes and proteins.

Xiaojing Lin, Jing Qu, Lijun Yin +2 more · 2023 · Biochimica et biophysica acta. Molecular and cell biology of lipids · Elsevier · added 2026-04-24
Our previous studies have implicated an important role of adipokine chemerin in exercise-induced improvements of glycolipid metabolism and fatty liver in diabetes rat, but the underlying mechanisms re Show more
Our previous studies have implicated an important role of adipokine chemerin in exercise-induced improvements of glycolipid metabolism and fatty liver in diabetes rat, but the underlying mechanisms remain unknown. This study first used an exogenous chemerin supplement to clarify the roles of decreased chemerin in exercised diabetes mice and possible mechanisms of glucose and lipid metabolism key enzymes and proteins [such as adipose triglyceride lipase (ATGL), lipoprotein lipase (LPL), phosphoenolpyruvate carboxykinase (PEPCK), and glucose transporter 4 (GLUT4)]. In addition, two kinds of adipose-specific chemerin knockout mice were generated to demonstrate the regulation of chemerin on glucose and lipid metabolism enzymes and proteins. We found that in diabetes mice, exercise-induced improvements of glucose and lipid metabolism and fatty liver, and exercise-induced increases of ATGL, LPL, and GLUT4 in liver, gastrocnemius and fat were reversed by exogenous chemerin. Furthermore, in chemerin knockdown mice, chemerin(-/-)∙adiponectin mice had lower body fat mass, improved blood glucose and lipid, and no fatty liver; while chemerin(-/-)∙fabp4 mice had hyperlipemia and unchanged body fat mass. Peroxisome proliferator-activated receptor γ (PPARγ), ATGL, LPL, GLUT4 and PEPCK in the liver and gastrocnemius had improve changes in chemerin(-/-)·adiponectin mice while deteriorated alterations in chemerin(-/-)·fabp4 mice, although PPARγ, ATGL, LPL, and GLUT4 increased in the fat of two kinds of chemerin(-/-) mice. CONCLUSIONS: Decreased chemerin exerts an important role in exercise-induced improvements of glucose and lipid metabolism and fatty liver in diabetes mice, which was likely to be through PPARγ mediating elevations of ATGL, LPL and GLUT4 in peripheral metabolic organs. Show less
no PDF DOI: 10.1016/j.bbalip.2023.159409
LPL

Effects of lysophospholipids and multi-enzymes on growth performance, antioxidant capacity, intestinal health, and cecal microflora of male cherry valley ducks.

Qianqian Zhang, Jian Li, Jianping Wang +8 more · 2023 · Journal of animal science · Oxford University Press · added 2026-04-24
Improvement of nutrient utilization to promote growth performance is always pursued in poultry. In this study, a total of 360 1-d-old male ducklings was randomly assigned to 3 treatments in terms of d Show more
Improvement of nutrient utilization to promote growth performance is always pursued in poultry. In this study, a total of 360 1-d-old male ducklings was randomly assigned to 3 treatments in terms of diet treatment groups. Three treatments were as follows: basal diet (Con group) or basal diet supplemented with 300 mg/kg multi-enzymes (ENZ group) or 500 mg/kg lysophospholipids (LPL group). On day 42, ducks were slaughtered for samplings. The results revealed that supplementary LPL improved the body weight (BW) at day 14 and average daily gain (ADG) during days 1 to 14 and improved the feed conversion rate (FCR) for the overall period (P < 0.05) by improving nutrient utilization of dry matter and ether extract (P < 0.05) compared with the Con group. Dietary ENZ improved the FCR from days 15-42 and 1-42, and nitrogen utilization (P < 0.05) compared with the Con group. Jejunal villus height and villus height/crypt depth ratio were higher (P < 0.05) in the LPL group and tended to be higher (P < 0.1) in the ENZ group compared to the Con group. Supplementation with either LPL or ENZ reduced interleukin-1β concentration in jejunal mucus (P < 0.05). Both LPL and ENZ enhanced serum total superoxide dismutase activity (P < 0.05), whereas only supplementation with LPL elevated total antioxidant capacity (P < 0.05). In terms of cecal microbiota, microbial richness tended to be reduced by LPL, with low observed-OTUs and Chao1 (0.05 < P < 0.1). Supplementation with ENZ led to higher abundances of cellulolytic bacteria such as Fibrobacterota, [Eubacterium]_xylanophilum_group, and Bifidobacterium. Overall, both LPL and ENZ improved FCR, which may be relevant to ameliorative intestinal health, overall antioxidant ability, and cecal microbiome. Show less
no PDF DOI: 10.1093/jas/skad361
LPL

MACF1 overexpression in BMSCs alleviates senile osteoporosis in mice through TCF4/miR-335-5p signaling pathway.

Kewen Zhang, Wuxia Qiu, Hui Li +5 more · 2023 · Journal of orthopaedic translation · Elsevier · added 2026-04-24
The decreased osteogenic differentiation ability of mesenchymal stem cells (MSCs) is one of the important reasons for SOP. Inhibition of Wnt signaling in MSCs is closely related to SOP. Microtubule ac Show more
The decreased osteogenic differentiation ability of mesenchymal stem cells (MSCs) is one of the important reasons for SOP. Inhibition of Wnt signaling in MSCs is closely related to SOP. Microtubule actin crosslinking factor 1 (MACF1) is an important regulator in Wnt/β-catenin signal transduction. However, whether the specific expression of MACF1 in MSC regulates SOP and its mechanism remains unclear. We established MSC-specific Prrx1 (Prx1) promoter-driven MACF1 conditional knock-in (MACF-KI) mice, naturally aged male mice, and ovariectomized female mice models. Micro-CT, H&E staining, double calcein labeling, and the three-point bending test were used to explore the effects of MACF1 on bone formation and bone microstructure in the SOP mice model. Bioinformatics analysis, ChIP-PCR, qPCR, and ALP staining were used to explore the effects and mechanisms of MACF1 on MSCs' osteogenic differentiation. Microarray analysis revealed that the expression of MACF1 and positive regulators of the Wnt pathway (such as TCF4, β-catenin, Dvl) was decreased in human MSCs (hMSCs) isolated from aged osteoporotic than non-osteoporotic patients. The ALP activity and osteogenesis marker genes (Alp, Runx2, and Bglap) expression in mouse MSCs was downregulated during aging. Furthermore, Micro-CT analysis of the femur from 2-month-old MSC-specific Prrx1 (Prx1) promoter-driven MACF1 conditional knock-in (MACF-cKI) mice showed no significant trabecular bone changes compared to wild-type littermate controls, whereas 18- and 21-month-old MACF1 c-KI animals displayed increased bone mineral densities (BMD), improved bone microstructure, and increased maximum compression stress. In addition, the ovariectomy (OVX)-induced osteoporosis model of MACF1 c-KI mice had significantly higher trabecular volume and number, and increased bone formation rate than that in control mice. Mechanistically, ChIP-PCR showed that TCF4 could bind to the promoter region of the host gene miR-335-5p. Moreover, MACF1 could regulate the expression of miR-335-5p by TCF4 during the osteogenic differentiation of MSCs. These data indicate that MACF1 positively regulates MSCs osteogenesis and bone formation through the TCF4/miR-335-5p signaling pathway in SOP, suggesting that targeting MACF1 may be a novel therapeutic approach against SOP. MACF1, an important switch in the Wnt signaling pathway, can alleviate SOP through the TCF4/miR-335-5p signaling pathway in mice model. It might act as a therapeutic target for the treatment of SOP to improve bone function. Show less
📄 PDF DOI: 10.1016/j.jot.2023.02.003
MACF1

Comparison of the mutation patterns between tumor tissue and cell-free DNA in stage IV gastric cancer.

Ching-Yun Kung, Wen-Liang Fang, Yi-Ping Hung +7 more · 2023 · Aging · Impact Journals · added 2026-04-24
Compared to stage I-III gastric cancer (GC), the level of cell-free DNA (cfDNA) was significantly higher in stage IV GC. The mutation patterns of different metastatic patterns between cfDNA and tumor Show more
Compared to stage I-III gastric cancer (GC), the level of cell-free DNA (cfDNA) was significantly higher in stage IV GC. The mutation patterns of different metastatic patterns between cfDNA and tumor DNA in stage IV GC have not yet been reported. We used next-generation sequencing (NGS) to analyze cfDNA and tumor DNA in 56 stage IV GC patients. Tumor DNA and cfDNA were analyzed using a 29-gene NGS panel. In tumor samples, the most commonly mutated gene was Show less
📄 PDF DOI: 10.18632/aging.204512
MACF1

Potentially functional genetic variants in RPS6KA4 and MAP2K5 in the MAPK signaling pathway predict HBV-related hepatocellular carcinoma survival.

Moqin Qiu, Qiuling Lin, Yingchun Liu +9 more · 2023 · Molecular carcinogenesis · Wiley · added 2026-04-24
Hepatocellular carcinoma (HCC) ranks the third leading cause of cancer deaths with a dismal 5-year survival rate. The mitogen-activated protein kinase (MAPK) signaling pathway is abnormally activated Show more
Hepatocellular carcinoma (HCC) ranks the third leading cause of cancer deaths with a dismal 5-year survival rate. The mitogen-activated protein kinase (MAPK) signaling pathway is abnormally activated in HCC to promote growth and aggressive metastatic potential of cancer cells. Therefore, genetic variants in the MAPK signaling pathway may serve as potential predictors of Hepatitis B virus (HBV)-related HCC survival. In the present study, we performed a two-stage survival analysis to evaluate the associations between 10,912 single nucleotide polymorphisms (SNPs) in 79 MAPK signaling pathway genes and the overall survival (OS) of 866 HBV-related HCC patients, followed by functional annotation. In combined datasets, we identified two novel and potential functional SNPs (RPS6KA4 rs600377 T>G and MAP2K5 rs17300363 A>C) as prognostic factors for HBV-related HCC, with adjusted allelic hazards ratios of 1.24 (95% confidence interval [CI] = 1.05-1.46, p = 0.010) and 1.48 (1.15-1.91, p = 0.001), respectively. Furthermore, their combined risk genotypes also predicted a poor survival in a dose-response manner in the combined data set (P Show less
no PDF DOI: 10.1002/mc.23583
MAP2K5

The DOT1L-MLLT10 complex regulates male fertility and promotes histone removal during spermiogenesis.

Huijuan Lin, Isabella G Cossu, N Adrian Leu +4 more · 2023 · Development (Cambridge, England) · added 2026-04-24
Histone modifications regulate chromatin remodeling and gene expression in development and diseases. DOT1L, the sole histone H3K79 methyltransferase, is essential for embryonic development. Here, we r Show more
Histone modifications regulate chromatin remodeling and gene expression in development and diseases. DOT1L, the sole histone H3K79 methyltransferase, is essential for embryonic development. Here, we report that DOT1L regulates male fertility in mouse. DOT1L associates with MLLT10 in testis. DOT1L and MLLT10 localize to the sex chromatin in meiotic and post-meiotic germ cells in an inter-dependent manner. Loss of either DOT1L or MLLT10 leads to reduced testis weight, decreased sperm count and male subfertility. H3K79me2 is abundant in elongating spermatids, which undergo the dramatic histone-to-protamine transition. Both DOT1L and MLLT10 are essential for H3K79me2 modification in germ cells. Strikingly, histones are substantially retained in epididymal sperm from either DOT1L- or MLLT10-deficient mice. These results demonstrate that H3K79 methylation promotes histone replacement during spermiogenesis. Show less
no PDF DOI: 10.1242/dev.201501
MLLT10

RNA sequencing of myeloid sarcoma, shed light on myeloid sarcoma stratification.

Yunfan Yang, Yang Shu, Yuan Tang +8 more · 2023 · Cancer medicine · Wiley · added 2026-04-24
Myeloid sarcoma (MS) is a rare, extramedullary tumor consisting of myeloid blasts. Little is known about the genetic background of MS and the prognostic value of genetic abnormalities in MS. In partic Show more
Myeloid sarcoma (MS) is a rare, extramedullary tumor consisting of myeloid blasts. Little is known about the genetic background of MS and the prognostic value of genetic abnormalities in MS. In particular, the broad variety of gene fusions that occur in MS is marginally covered by traditional testing methods due to lack of fresh tumor specimens. Here, we analyzed the clinical and genetic features of 61 MS cases. We performed RNA sequencing (RNA-seq) on formalin-fixed paraffin-embedded (FFPE) or fresh samples to analyze fusion genes in 26 cases. In addition, we performed genetic abnormalities-based risk stratification using fusion genes and gene mutations. A total of 305 fusion genes were identified in 22 cases, including the following five recurrent fusion genes: RUNX1-RUNX1T1, CBFβ-MYH11, ETV6-MECOM, FUS-ERG, and PICALM-MLLT10. The prognosis in the adverse-risk group was significantly worse than that in the favorable/intermediate-risk group (median survival: 12 months vs. not reached; p = 0.0004). These results indicated the efficacy of RNA-seq using FFPE-derived RNA as a clinical routine for detecting fusion genes, which can be used as markers for risk stratification in MS. Show less
📄 PDF DOI: 10.1002/cam4.5654
MLLT10

Multiplex immunohistochemistry defines two cholesterol metabolism patterns predicting immunotherapeutic outcomes in gastric cancer.

Wei Tang, Guanghua Li, Qi Lin +3 more · 2023 · Journal of translational medicine · BioMed Central · added 2026-04-24
The role of cholesterol metabolism in gastric cancer (GC) and its implications for tumor characteristics and immunotherapy response remain poorly understood. In this study, our aim was to investigate Show more
The role of cholesterol metabolism in gastric cancer (GC) and its implications for tumor characteristics and immunotherapy response remain poorly understood. In this study, our aim was to investigate this role, identify associated metabolic subtypes, and assess their clinical implications in GC. We conducted a comprehensive analysis of cholesterol metabolism genes (CMGs) using transcriptomic data from TCGA and GEO. Based on 23 representative CMGs, we classified GC into metabolic subtypes. We evaluated clinical features and immune cell infiltration between these subtypes. Additionally, we identified a CMG signature and assessed its clinical relevance in GC. We retrospectively enrolled thirty-five GC patients receiving chemotherapy plus a PD-1 inhibitor to assess the CMG signature using multiplex immunohistochemistry. Our analysis revealed two cholesterol metabolism subtypes in GC: Cholesterol Metabolism Type 1 (CMT1) and Cholesterol Metabolism Type 2 (CMT2). These subtypes exhibited distinct patterns: CMT1 indicated heightened cholesterol biosynthesis, while CMT2 showed abnormal cholesterol transport. CMT2 was associated with unfavorable clinical features, enriched malignant pathways, and a pro-tumor immune microenvironment. Furthermore, we developed a five-CMG prognostic signature (ABCA1, NR1H3, TSPO, NCEH1, and HMGCR) that effectively predicted the prognosis of patients with GC and their response to chemotherapy plus a PD-1 inhibitor. This signature was validated in a clinical cohort using multiplex immunohistochemistry. Our results highlight the effectiveness of cholesterol metabolism patterns as biomarkers for predicting the prognosis and immunotherapy response in GC. The expression of cholesterol metabolism genes and the assessment of cholesterol metabolism patterns have the potential to predict the outcome of immunotherapy and guide treatment strategies. Show less
no PDF DOI: 10.1186/s12967-023-04758-4
NR1H3

The cellular trajectories of tumor-associated macrophages decipher the heterogeneity of pancreatic cancer.

Jiajing Lin, Fengchun Lu, Yuwei Wu +2 more · 2023 · Functional & integrative genomics · Springer · added 2026-04-24
Emerging evidence indicates that the interactions and dynamic changes among tumor-associated macrophages (TAMs) are pivotal in molding the tumor microenvironment (TME), thereby influencing diverse cli Show more
Emerging evidence indicates that the interactions and dynamic changes among tumor-associated macrophages (TAMs) are pivotal in molding the tumor microenvironment (TME), thereby influencing diverse clinical outcomes. However, the potential clinical ramifications of these evolutionary shifts in tumor-associated macrophages within pancreatic adenocarcinoma (PAAD) remain largely unexamined. Single-cell RNA sequencing (scRNA-seq) data were retrieved from the Tumor Immune Single-cell Hub. The Seurat and Monocle algorithms were employed to elucidate the progression of TAMs, using non-negative matrix factorization (NMF) to determine molecular classifications. Subsequently, the prognosis, biological characteristics, genomic modifications, and immune landscape across various clusters were interpreted. Furthermore, the sensitivity of potential therapeutic drugs between subtypes was predicted. Cellular experiments were conducted to explore the function of the NR1H3 gene in pancreatic cancer. These experiments encompassed gene knockdown, proliferation assessment, clone formation evaluation, transwell examination, and apoptosis analysis. Trajectory gene expression analysis of tumor-associated macrophages identified three disparate clusters, each associated with different clinical outcomes Compared to clusters C1 and C2, cluster C3 is seemingly at a less advanced pathological stage and associates with a relatively favorable prognosis. Further investigation revealed pronounced genetic instability in cluster C2, whereas cluster C3 demonstrated notable genetic stability. Cluster C1, characterized as "immune-hot," exhibits an abundance of immune cells and elevated immune checkpoint expression, suggesting its suitability for immunotherapy. Furthermore, several potential therapeutic agents have been pinpointed, potentially facilitating the clinical application of these insights. Cell assays indicated that NR1H3 knockdown markedly induced apoptosis and suppressed clonogenesis, migration, and proliferation of pancreatic cancer cells in the PTAU-8988 and PANC-1 cell lines. Overall, our study discerned three clusters with unique characteristics, defined by the evolution of TAMs. We propose customized therapeutic strategies for patients within these specific clusters to improve clinical outcomes and optimize clinical management. Show less
no PDF DOI: 10.1007/s10142-023-01266-y
NR1H3

Bile acid-dependent transcription factors and chromatin accessibility determine regional heterogeneity of intestinal antimicrobial peptides.

Yue Wang, Yanbo Yu, Lixiang Li +20 more · 2023 · Nature communications · Nature · added 2026-04-24
Antimicrobial peptides (AMPs) are important mediators of intestinal immune surveillance. However, the regional heterogeneity of AMPs and its regulatory mechanisms remain obscure. Here, we clarified th Show more
Antimicrobial peptides (AMPs) are important mediators of intestinal immune surveillance. However, the regional heterogeneity of AMPs and its regulatory mechanisms remain obscure. Here, we clarified the regional heterogeneity of intestinal AMPs at the single-cell level, and revealed a cross-lineages AMP regulation mechanism that bile acid dependent transcription factors (BATFs), NR1H4, NR1H3 and VDR, regulate AMPs through a ligand-independent manner. Bile acids regulate AMPs by perturbing cell differentiation rather than activating BATFs signaling. Chromatin accessibility determines the potential of BATFs to regulate AMPs at the pre-transcriptional level, thus shaping the regional heterogeneity of AMPs. The BATFs-AMPs axis also participates in the establishment of intestinal antimicrobial barriers of fetuses and the defects of antibacterial ability during Crohn's disease. Overall, BATFs and chromatin accessibility play essential roles in shaping the regional heterogeneity of AMPs at pre- and postnatal stages, as well as in maintenance of antimicrobial immunity during homeostasis and disease. Show less
no PDF DOI: 10.1038/s41467-023-40565-7
NR1H3

A Multicenter Analysis of Abnormal Chromosomal Microarray Findings in Congenital Heart Disease.

Benjamin J Landis, Lindsey R Helvaty, Gabrielle C Geddes +13 more · 2023 · Journal of the American Heart Association · added 2026-04-24
Background Chromosomal microarray analysis (CMA) provides an opportunity to understand genetic causes of congenital heart disease (CHD). The methods for describing cardiac phenotypes in patients with Show more
Background Chromosomal microarray analysis (CMA) provides an opportunity to understand genetic causes of congenital heart disease (CHD). The methods for describing cardiac phenotypes in patients with CMA abnormalities have been inconsistent, which may complicate clinical interpretation of abnormal testing results and hinder a more complete understanding of genotype-phenotype relationships. Methods and Results Patients with CHD and abnormal clinical CMA were accrued from 9 pediatric cardiac centers. Highly detailed cardiac phenotypes were systematically classified and analyzed for their association with CMA abnormality. Hierarchical classification of each patient into 1 CHD category facilitated broad analyses. Inclusive classification allowing multiple CHD types per patient provided sensitive descriptions. In 1363 registry patients, 28% had genomic disorders with well-recognized CHD association, 67% had clinically reported copy number variants (CNVs) with rare or no prior CHD association, and 5% had regions of homozygosity without CNV. Hierarchical classification identified expected CHD categories in genomic disorders, as well as uncharacteristic CHDs. Inclusive phenotyping provided sensitive descriptions of patients with multiple CHD types, which occurred commonly. Among CNVs with rare or no prior CHD association, submicroscopic CNVs were enriched for more complex types of CHD compared with large CNVs. The submicroscopic CNVs that contained a curated CHD gene were enriched for left ventricular obstruction or septal defects, whereas CNVs containing a single gene were enriched for conotruncal defects. Neuronal-related pathways were over-represented in single-gene CNVs, including top candidate causative genes Show less
no PDF DOI: 10.1161/JAHA.123.029340
NRXN3

Isoforskolin modulates AQP4-SPP1-PIK3C3 related pathway for chronic obstructive pulmonary disease via cAMP signaling.

Haochang Lin, Sha Cheng, Songye Yang +11 more · 2023 · Chinese medicine · BioMed Central · added 2026-04-24
Cyclic adenosine monophosphate (cAMP) levels are directly activated by adenylate cyclase (AC) and play an anti-inflammatory role in chronic obstructive pulmonary disease (COPD). Previously, we have sh Show more
Cyclic adenosine monophosphate (cAMP) levels are directly activated by adenylate cyclase (AC) and play an anti-inflammatory role in chronic obstructive pulmonary disease (COPD). Previously, we have shown that isoforskolin (ISOF) can effectively activate AC1 and AC2 in vitro, improve pulmonary ventilation and reduce the inflammatory response in COPD model rats, supporting that ISOF may be a potential drug for the prevention and treatment of COPD, but the mechanism has not been explored in detail. The potential pharmacological mechanisms of ISOF against COPD were analyzed by network pharmacology and multi-omics based on pharmacodynamic study. To use specific agonists, inhibitors and/or SiRNA for gene regulation function studies, combined qPCR, WB were applied to detect changes in mRNA and protein expression of important targets PIK3C3, AKT, mTOR, SPP1 and AQP4 which related to ISOF effect on COPD. And the key inflammatory factors detected by ELISA. Bioinformatics suggested that the anti-COPD pharmacological mechanism of ISOF was related to PI3K-AKT signaling pathway, and suggested target protein like PIK3C3, AQP4, SPP1, AKT, mTOR. Using the AQP4 inhibitor,or inhibiting SPP1 expression by siRNA-SPP1 could block the PIK3C3-AKT-mTOR pathway and ameliorate chronic inflammation. ISOF showed cAMP-promoting effect then suppressed AQP4 expression, together with decreased level of IL-1β, IL-6, and IL-8. These findings demonstrate ISOF controlled the cAMP-regulated PIK3C3-AKT-mTOR pathway, thereby alleviating inflammatory development in COPD. The cAMP/AQP4/PIK3C3 axis also modulate Th17/Treg differentiation, revealed potential therapeutic targets for this disease. Show less
no PDF DOI: 10.1186/s13020-023-00778-w
PIK3C3

A/(H1N1) pdm09 NS1 promotes viral replication by enhancing autophagy through hijacking the IAV negative regulatory factor LRPPRC.

Xing Guo, Zhenyu Zhang, Chaohui Lin +11 more · 2023 · Autophagy · Taylor & Francis · added 2026-04-24
The quadrilateral reassortant IAV A/(H1N1) pdm09 is the pathogen responsible for the first influenza pandemic of the 21st century. The virus spread rapidly among hosts causing high mortality within hu Show more
The quadrilateral reassortant IAV A/(H1N1) pdm09 is the pathogen responsible for the first influenza pandemic of the 21st century. The virus spread rapidly among hosts causing high mortality within human population. Efficient accumulation of virions is known to be important for the rapid transmission of virus. However, the mechanism by which A/(H1N1) pdm09 promotes its rapid replication has not been fully studied. Here, we found the NS1 of A/(H1N1) pdm09 mediated complete macroautophagy/autophagy, and then facilitated self-replication, which may be associated with the more rapid spread of this virus compared with H1N1 Show less
no PDF DOI: 10.1080/15548627.2022.2139922
PIK3C3

WHOLE GENOME SEQUENCING ANALYSIS OF BODY MASS INDEX IDENTIFIES NOVEL AFRICAN ANCESTRY-SPECIFIC RISK ALLELE.

Xinruo Zhang, Jennifer A Brody, Mariaelisa Graff +120 more · 2023 · medRxiv : the preprint server for health sciences · Cold Spring Harbor Laboratory · added 2026-04-24
Xinruo Zhang, Jennifer A Brody, Mariaelisa Graff, Heather M Highland, Nathalie Chami, Hanfei Xu, Zhe Wang, Kendra Ferrier, Geetha Chittoor, Navya S Josyula, Xihao Li, Zilin Li, Matthew A Allison, Diane M Becker, Lawrence F Bielak, Joshua C Bis, Meher Preethi Boorgula, Donald W Bowden, Jai G Broome, Erin J Buth, Christopher S Carlson, Kyong-Mi Chang, Sameer Chavan, Yen-Feng Chiu, Lee-Ming Chuang, Matthew P Conomos, Dawn L DeMeo, Margaret Du, Ravindranath Duggirala, Celeste Eng, Alison E Fohner, Barry I Freedman, Melanie E Garrett, Xiuqing Guo, Chris Haiman, Benjamin D Heavner, Bertha Hidalgo, James E Hixson, Yuk-Lam Ho, Brian D Hobbs, Donglei Hu, Qin Hui, Chii-Min Hwu, Rebecca D Jackson, Deepti Jain, Rita R Kalyani, Sharon L R Kardia, Tanika N Kelly, Ethan M Lange, Michael LeNoir, Changwei Li, Loic Le Marchand, Merry-Lynn N McDonald, Caitlin P McHugh, Alanna C Morrison, Take Naseri, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Jeffrey O'Connell, Christopher J O'Donnell, Nicholette D Palmer, James S Pankow, James A Perry, Ulrike Peters, Michael H Preuss, D C Rao, Elizabeth A Regan, Sefuiva M Reupena, Dan M Roden, Jose Rodriguez-Santana, Colleen M Sitlani, Jennifer A Smith, Hemant K Tiwari, Ramachandran S Vasan, Zeyuan Wang, Daniel E Weeks, Jennifer Wessel, Kerri L Wiggins, Lynne R Wilkens, Peter W F Wilson, Lisa R Yanek, Zachary T Yoneda, Wei Zhao, Sebastian Zöllner, Donna K Arnett, Allison E Ashley-Koch, Kathleen C Barnes, John Blangero, Eric Boerwinkle, Esteban G Burchard, April P Carson, Daniel I Chasman, Yii-der Ida Chen, Joanne E Curran, Myriam Fornage, Victor R Gordeuk, Jiang He, Susan R Heckbert, Lifang Hou, Marguerite R Irvin, Charles Kooperberg, Ryan L Minster, Braxton D Mitchell, Mehdi Nouraie, Bruce M Psaty, Laura M Raffield, Alexander P Reiner, Stephen S Rich, Jerome I Rotter, M Benjamin Shoemaker, Nicholas L Smith, Kent D Taylor, Marilyn J Telen, Scott T Weiss, Yingze Zhang, Nancy Heard-Costa, Yan V Sun, Xihong Lin, L Adrienne Cupples, Leslie A Lange, Ching-Ti Liu, Ruth J F Loos, Kari E North, Anne E Justice Show less
Obesity is a major public health crisis associated with high mortality rates. Previous genome-wide association studies (GWAS) investigating body mass index (BMI) have largely relied on imputed data fr Show more
Obesity is a major public health crisis associated with high mortality rates. Previous genome-wide association studies (GWAS) investigating body mass index (BMI) have largely relied on imputed data from European individuals. This study leveraged whole-genome sequencing (WGS) data from 88,873 participants from the Trans-Omics for Precision Medicine (TOPMed) Program, of which 51% were of non-European population groups. We discovered 18 BMI-associated signals ( Show less
no PDF DOI: 10.1101/2023.08.21.23293271
POC5

The new landscape of differentially expression proteins in placenta tissues of gestational diabetes based on iTRAQ proteomics.

Li Ge, Pingping Huang, Haiyan Miao +7 more · 2023 · Placenta · Elsevier · added 2026-04-24
Gestational diabetes mellitus (GDM) refers to abnormal glucose tolerance that occurs or is firstly diagnosed during pregnancy. GDM is related to various adverse pregnancy outcomes, but GDM pathogeny h Show more
Gestational diabetes mellitus (GDM) refers to abnormal glucose tolerance that occurs or is firstly diagnosed during pregnancy. GDM is related to various adverse pregnancy outcomes, but GDM pathogeny has not been fully elucidated. Nevertheless, previous studies have observed that many proteins in the placentas of patients with GDM are dysregulated. The present study aimed to establish a novel differentially expressed protein (DEP) landscape of GDM and normal maternal placentas and to explore the possible connection between DEPs and GDM pathogenesis. This study provides new insights into the mechanism of GDM and should make an important contribution to the development of biomarkers. The morphological characteristics of the placenta were observed on 30 GDM and normal maternal placental tissues stained with haematoxylin and eosin. Isobaric tags for relative and absolute quantitation (iTRAQ) was used in the proteomics screening of the DEPs of the normal and GDM maternal placentas. Bioinformatics analysis was performed on the DEPs, and parallel reaction monitoring (PRM) was performed to verify the DEPs. Finally, the quantitative analysis of iTRAQ and PRM was verified by immunohistochemical assay. A total of 68 DEPs in the GDM placenta were identified with iTRAQ proteomics experiment, comprising 21 up-regulated and 47 down-regulated DEPs. Bioinformatics analysis showed that the regulation of transport, catabolic process of non-coding RNA, cytoskeleton and cell binding were the most abundant Gene Ontology terms, and RNA degradation was an important pathway for significant enrichment. Protein-protein interaction network analysis showed that heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1), heterogeneous nuclear ribonucleoprotein A/B (HNRNPAB), heterogeneous nuclear ribonucleoprotein L (HNRNPL) and heterogeneous nuclear ribonucleoprotein A3 (HNRNPA3) were the cores of the up-regulated proteins. Band 3 anion transport protein (SLC4A1), spectrin beta chain erythrocytic (SPTB), ankyrin-1 (ANK1), spectrin beta chain non-erythrocytic 2 (SPTBN2), D-3-phosphoglycerate dehydrogenase (PHGDH) and exosome complex component RRP42 (EXOSC7) were the cores of the down-regulated proteins. These proteins are involved in the binding, splicing, processing, transport and degradation of RNA and in the formation and maintenance of the cytoskeleton. PRM verification results showed that seven proteins, namely, epiplakin (EPPK1), cold-inducible RNA-binding protein (CIRBP), HNRNPA2B1, HNRNPAB, HNRNPL, Ras-related protein Rab-21 (RAB21) and Ras-related protein Rab-3B (RAB3B), were up-regulated, whereas SPTB and SLC4A1 were down-regulated. The results of immunohistochemical assay also showed that the expression of five proteins, namely EPPK1, HNRNPA2B1, HNRNPAB, CIRBP and RAB21, were significantly higher in GDM placental tissues (P < 0.01). The GDM placentas showed changes in the morphological evaluation, including poor villous maturation, obvious increase in the number of syncytiotrophoblast nodules, thickening of the wall of dry villous arterioles with lumen stenosis, increased fibrinous exudation and excessive filling of villous interstitial vessels. Differentially expressed proteins related to a variety of biological processes in the GDM placenta were found. Fourteen proteins, namely, HNRNPA2B1, HNRNPAB, HNRNPL, HNRNPA3, EPPK1, CIRBP, RAB21, RAB3B, SLC4A1, SPTB, ANK1, SPTBN2, PHGDH and EXOSC7, which were differentially expressed in the placenta, may play an important role in regulating the occurrence and development of gestational diabetes through multi-channel and multi-link regulation. Show less
no PDF DOI: 10.1016/j.placenta.2022.11.012
RAB21

Liraglutide intervention improves high-glucose-induced reactive gliosis of Müller cells and ECM dysregulation.

Yongyan Shan, Xinyuan Gao, Kangqi Zhao +8 more · 2023 · Molecular and cellular endocrinology · Elsevier · added 2026-04-24
Reactive gliosis of Müller cells plays an important role in the pathogenesis of diabetic retinopathy (DR). Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been shown to improve D Show more
Reactive gliosis of Müller cells plays an important role in the pathogenesis of diabetic retinopathy (DR). Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been shown to improve DR by inhibiting reactive gliosis. However, the mechanism of inhibition has yet to be elucidated. This study investigated the effects of liraglutide on Müller glia reactivity in the early stages of DR and the underlying mechanisms. Proteomics combined with bioinformatics analysis, HE staining, and immunofluorescence staining revealed ganglion cell loss, reactive gliosis of Müller cells, and extracellular matrix (ECM) imbalance in rats with early stages of DR. High glucose (HG) exposure up-regulated GFAP and TNF-α expression and down-regulated ITGB1 expression and FN1 content in extracellular fluid in rMC1 cells, thereby promoting reactive gliosis. GLP-1R knockdown and HG+DAPT inhibition experiments show that liraglutide balances ECM levels by inhibiting activation of the Notch1/Hes1 pathway and ameliorates high-glucose-induced Müller glia reactivity. Thus, the study provides new targets and ideas for improvement of DR in early stages. Show less
no PDF DOI: 10.1016/j.mce.2023.112013
RMC1

P2X7 Is Involved in the Mouse Retinal Degeneration via the Coordinated Actions in Different Retinal Cell Types.

Ponarulselvam Sekar, George Hsiao, Yuan-Shen Chen +2 more · 2023 · Antioxidants (Basel, Switzerland) · MDPI · added 2026-04-24
Adenosine triphosphate (ATP) released from dying cells with high concentrations is sensed as a danger signal by the P2X7 receptor. Sodium iodate (NaIO
no PDF DOI: 10.3390/antiox12010141
RMC1

MYH10 Combines with MYH9 to Recruit USP45 by Deubiquitinating Snail and Promotes Serous Ovarian Cancer Carcinogenesis, Progression, and Cisplatin Resistance.

Longyang Liu, Chunlin Chen, Ping Liu +10 more · 2023 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
The poor prognosis of serous ovarian cancer (SOC) is due to its high invasive capacity and cisplatin resistance of SOC cells, whereas the molecular mechanisms remain poorly understood. In the present Show more
The poor prognosis of serous ovarian cancer (SOC) is due to its high invasive capacity and cisplatin resistance of SOC cells, whereas the molecular mechanisms remain poorly understood. In the present study, the expression and function of non-muscle myosin heavy chain IIB (MYH10) in SOC are identified by immunohistochemistry, in vitro, and in vivo studies, respectively. The mechanism of MYH10 is demonstrated by co-immunoprecipitation, GST pull-down, confocal laser assays, and so on. The results show that the knockdown of MYH10 suppressed SOC cell proliferation, migration, invasion, metastasis, and cisplatin resistance both in vivo and in vitro. Further studies confirm that the MYH10 protein functional domain combines with non-muscle myosin heavy chain IIA (MYH9) to recruit the deubiquitinating enzyme Ubiquitin-specific proteases 45 and deubiquitinates snail to inhibit snail degradation, eventually promoting tumorigenesis, progression, and cisplatin resistance in SOC. In clinical samples, MYH10 expression is significantly elevated in SOC samples compared to the paratumor samples. And the expression of MYH10 is positively correlated with MYH9 expression. MYH10+/MYH9+ co-expression is an independent prognostic factor for predicting SOC patient survival. These findings uncover a key role of the MYH10-MYH9-snail axis in SOC carcinogenesis, progression, and cisplatin resistance, and provide potential novel therapeutic targets for SOC intervention. Show less
no PDF DOI: 10.1002/advs.202203423
SNAI1

Integrative analysis of circadian clock with prognostic and immunological biomarker identification in ovarian cancer.

Lianfang Zhao, Yuqin Tang, Jiayan Yang +4 more · 2023 · Frontiers in molecular biosciences · Frontiers · added 2026-04-24
no PDF DOI: 10.3389/fmolb.2023.1208132
SNRPC

lncRNA

Zhen Zhang, Yun-Xin Lu, Fangzhou Liu +16 more · 2023 · Proceedings of the National Academy of Sciences of the United States of America · National Academy of Sciences · added 2026-04-24
Notch has been implicated in human cancers and is a putative therapeutic target. However, the regulation of Notch activation in the nucleus remains largely uncharacterized. Therefore, characterizing t Show more
Notch has been implicated in human cancers and is a putative therapeutic target. However, the regulation of Notch activation in the nucleus remains largely uncharacterized. Therefore, characterizing the detailed mechanisms governing Notch degradation will identify attractive strategies for treating Notch-activated cancers. Here, we report that the long noncoding RNA (lncRNA) Show less
no PDF DOI: 10.1073/pnas.2206694120
WWP2

Activation of E3 ubiquitin ligase WWP2 by non-receptor tyrosine kinase ACK1.

Jun Zhu, Ziluo Peng, Xianyan Tian +4 more · 2023 · IUBMB life · Wiley · added 2026-04-24
WW domain containing E3 ubiquitin protein ligase 2 (WWP2) is a member of the NEDD4 E3 ubiquitin ligase family. WWP2 ligase activity is regulated by the 2, 3-linker auto-inhibition. Tyrosine phosphoryl Show more
WW domain containing E3 ubiquitin protein ligase 2 (WWP2) is a member of the NEDD4 E3 ubiquitin ligase family. WWP2 ligase activity is regulated by the 2, 3-linker auto-inhibition. Tyrosine phosphorylation of the 2, 3-linker was identified as an activating means for releasing the auto-inhibition of WWP2. However, the tyrosine kinase (TK) for the phosphorylation and activation remains unknown. In this report, we have found that non-receptor TK ACK1 binds to the WW3 domain of WWP2 and phosphorylates WWP2. ACK1 phosphorylates WWP2 at the 2, 3-linker and partially activates the ubiquitination ligase activity. Unexpectedly, tyrosine phosphorylation of the 2, 3-linker seems not a major mode for activation of WWP2, as ACK1 causes much higher activation of the 2, 3-linker tyrosine phosphorylation defective mutants of WWP2 than that of wild-type WWP2. Furthermore, epidermal growth factor (EGF) stimulates tyrosine phosphorylation of WWP2 and this EGF-stimulated phosphorylation of WWP2 is mediated by ACK1. Finally, knockdown of WWP2 by shWWP2 inhibits the EGF-dependent cell proliferation of lung cancer A549 cells, suggesting that WWP2 may function in the EGFR signaling in lung cancer progression. Taken together, our findings have revealed a novel mechanism underlying activation of WWP2. Show less
no PDF DOI: 10.1002/iub.2705
WWP2

Design of Potent and Proteolytically Stable Biaryl-Stapled GLP-1R/GIPR Peptide Dual Agonists.

Yifang Yang, Candy Lee, Reddy Rajasekhar Reddy +5 more · 2022 · ACS chemical biology · ACS Publications · added 2026-04-24
Recent clinical trials have revealed that the chimeric peptide hormones simultaneously activating glucagon-like peptide-1 receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide receptor (G Show more
Recent clinical trials have revealed that the chimeric peptide hormones simultaneously activating glucagon-like peptide-1 receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide receptor (GIPR) demonstrate superior efficacy in glycemic control and body weight reduction, better than those activating the GLP-1R alone. However, the linear peptide-based GLP-1R/GIPR dual agonists are susceptible to proteolytic cleavage by common digestive enzymes present in the gastrointestinal tract and thus not suitable for oral administration. Here, we report the design and synthesis of biaryl-stapled peptides, with and without fatty diacid attachment, that showed potent GLP-1R/GIPR dual agonist activities. Compared to a linear peptide dual agonist and semaglutide, the biaryl-stapled peptides displayed drastically improved proteolytic stability against the common digestive enzymes. Furthermore, two stapled peptides showed excellent efficacy in an oral glucose tolerance test in mice, owing to their potent receptor activity in vitro and good pharmacokinetics exposure upon subcutaneous injection. By exploring a more comprehensive set of biaryl staplers, we expect that this stapling method could facilitate the design of the stapled peptide-based dual agonists suitable for oral administration. Show less
📄 PDF DOI: 10.1021/acschembio.2c00175
GIPR

Pharmacological Evaluation of Melanocortin 2 Receptor Accessory Protein 2 on Axolotl Neural Melanocortin Signaling.

Xiaozhu Wang, Song Xue, Xiaowei Lei +11 more · 2022 · Frontiers in endocrinology · Frontiers · added 2026-04-24
The Melanocortin-3 receptor (MC3R) and Melanocortin-4 receptor (MC4R), two members of the key hypothalamic neuropeptide signaling, function as complex mediators to control the central appetitive and e Show more
The Melanocortin-3 receptor (MC3R) and Melanocortin-4 receptor (MC4R), two members of the key hypothalamic neuropeptide signaling, function as complex mediators to control the central appetitive and energy homeostasis. The melanocortin 2 receptor accessory protein 2 (MRAP2) is well-known for its modulation on the trafficking and signaling of MC3R and MC4R in mammals. In this study, we cloned and elucidated the pharmacological profiles of MRAP2 on the regulation of central melanocortin signaling in a relatively primitive poikilotherm amphibian species, the Mexican axolotl ( Show less
📄 PDF DOI: 10.3389/fendo.2022.820896
MC4R

Histone deacetylase 6 inhibition restores leptin sensitivity and reduces obesity.

Işın Çakır, Colleen K Hadley, Pauline Lining Pan +12 more · 2022 · Nature metabolism · Nature · added 2026-04-24
The adipose tissue-derived hormone leptin can drive decreases in food intake while increasing energy expenditure. In diet-induced obesity, circulating leptin levels rise proportionally to adiposity. D Show more
The adipose tissue-derived hormone leptin can drive decreases in food intake while increasing energy expenditure. In diet-induced obesity, circulating leptin levels rise proportionally to adiposity. Despite this hyperleptinemia, rodents and humans with obesity maintain increased adiposity and are resistant to leptin's actions. Here we show that inhibitors of the cytosolic enzyme histone deacetylase 6 (HDAC6) act as potent leptin sensitizers and anti-obesity agents in diet-induced obese mice. Specifically, HDAC6 inhibitors, such as tubastatin A, reduce food intake, fat mass, hepatic steatosis and improve systemic glucose homeostasis in an HDAC6-dependent manner. Mechanistically, peripheral, but not central, inhibition of HDAC6 confers central leptin sensitivity. Additionally, the anti-obesity effect of tubastatin A is attenuated in animals with a defective central leptin-melanocortin circuitry, including db/db and MC4R knockout mice. Our results suggest the existence of an HDAC6-regulated adipokine that serves as a leptin-sensitizing agent and reveals HDAC6 as a potential target for the treatment of obesity. Show less
📄 PDF DOI: 10.1038/s42255-021-00515-3
MC4R

Mesenchymal Stromal Cells Overexpressing Farnesoid X Receptor Exert Cardioprotective Effects Against Acute Ischemic Heart Injury by Binding Endogenous Bile Acids.

Yunlong Xia, Xinyue Xu, Yongzhen Guo +14 more · 2022 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Bile acid metabolites have been increasingly recognized as pleiotropic signaling molecules that regulate cardiovascular functions, but their role in mesenchymal stromal cells (MSC)-based therapy has n Show more
Bile acid metabolites have been increasingly recognized as pleiotropic signaling molecules that regulate cardiovascular functions, but their role in mesenchymal stromal cells (MSC)-based therapy has never been investigated. It is found that overexpression of farnesoid X receptor (FXR), a main receptor for bile acids, improves the retention and cardioprotection of adipose tissue-derived MSC (ADSC) administered by intramyocardial injection in mice with myocardial infarction (MI), which shows enhanced antiapoptotic, proangiogenic, and antifibrotic effects. RNA sequencing, LC-MS/MS, and loss-of-function studies reveal that FXR overexpression promotes ADSC paracrine angiogenesis via Angptl4. FXR overexpression improves ADSC survival in vivo but fails in vitro. By performing bile acid-targeted metabolomics using ischemic heart tissue, 19 bile acids are identified. Among them, cholic acid and deoxycholic acid significantly increase Angptl4 secretion from ADSC overexpressing FXR and further improve their proangiogenic capability. Moreover, ADSC overexpressing FXR shows significantly lower apoptosis by upregulating Nqo-1 expression only in the presence of FXR ligands. Retinoid X receptor α is identified as a coactivator of FXR. It is first demonstrated that there is a bile acid pool in the myocardial microenvironment. Targeting the bile acid-FXR axis may be a novel strategy for improving the curative effect of MSC-based therapy for MI. Show less
📄 PDF DOI: 10.1002/advs.202200431
ANGPTL4

Angiopoietin-Like Protein 4 Is Involved in Manganese Superoxide Dismutase-Mediated Suppression of Breast Cancer Cell Growth.

P Li, X Zeng, Y Liu +1 more · 2022 · Bulletin of experimental biology and medicine · Springer · added 2026-04-24
P Li, X Zeng, Y Liu, M Lin Show less
This study aims to understand the molecular basis of manganese superoxide dismutase (MnSOD) impacts on breast cancer cell growth. Modulation of the level of MnSOD by genetic engineering led significan Show more
This study aims to understand the molecular basis of manganese superoxide dismutase (MnSOD) impacts on breast cancer cell growth. Modulation of the level of MnSOD by genetic engineering led significant changes in the expression of angiopoietin-like protein 4 (ANGPTL4) and activity of peroxisome proliferator-activated receptor α (PPARα) in MCF7 cells. PPARα agonist increased ANGPTL4 expression inhibited by MnSOD. Proliferation of MCF7 cells was inhibited by MnSOD, however, ANGPTL4 transduction into MCF7 cells with MnSOD overexpression significantly stimulated cell proliferation. MnSOD induced G0/G1 cell cycle arrest, nevertheless, ANGPTL4 transduction significantly reduced the percentage of cells in G0/G1 phase overexpressing MnSOD. In conclusion, MnSOD suppressed the expression of ANGPTL4 in breast cancer cells via the PPARα signaling pathway, and ANGPTL4 was involved in MnSOD-mediated proliferation inhibition and cell cycle arrest. Show less
📄 PDF DOI: 10.1007/s10517-022-05526-y
ANGPTL4

Increased angiopoietin-like 4 expression ameliorates inflammatory bowel diseases via suppressing CD8

Xiaoyuan Zhang, Jing Tu, Shizhen Ding +6 more · 2022 · Biochemical and biophysical research communications · Elsevier · added 2026-04-24
Angiopoietin-like 4 (ANGPTL4) is involved in inflammation-associated diseases, such as rheumatoid arthritis, type 2 diabetes, atherosclerosis, and chronic obstructive pulmonary disease. The role of AN Show more
Angiopoietin-like 4 (ANGPTL4) is involved in inflammation-associated diseases, such as rheumatoid arthritis, type 2 diabetes, atherosclerosis, and chronic obstructive pulmonary disease. The role of ANGPTL4 in the pathogenesis of inflammatory bowel disease (IBD) remains unknown. Here, the plasma ANGPTL4 levels peaked on days 3 and 5, and expression of ANGPTL4 of inflamed colons peaked on days 5 and 7 in mice with dextran sulfate sodium (DSS)-induced colitis. Simultaneously, CD8 Show less
no PDF DOI: 10.1016/j.bbrc.2022.03.153
ANGPTL4

ANGPTL4 negatively regulates the progression of osteosarcoma by remodeling branched-chain amino acid metabolism.

Shanyi Lin, Yu Miao, Xu Zheng +7 more · 2022 · Cell death discovery · Nature · added 2026-04-24
Angiopoietin-like-4 (ANGPTL4), a secreted glycoprotein that is mainly known as a regulator in lipid metabolism, now, is also indicated to be involved in the regulation of cancer progression and metast Show more
Angiopoietin-like-4 (ANGPTL4), a secreted glycoprotein that is mainly known as a regulator in lipid metabolism, now, is also indicated to be involved in the regulation of cancer progression and metastasis. However, little is known about not only biological functions, but also underlying mechanism of ANGPTL4 in the progression of osteosarcoma (OS). Here, we discovered that ANGPTL4 is downregulated in OS, and is associated with branched-chain amino acid (BCAA) metabolism. The BCAAs (valine, leucine, and isoleucine) are essential amino acids that play an important role in metabolic regulation. Aberrant BCAA metabolism is also found in various cancers and is associated with tumor progression, including proliferation, invasion, and metastasis. In this study, we indicated that the negative relation between the expression of ANGPTL4 and BCAA catabolism in OS samples and cell lines. The knockdown of ANGPTL4 in OS cells resulted in the accumulation of BCAAs, which in turn activated the mTOR signaling pathway, enhancing OS cell proliferation. Thus, reduced expression of ANGPTL4 is associated with the progression of OS. Taken together, our results demonstrated that the ANGPTL4/BCAA/mTOR axis is an important pathway in OS progression and may be a potential therapeutic target to slow OS progression. Show less
📄 PDF DOI: 10.1038/s41420-022-01029-x
ANGPTL4