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Your search keyword '"Guan, Dongxian"' showing total 12 results
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12 results on '"Guan, Dongxian"'

1. Gut microbial co-metabolite 2-methylbutyrylcarnitine exacerbates thrombosis via binding to and activating integrin α2β1

Author

Huang, Kan, Li, Zilun, He, Xi, Dai, Jun, Huang, Bingding, Shi, Yongxia, Fan, Dongxiao, Zhang, Zefeng, Liu, Yunchong, Li, Na, Zhang, Zhongyu, Peng, Jiangyun, Liu, Chenshu, Zeng, Renli, Cen, Zhipeng, Wang, Tengyao, Yang, Wenchao, Cen, Meifeng, Li, Jingyu, Yuan, Shuai, Zhang, Lu, Hu, Dandan, Huang, Shuxiang, Chen, Pin, Lai, Peilong, Lin, Liyan, Wen, Jielu, Zhao, Zhengde, Huang, Xiuyi, Yuan, Lining, Zhou, Lifang, Wu, Haoliang, Huang, Lihua, Feng, Kai, Wang, Jian, Liao, Baolin, Cai, Weiping, Deng, Xilong, Li, Yueping, Li, Jianping, Hu, Zhongwei, Yang, Li, Li, Jiaojiao, Zhuo, Youguang, Zhang, Fuchun, Lin, Lin, Luo, Yifeng, Zhang, Wei, Ni, Qianlin, Hong, Xiqiang, Chang, Guangqi, Zhang, Yang, Guan, Dongxian, Cai, Weikang, Lu, Yutong, Li, Fang, Yan, Li, Ren, Meng, Li, Linghua, and Chen, Sifan

Published
2024
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2. Prolonged hypoxia alleviates prolyl hydroxylation-mediated suppression of RIPK1 to promote necroptosis and inflammation

Author

Zhang, Tao, Xu, Daichao, Liu, Jianping, Wang, Min, Duan, Li-Juan, Liu, Min, Meng, Huyan, Zhuang, Yuan, Wang, Huibing, Wang, Yingnan, Lv, Mingming, Zhang, Zhengyi, Hu, Jia, Shi, Linyu, Guo, Rui, Xie, Xingxing, Liu, Hui, Erickson, Emily, Wang, Yaru, Yu, Wenyu, Dang, Fabin, Guan, Dongxian, Jiang, Cong, Dai, Xiaoming, Inuzuka, Hiroyuki, Yan, Peiqiang, Wang, Jingchao, Babuta, Mrigya, Lian, Gewei, Tu, Zhenbo, Miao, Ji, Szabo, Gyongyi, Fong, Guo-Hua, Karnoub, Antoine E., Lee, Yu-Ru, Pan, Lifeng, Kaelin, Jr., William G., Yuan, Junying, and Wei, Wenyi

Published
2023
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4. Imatinib and methazolamide ameliorate COVID-19-induced metabolic complications via elevating ACE2 enzymatic activity and inhibiting viral entry

Author

Li, Zilun, Peng, Meixiu, Chen, Pin, Liu, Chenshu, Hu, Ao, Zhang, Yixin, Peng, Jiangyun, Liu, Jiang, Li, Yihui, Li, Wenxue, Zhu, Wei, Guan, Dongxian, Zhang, Yang, Chen, Hongyin, Li, Jiuzhou, Fan, Dongxiao, Huang, Kan, Lin, Fen, Zhang, Zefeng, Guo, Zeling, Luo, Hengli, He, Xi, Zhu, Yuanyuan, Li, Linghua, Huang, Bingding, Cai, Weikang, Gu, Lei, Lu, Yutong, Deng, Kai, Yan, Li, and Chen, Sifan

Published
2022
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7. IL1R1 is required for celastrol's leptin-sensitization and antiobesity effects

Author

Feng, Xudong, Guan, Dongxian, Auen, Thomas, Choi, Jae Won, Salazar Hernández, Mario Andrés, Lee, Jaemin, and Chun, Hyonho

Subjects
Quinones -- Testing, Leptin -- Testing, Anti-obesity agents -- Testing, Body weight -- Health aspects -- Genetic aspects, Obesity, Diabetes therapy, Brain, Interleukins, Type 2 diabetes, Biological sciences, Health
Abstract

Celastrol, a pentacyclic triterpene, is the most potent antiobesity agent that has been reported thus far.sup.1. The mechanism of celastrol's leptin-sensitizing and antiobesity effects has not yet been elucidated. In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol's action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. We demonstrate that IL1R1-deficient mice are completely resistant to the effects of celastrol in leptin sensitization and treatment of obesity, diabetes, and nonalcoholic steatohepatitis. Thus, we conclude that IL1R1 is a gatekeeper for celastrol's metabolic actions. IL1R1 is a gatekeeper for celastrol's metabolic actions., Author(s): Xudong Feng [sup.1] , Dongxian Guan [sup.1] , Thomas Auen [sup.1] , Jae Won Choi [sup.1] , Mario Andrés Salazar Hernández [sup.1] , Jaemin Lee [sup.1] , Hyonho Chun [...]

Published
2019
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12. Metabolic orchestration of cell death by AMPK-mediated phosphorylation of RIPK1.

Author

Zhang T, Xu D, Trefts E, Lv M, Inuzuka H, Song G, Liu M, Lu J, Liu J, Chu C, Wang M, Wang H, Meng H, Liu H, Zhuang Y, Xie X, Dang F, Guan D, Men Y, Jiang S, Jiang C, Dai X, Liu J, Wang Z, Yan P, Wang J, Tu Z, Babuta M, Erickson E, Hillis AL, Dibble CC, Asara JM, Szabo G, Sicinski P, Miao J, Lee YR, Pan L, Shaw RJ, Yuan J, and Wei W

Subjects
Animals, Mice, Phosphorylation, Inflammation metabolism, Ischemia metabolism, AMP-Activated Protein Kinases genetics, AMP-Activated Protein Kinases metabolism, Necroptosis, Stress, Physiological, Energy Metabolism, Receptor-Interacting Protein Serine-Threonine Kinases genetics, Receptor-Interacting Protein Serine-Threonine Kinases metabolism
Abstract

Adenosine monophosphate-activated protein kinase (AMPK) activity is stimulated to promote metabolic adaptation upon energy stress. However, sustained metabolic stress may cause cell death. The mechanisms by which AMPK dictates cell death are not fully understood. We report that metabolic stress promoted receptor-interacting protein kinase 1 (RIPK1) activation mediated by TRAIL receptors, whereas AMPK inhibited RIPK1 by phosphorylation at Ser 415 to suppress energy stress-induced cell death. Inhibiting pS415-RIPK1 by Ampk deficiency or RIPK1 S415A mutation promoted RIPK1 activation. Furthermore, genetic inactivation of RIPK1 protected against ischemic injury in myeloid Ampkα1 -deficient mice. Our studies reveal that AMPK phosphorylation of RIPK1 represents a crucial metabolic checkpoint, which dictates cell fate response to metabolic stress, and highlight a previously unappreciated role for the AMPK-RIPK1 axis in integrating metabolism, cell death, and inflammation.

Published
2023
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