Search

Your search keyword '"Dang, Fabin"' showing total 25 results
Start Over Author "Dang, Fabin"
25 results on '"Dang, Fabin"'

1. Reciprocal antagonism of PIN1-APC/CCDH1 governs mitotic protein stability and cell cycle entry

Author

Ke, Shizhong, Dang, Fabin, Wang, Lin, Chen, Jia-Yun, Naik, Mandar T., Li, Wenxue, Thavamani, Abhishek, Kim, Nami, Naik, Nandita M., Sui, Huaxiu, Tang, Wei, Qiu, Chenxi, Koikawa, Kazuhiro, Batalini, Felipe, Stern Gatof, Emily, Isaza, Daniela Arango, Patel, Jaymin M., Wang, Xiaodong, Clohessy, John G., Heng, Yujing J., Lahav, Galit, Liu, Yansheng, Gray, Nathanael S., Zhou, Xiao Zhen, Wei, Wenyi, Wulf, Gerburg M., and Lu, Kun Ping

Published
2024
Full Text
View/download PDF

4. 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
Full Text
View/download PDF

10. USP2 inhibition prevents infection with ACE2-dependent coronaviruses in vitro and is protective against SARS-CoV-2 in mice

Author

Dang, Fabin, primary, Bai, Lei, additional, Dong, Jiazhen, additional, Hu, Xiaoping, additional, Wang, Jingchao, additional, Paulo, Joao A., additional, Xiong, Yan, additional, Liang, Xiaowei, additional, Sun, Yishuang, additional, Chen, Yuncai, additional, Guo, Ming, additional, Wang, Xin, additional, Huang, Zhixiang, additional, Inuzuka, Hiroyuki, additional, Chen, Li, additional, Chu, Chen, additional, Liu, Jianping, additional, Zhang, Tao, additional, Rezaeian, Abdol-Hossein, additional, Liu, Jing, additional, Kaniskan, Husnu Ümit, additional, Zhong, Bo, additional, Zhang, Jinfang, additional, Letko, Michael, additional, Jin, Jian, additional, Lan, Ke, additional, and Wei, Wenyi, additional

Published
2023
Full Text
View/download PDF

12. Reciprocal antagonism of PIN1-APC/CCDH1 governs mitotic protein stability and cell cycle entry.

Author

Ke, Shizhong, Dang, Fabin, Wang, Lin, Chen, Jia-Yun, Naik, Mandar T., Li, Wenxue, Thavamani, Abhishek, Kim, Nami, Naik, Nandita M., Sui, Huaxiu, Tang, Wei, Qiu, Chenxi, Koikawa, Kazuhiro, Batalini, Felipe, Stern Gatof, Emily, Isaza, Daniela Arango, Patel, Jaymin M., Wang, Xiaodong, Clohessy, John G., and Heng, Yujing J.

Abstract

Induced oncoproteins degradation provides an attractive anti-cancer modality. Activation of anaphase-promoting complex (APC/CCDH1) prevents cell-cycle entry by targeting crucial mitotic proteins for degradation. Phosphorylation of its co-activator CDH1 modulates the E3 ligase activity, but little is known about its regulation after phosphorylation and how to effectively harness APC/CCDH1 activity to treat cancer. Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1)-catalyzed phosphorylation-dependent cis-trans prolyl isomerization drives tumor malignancy. However, the mechanisms controlling its protein turnover remain elusive. Through proteomic screens and structural characterizations, we identify a reciprocal antagonism of PIN1-APC/CCDH1 mediated by domain-oriented phosphorylation-dependent dual interactions as a fundamental mechanism governing mitotic protein stability and cell-cycle entry. Remarkably, combined PIN1 and cyclin-dependent protein kinases (CDKs) inhibition creates a positive feedback loop of PIN1 inhibition and APC/CCDH1 activation to irreversibly degrade PIN1 and other crucial mitotic proteins, which force permanent cell-cycle exit and trigger anti-tumor immunity, translating into synergistic efficacy against triple-negative breast cancer. Unveiling the regulation of mitotic protein degradation is crucial for cancer therapy. Here, the authors reveal that a reciprocal inhibition of PIN1-APC/CCDH1 controls the cell cycle and mitotic protein degradation, offering a synergistic anti-tumor strategy. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

20. PTEN Methylation by NSD2 Controls Cellular Sensitivity to DNA Damage

Author

Zhang, Jinfang, primary, Lee, Yu-Ru, additional, Dang, Fabin, additional, Gan, Wenjian, additional, Menon, Archita Venugopal, additional, Katon, Jesse M., additional, Hsu, Chih-Hung, additional, Asara, John M., additional, Tibarewal, Priyanka, additional, Leslie, Nicholas R., additional, Shi, Yang, additional, Pandolfi, Pier Paolo, additional, and Wei, Wenyi, additional

Published
2019
Full Text
View/download PDF

24. 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
Full Text
View/download PDF

25. Reciprocal inhibition of PIN1 and APC/C CDH1 controls timely G1/S transition and creates therapeutic vulnerability.

Author

Ke S, Dang F, Wang L, Chen JY, Naik MT, Thavamani A, Liu Y, Li W, Kim N, Naik NM, Sui H, Tang W, Qiu C, Koikawa K, Batalini F, Wang X, Clohessy JG, Heng YJ, Lahav G, Gray NS, Zho XZ, Wei W, Wulf GM, and Lu KP

Abstract

Cyclin-dependent kinases (CDKs) mediated phosphorylation inactivates the anaphase-promoting complex (APC/C CDH1 ), an E3 ubiquitin ligase that contains the co-activator CDH1, to promote G1/S transition. PIN1 is a phosphorylation-directed proline isomerase and a master cancer signaling regulator. However, little are known about APC/C CDH1 regulation after phosphorylation and about PIN1 ubiquitin ligases. Here we uncover a domain-oriented reciprocal inhibition that controls the timely G1/S transition: The non-phosphorylated APC/C CDH1 E3 ligase targets PIN1 for degradation in G1 phase, restraining G1/S transition; APC/C CDH1 itself, after phosphorylation by CDKs, is inactivated by PIN1-catalyzed isomerization, promoting G1/S transition. In cancer, PIN1 overexpression and APC/C CDH1 inactivation reinforce each other to promote uncontrolled proliferation and tumorigenesis. Importantly, combined PIN1- and CDK4/6-inhibition reactivates APC/C CDH1 resulting in PIN1 degradation and an insurmountable G1 arrest that translates into synergistic anti-tumor activity against triple-negative breast cancer in vivo. Reciprocal inhibition of PIN1 and APC/C CDH1 is a novel mechanism to control timely G1/S transition that can be harnessed for synergistic anti-cancer therapy.

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results