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12 results on '"Ci, Yanpeng"'

2. Cyclin DCDK4 kinase destabilizes PD-L1 via cullin 3SPOP to control cancer immune surveillance

Author

Zhang, Jinfang, Bu, Xia, Wang, Haizhen, Zhu, Yasheng, Geng, Yan, Nihira, Naoe Taira, Tan, Yuyong, Ci, Yanpeng, Wu, Fei, Dai, Xiangpeng, Guo, Jianping, Huang, Yu-Han, Fan, Caoqi, Ren, Shancheng, Sun, Yinghao, Freeman, Gordon J., Sicinski, Piotr, and Wei, Wenyi

Subjects
Cancer treatment -- Methods, Apoptosis -- Research, Phosphotransferases -- Physiological aspects, Cancer research, Ligands (Biochemistry) -- Physiological aspects, Immune response -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Jinfang Zhang [1]; Xia Bu [2]; Haizhen Wang [3]; Yasheng Zhu [4]; Yan Geng [3]; Naoe Taira Nihira [1]; Yuyong Tan [1, 5]; Yanpeng Ci [1, 6]; Fei Wu [...]

Published
2018
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7. Evolution and extensive reassortment of H5 influenza viruses isolated from wild birds in China over the past decade

Author

Cui, Yanfang, primary, Li, Yulei, additional, Li, Minghui, additional, Zhao, Lu, additional, Wang, Deli, additional, Tian, Jingman, additional, Bai, Xiaoli, additional, Ci, Yanpeng, additional, Wu, Shanshan, additional, Wang, Fei, additional, Chen, Xiaomei, additional, Ma, Shujie, additional, Qu, Zhiyuan, additional, Yang, Cen, additional, Liu, Liling, additional, Shi, Jianzhong, additional, Guan, Yuntao, additional, Zeng, Xianying, additional, Tian, Guobin, additional, Cui, Pengfei, additional, Deng, Guohua, additional, Jiang, Yongping, additional, Chen, Pucheng, additional, Liu, Jinxiong, additional, Wang, Xiurong, additional, Bao, Hongmei, additional, Jiang, Li, additional, Suzuki, Yasuo, additional, Li, Chengjun, additional, Li, Yanbing, additional, and Chen, Hualan, additional

Published
2020
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8. Cyclin D–CDK4 kinase destabilizes PD-L1 via cullin 3–SPOP to control cancer immune surveillance

Author

Zhang, Jinfang, primary, Bu, Xia, additional, Wang, Haizhen, additional, Zhu, Yasheng, additional, Geng, Yan, additional, Nihira, Naoe Taira, additional, Tan, Yuyong, additional, Ci, Yanpeng, additional, Wu, Fei, additional, Dai, Xiangpeng, additional, Guo, Jianping, additional, Huang, Yu-Han, additional, Fan, Caoqi, additional, Ren, Shancheng, additional, Sun, Yinghao, additional, Freeman, Gordon J., additional, Sicinski, Piotr, additional, and Wei, Wenyi, additional

Published
2017
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10. SCFβ-TRCP E3 ubiquitin ligase targets the tumor suppressor ZNRF3 for ubiquitination and degradation.

Author

Ci, Yanpeng, Li, Xiaoning, Chen, Maorong, Zhong, Jiateng, North, Brian J., Inuzuka, Hiroyuki, He, Xi, Li, Yu, Guo, Jianping, and Dai, Xiangpeng

Abstract

Wnt signaling has emerged as a major regulator of tissue development by governing the self-renewal and maintenance of stem cells in most tissue types. As a key upstream regulator of the Wnt pathway, the transmembrane E3 ligase ZNRF3 has recently been established to play a role in negative regulation of Wnt signaling by targeting Frizzled (FZD) receptor for ubiquitination and degradation. However, the upstream regulation of ZNRF3, in particular the turnover of ZNRF3, is still unclear. Here we report that ZNRF3 is accumulated in the presence of proteasome inhibitor treatment independent of its E3-ubiquitin ligase activity. Furthermore, the Cullin 1-specific SCF complex containing β-TRCP has been identified to directly interact with and ubiquitinate ZNRF3 thereby regulating its protein stability. Similar with the degradation of β-catenin by β-TRCP, ZNRF3 is ubiquitinated by β-TRCP in both CKI-phosphorylation- and degron-dependent manners. Thus, our findings not only identify a novel substrate for β-TRCP oncogenic regulation, but also highlight the dual regulation of Wnt signaling by β-TRCP in a context-dependent manner where β-TRCP negatively regulates Wnt signaling by targeting β-catenin, and positively regulates Wnt signaling by targeting ZNRF3. [ABSTRACT FROM AUTHOR]

Published
2018
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12. SCFβ-TRCPE3 ubiquitin ligase targets the tumor suppressor ZNRF3 for ubiquitination and degradation

Author

Ci, Yanpeng, Li, Xiaoning, Chen, Maorong, Zhong, Jiateng, North, Brian, Inuzuka, Hiroyuki, He, Xi, Li, Yu, Guo, Jianping, and Dai, Xiangpeng

Abstract

Wnt signaling has emerged as a major regulator of tissue development by governing the self-renewal and maintenance of stem cells in most tissue types. As a key upstream regulator of the Wnt pathway, the transmembrane E3 ligase ZNRF3 has recently been established to play a role in negative regulation of Wnt signaling by targeting Frizzled (FZD) receptor for ubiquitination and degradation. However, the upstream regulation of ZNRF3, in particular the turnover of ZNRF3, is still unclear. Here we report that ZNRF3 is accumulated in the presence of proteasome inhibitor treatment independent of its E3-ubiquitin ligase activity. Furthermore, the Cullin 1-specific SCF complex containing β-TRCP has been identified to directly interact with and ubiquitinate ZNRF3 thereby regulating its protein stability. Similar with the degradation of β-catenin by β-TRCP, ZNRF3 is ubiquitinated by β-TRCP in both CKI-phosphorylation- and degron-dependent manners. Thus, our findings not only identify a novel substrate for β-TRCP oncogenic regulation, but also highlight the dual regulation of Wnt signaling by β-TRCP in a context-dependent manner where β-TRCP negatively regulates Wnt signaling by targeting β-catenin, and positively regulates Wnt signaling by targeting ZNRF3.

Published
2018
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