赌博app

性别: 男
工作电话:020-84110415
职称: 副教授
电子邮件:[email protected]
导师类型: 博士生导师
学历: 博士
学科方向
071009-细胞生物学
071010-生物化学与分子生物学

研究方向

（1）免疫-代谢的分子作用机制
（2）非经典自噬的发生和调控机理
（3）抗病毒信号通路及干预策略研究

个人经历

2019/05至今  赌博app-网络赌博软件   副教授
2016/07-2019/04  赌博app-网络赌博软件   特聘副研究员
2013/09-2016/06  中山大学中山医学院  理学博士

讲授课程

《细胞生物学前沿》
《细胞信号转导》（本研贯通课）
《科技论文写作》
《免疫学实验》
《现代生命科学进展》

学术成就

金寿恒  副教授，博士生导师。攻读博士研究生学位开始，师从崔隽教授从事分子免疫调控研究。近年来，以第一作者/通讯作者（含共同）完成SCI研究性论文10篇，主要聚焦在固有免疫调控网络研究，鉴定了多个在抗病毒免疫应答过程的关键蛋白因子，并阐释了它们的效应机制，揭示了细胞自噬途径与抗病毒固有免疫应答交互渗透的工作模型，为抗感染和炎性疾病的治疗提供了理论依据和分子基础。
具体学术发现有：（1）阐述了经典自噬过程的多层次调控机制，详细研究了去泛素化酶蛋白和m6A RNA修饰严密控制细胞自噬发生的分子机理（EMBO Journal 2016；Cell Research 2018；Autophagy 2020b；Cell Reports 2020）；（2）揭示了内质网稳态与自噬调节固有免疫信号转导反应的效应机制（Molecular Cell 2017；Autophagy 2020a；EMBO Journal 2024）；（3）发现并阐释了干预细胞自噬可以治疗病毒感染及炎症性疾病的机制（Nature Communications 2022；Cell Death & Differentiation 2022；Autophagy 2023）。研究成果受到《中国科学报》、国家自然科学基金委科学传播中心官网、科学网等关注和报道。

承担课题

国家自然科学基金面上项目，2022/01-2025/12，主持，在研
国家自然科学基金面上项目，2020/01-2023/12，主持，结题
中央高校基本科研业务费中山大学创新人才培育计划项目，2023/01-2024/12，主持，结题
国家自然科学基金青年项目，2018/01-2020/12，主持，结题
中央高校基本科研业务费中山大学青年教师培育项目，2018/01-2020/12，主持，结题

论文专著

[1] ER-phagy restrains inflammatory responses through its receptor UBAC2, Xing He, Haowei He, Zitong Hou, Zheyu Wang, Qinglin Shi, Tao Zhou, Yaoxing Wu, Yunfei Qin, Jun Wang, Zhe Cai, Jun Cui, Shouheng Jin*, EMBO Journal 2024, 43(21):5057-5084;
[2] ATG4B antagonizes antiviral immunity by GABARAP-directed autophagic degradation of TBK1, Weihong Xie^#, Chenqiu Zhang^#, Zheyu Wang, Hui Chen, Tonghui Gu, Tao Zhou, Yaoxing Wu, Fan Xia, Min Li, Jun Wang, Renjie Jiao, Jun Cui, Shouheng Jin*, Autophagy 2023, 19(11):2853-2868;
[3] Suppression of ACE2 SUMOylation protects against SARS-CoV-2 infection through TOLLIP-mediated selective autophagy, Shouheng Jin^#, *, Xing He^#, Ling Ma, Zhen Zhuang, Yiliang Wang, Meng Lin, Sihui Cai, Lu Wei, Zheyu Wang, Zhiyao Zhao, Yaoxing Wu, Lin Sun, Chunwei Li, Weihong Xie, Yong Zhao, Zhou Songyang, Ke Peng, Jincun Zhao, Jun Cui*, Nature Communications 2022, 13(1):5204;
[4] Palmitoylation restricts SQSTM1/p62-mediated autophagic degradation of NOD2 to modulate inflammation, Lingli Zhou^#, Xing He^#, Liqiu Wang, Ping Wei, Zhe Cai, Song Zhang, Shouheng Jin*, Huasong Zeng*, Jun Cui*, Cell Death & Differentiation 2022, 29(8):1541-1551;
[5] Igniting autophagy through the regulation of phase separation, Shouheng Jin^#, *, Jun Cui*, 
Signal Transduction and Target Therapy 2020, 5(1):49, DOI: 10.1038/s41392-020-0154-6;
[6] High-throughput screening of functional deubiquitinating enzymes in autophagy, Shuo Tian^#, Shouheng Jin^#, Yaoxing Wu#, Tao Liu, Man Luo, Jiayu Ou, Weihong Xie, Jun Cui*, Autophagy 2020, 17(6):1367-1378; 
[7] The NEDD4-USP13 axis facilitates autophagy via deubiquitinating PIK3C3, Weihong Xie, Shouheng Jin*, Jun Cui*, Autophagy 2020, 16(6):1150-1151;
[8] Auto-ubiquitination of NEDD4-1 recruits USP13 to facilitate autophagy through deubiquitinating VPS34, Weihong Xie^#, Shouheng Jin^#, Yaoxing Wu, Huifang Xian, Shuo Tian, Di-Ao Liu, Zhiyong Guo, Jun Cui*, Cell Reports 2020, 30(8):2807-2819；
[9] LRRC59 modulates type I interferon signaling by restraining the SQSTM1/p62-mediated autophagic degradation of pattern recognition receptor DDX58/RIG-I, Huifang Xian^#, Shuai Yang^#, Shouheng Jin^#, *, Yuxia Zhang, Jun Cui*, Autophagy 2020, 22:16(3):408-418;
[10] The cross-regulation between autophagy and type I interferon signaling in host defense, Shouheng Jin*, Advances in Experimental Medicine and Biology 2019, 1209:125-144, DOI: 10.1007/978-981-15-0606-2_8;
[11] m6A RNA modification controls autophagy through upregulating ULK1 protein abundance, Shouheng Jin^#, Xiya Zhang^#, Yanyan Miao^#, Puping Liang, Kaiyu Zhu, Yuanchu She, Yaoxing Wu, Di-Ao Liu, Junjiu Huang, Jian Ren*, Jun Cui*, Cell Research 2018, 28(9):955-957; 
[12] BST2 inhibits type I IFN (interferon) signaling by accelerating MAVS degradation through CALCOCO2-directed autophagy, Shouheng Jin^#, Jun Cui*, Autophagy 2018, 14(1):171-172; 
[13] Tetherin suppresses type I interferon signaling by targeting MAVS for NDP52-mediated selective autophagic degradation in human cells, Shouheng Jin, Shuo Tian, Man Luo, Weihong Xie, Tao Liu, Tianhao Duan, Yaoxing Wu, Jun Cui*, Molecular Cell 2017, 68(2):308-322; 
[14] USP19 modulates autophagy and antiviral immune responses by deubiquitinating Beclin-1, Shouheng Jin^#, Shuo Tian^#, Yamei Chen^#, Chuanxia Zhang, Weihong Xie, Xiaojun Xia, Jun Cui*, Rong-Fu Wang*, EMBO Journal 2016, 35(8):866-880; 
[15] The BECN1-USP19 axis plays a role in the crosstalk between autophagy and antiviral immune responses, Jun Cui*, Shouheng Jin, Rong-Fu Wang*, Autophagy 2016, 12(7):1210-1211. 
注：^#第一作者，*通讯作者。