特聘研究员
博士后
博士
发掘预防与治疗传染性疾病的生物靶点。课题组主要探讨机体内病原微生物的致病机理;探讨宿主免疫系统、细胞代谢防御病原微生物的分子机理。包括:1.病原微生物的致病机理;2.机体抵抗病原微生物感染的分子机理;3.新抗菌分子的筛选和鉴定。课题组学术氛围浓厚,成员和谐友爱,共同进步,欢迎对感染、免疫、代谢等研究内容感兴趣的同学或研究人员加入我们课题组。
陈美欣博士师从长江学者崔隽教授,于2018年在中山大学获得博士学位。随后加入耶鲁大学医学院Jorge E. Galán双院院士(病原感染领域先驱)的课题组从事博士后研究工作,期间主要研究免疫代谢与抗感染免疫调控。2021年全职加入深圳湾实验室,任传染病研究所特聘研究员。陈美欣博士长期致力于宿主免疫与病原感染的互作。陈美欣博士的研究首次揭示DNA识别受体cGAS蛋白泛素化修饰在防御病原感染过程中的重要功能与调控机制,首次利用代谢物识别器等工具揭示宿主细胞中代谢物衣康酸的抗菌通路。陈美欣博士的研究工作揭示病原体致病与宿主防御病原感染的功能与机制,完善与填补有关宿主与病原互作的知识体系。陈美欣博士的成果发表于Science、Molecular Cell、Nature Microbiology、Advanced Science、Nature Communications等期刊,作为独立通讯作者成果投于Nature Metabolism(Revised and resubmitted)、Nature Microbiology(Submitted)国际著名期刊;申请专利三项;主持国家自然科学基金、深圳市医学院专项基金等;获取广东省珠江人才计划青年拔尖人才项目、深圳市国家级领军A类人才等荣誉。
线粒体代谢物衣康酸的抑菌通路
1.Chen, M.#, Sun, H. #, Boot, M., Shao, L., Chang, S.J., Wang, W., Lam, T.T., Lara-Tejero, M., Rego, E.H. and Galán, J.E. *, 2020. Itaconate is an effector of a Rab GTPase cell-autonomous host defense pathway against Salmonella. Science, 369(6502), pp.450-455.
2.Lian, H. #, Park, D. #,Chen, M., Schueder, F., Lara-Tejero, M., Liu, J., & Galán, J. E*, 2023. Parkinson’s disease kinase LRRK2 coordinates a cell-intrinsic itaconate-dependent defence pathway against intracellular Salmonella. Nature Microbiology, 1-16.
These pubilications demonstrate that Rab32/LRRK2 facilitates the delivery of itaconate to the Salmonella-containing vacuoles, which allows itaconate to inhibit bacterial growth. Our results have been cited by the itaconate expert Luke O’Neil for several times in articles/reviews. The HHMI professor John D. MacMicking cited our publication in their Science paper revealing the important antibacterial protein APOL3. Karine Auclairp group has repeated our key results successfully and made some other discoveries.
3.Chen, M.#, Zhao, Z. #, Meng, Q. #, Liang, P. #, Su, Z., Wu, Y., Huang, J. and Cui, J. *, 2019. TRIM14 Promotes Noncanonical NF‐kB Activation by Modulating p100/p52 Stability via Selective Autophagy. Advanced Science, p.1901261.
This paper demonstrates that TRIM14 enhances p100/p52 processing in Noncanonical NF-kB signaling. It has been cited by many groups. Jiankun Wu group repeated our key results and made some other discoveries.
4.Chen, M.#, Meng, Q. #, Qin, Y. #, Liang, P., Tan, P., He, L., Zhou, Y., Chen, Y., Huang, J. *, Wang, R.F. * and Cui, J. *, 2016. TRIM14 inhibits cGAS degradation mediated by selective autophagy receptor p62 to promote innate immune responses. Molecular cell, 64(1), pp.105-119.
This paper firstly demonstrated the mechanical details of cGAS ubiquitination, which was important in autophagic degradation of cGAS and resisting virus infection in innate immunity. It has been cited by many groups in their research articles or reviews, including Katherine A. Fitzgerald and Beth Levine, who are experts in the field of innate immunity and autophagy.
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