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Huangyuan TANG
唐华园

Assistant Investigator

Email:

tanghy@szbl.ac.cn

A Bit About Me

​

I received my Ph.D degree and Postdoctoral training at Peking University, where I uncovered the molecular mechanism underlying the metabolic reprogramming induced by IP3R-mediated calcium signaling that is essential for B cell maturation and proliferation. My research interests since then have been drawn to understanding how metabolism, (intracellular and extracellular) affect immune cell function.

 

Cellular metabolism is operated by a metabolic network consisting of more than 300 interconnecting metabolic pathways. This network property makes it possible that perturbations in certain metabolic site could lead to significant rearrangement of the overall network, which in turn induces prominent changes in cell function. I’m fascinated with this phenomenon and believe that dissecting the metabolic plasticity will certainly identify novel therapeutic strategies, through reprogramming immune cell activity, for immune-related disease treatment.

 

In terms of the extracellular metabolism, I’m particularly interested in the regulation of immune function by microbial metabolites. I have been trying to develop a novel genetic platform to report microbial metabolite receptor activity in live animal. By revealing the identity of the bacteria strain, the microbial metabolite and the corresponding receptor on immune cells, I hope to develop non-invasive therapies, such as microbiota modification and transplantation etc, for treating immune disorders.

​

EDUCATION AND PROFESSIONAL EXPERIENCE

  • 2021.6-2021.9   Assistant research fellow, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, China

  • 2017.10-2021.5  Postdoctoral Fellow, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, China

  • 2012.9-2017.7    Ph. D., Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University, Shenzhen, China

  • 2008.9-2012.7    Bachelor, Biological Sciences, Hunan Normal University, Hunan, China

 

GRANTS AND FUNDING

  • National Natural Science Foundation of China (Youth Foundation), Grant No. 31800767, Mechanistic study of the histone methyltransferases SETD2 in B lymphatic cell development, 2019/01-2020/12, CNY 160,000. Project leader

  • Shenzhen Basic Research Foundation, Grant No. JCYJ20170818090044949, The role of histone methyltransferases SETD2 in etiology of congenital heart disease, 2018/03-2020/03, CNY 500,000. Project leader

  • Guangdong Province Basic Research Foundation, Grant No. 2018A030310012, Mechanism of histone methylation modifications in etiology and pathology of congenital heart disease, 2018/05- 2021/04, CNY 100,000. Project leader

  • General Program of National Natural Science Foundation of China, Grant No. 81872783, The study of immuno-active multifunctional protein complexes in mediating antitumor activity of Chimeric antigen receptor (CAR)-redirected T lymphocytes, 2019/01-2021/12，CNY 570,000. Participant

  • Emergency Management Project of the National Natural Science Foundation of China，Grant No. 3174100332, Research and development of regulatory T cells with immune enhancing chimeric antigen receptor, 2018/01-2018/12, CNY 150,000. Participant

  • Basic Research Project of Shenzhen Science and Technology Plan, Grant No. CYJ20140509093817680, Mechanism of IP3 receptors of vascular smooth muscle cell in etiology and progression of hypertension, 2015/01-2016/12, CNY 300,000. Participant

  • General Program of National Natural Science Foundation of China Grant, Grant No. 31370823, The role of IP3 receptors in cardiomyocyte development and remodeling, 2014/01-2017/12，CNY 800,000. Participant

 

AWARD

  • 2017  NSFC/RGC Young Scholar Forum - Cardiovascular Ca2+ Signaling In Health and Disease, “Best Poster Presentation Award”

  • 2016  Peking University, “IKA Scholarship for Excellence”

  • 2015  Peking University, “Exceptional Research Award”

  • 2014  Peking University, “Power Leader Interdisciplinary Award”

​

PUBLICATION

  • H. Tang#*, Y. Li#, S. Wang#, J. Ji, X. Zhu, Y. Bao, C. Huang, Y. Luo, L. Huang, Y. Gao, C. Wei, J. Liu, X. Fang, L. Sun, K. Ouyang. IP3R-mediated Ca2+ signaling controls B cell proliferation through metabolic reprogramming. iScience. 2022 Apr 6;25(5):104209. doi: 10.1016/j.isci.2022.104209. （# equal contribution, * Corresponding author）

  • Y. Li#, H. Tang#, F. Chen#, J. Chen, H. Wang, Z. Chen, Y. Duan, X. Wang, L. Li, K. Ouyang .2021. SETD2 is essential for terminal differentiation of erythroblasts during fetal erythropoiesis, Biochem Biophys Res Commun. 552 (2021) 98-105. 10.1016/j.bbrc.2021.03.040. （# equal contribution）

  • Y. Duan#, H. Tang#, K. Mitchell-Silbaugh, X. Fang, Z. Han, K. Ouyang. 2020. Heat Shock Protein 60 in Cardiovascular Physiology and Diseases. Front Mol Biosci. doi: 10.3389/fmolb.2020.00073. （# equal contribution）

  • H. Tang, H. Wang, Q. Lin, F. Fan, F. Zhang, X. Peng, X. Fang, J. Liu, K. Ouyang. 2017. Loss of IP3 receptor-mediated Ca2+ release in mouse B cells results in abnormal B cell development and function. J Immunol. 199(2):570-580. doi: 10.4049/jimmunol.1700109.

  • Y. Duan, H. Wang, K. Mitchell-Silbaugh, S. Cai, F. Fan, Y. Li, H. Tang, G. Wang, X. Fang, J. Liu, N. Jia, R. Jing, K. Ouyang. 2019. Heat shock protein 60 regulates yolk sac erythropoiesis in mice. Cell Death Dis. 10:766. 10.1038/s41419-019-2014-2.

  • H. Wang, R. Jing, C. Trexler, Y. Li, H. Tang, Z. Pan , S.Zhu, B. Zhao, X. Fang, J. Liu, J. Chen, K. Ouyang. 2019. Deletion of IP3R1 by Pdgfrb-Cre in mice results in intestinal pseudo-obstruction and lethality. J Gastroenterol. 54(5):407-418.

  • Q. Lin, L. Zhao, R. Jing, C. Trexler, H. Wang, Y. Li, H. Tang, F. Huang, F. Zhang, X. Fang, J. Liu, N. Jia, J. Chen, K. Ouyang. 2019. Inositol 1,4,5‐Trisphosphate Receptors in Endothelial Cells Play an Essential Role in Vasodilation and Blood Pressure Regulation. J Am Heart Assoc. doi: 10.1161/JAHA.118.011704.

  • Y. Wang, J. Huang, W. Liu, X. Kou, H. Tang, H. Wang, X. Yu, S. Gao, K. Ouyang, HT. Yang. 2017. IP3R-mediated Ca2+ signals in hematopoietic and cardiac divergence of Flk1+ cells. J Mol Cell Biol. doi: 10.1093/jmcb/mjx014.

  • Q. Lin, G. Zhao, X. Fang, X. Peng, H. Tang, H. Wang, R. Jing, J. Liu, W. J. Lederer, J. Chen, and K. Ouyang. 2016. IP3 receptors regulate vascular smooth muscle contractility and hypertension. JCI Insight. 1:e89402 doi: 89410.81172/ jci.insight.89402.

  • K. Ouyang, R. Leandro Gomez-Amaro, D. L. Stachura, H. Tang, X. Peng, X. Fang, D.Traver, S. M. Evans, and J. Chen. 2014. Loss of IP3R-dependent Ca2+ signalling in thymocytes leads to aberrant development and acute lymphoblastic leukemia. Nat Commun. 5:4814 doi: 4810.1038/ncomms5814.

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