SELF-INTRODUCTION：

Dr. Mo Chen is an assistant professor in the Department of Pharmacology at the School of Medicine. She obtained her PhD from the National University of Singapore in 2013 and worked as a postdoctoral research fellow at the same university from 2014 to 2017. From 2017 to 2023, she served as a postdoctoral research associate and scientist at the University of Wisconsin Madison in the United States. In April 2023, she joined the Department of Pharmacology at the School of Medicine of the Southern University of Science and Technology.

Her main research interests are the molecular mechanisms of lipid signaling pathways in organelles, including lipid transfer proteins, phosphoinositide metabolism, lipid-protein complexes, lipid effector proteins, and related disease mechanisms. As the first/co-first author, she has published three articles in the authoritative journal of cell biology, Nature Cell Biology, and two articles in Cell Death & Differentiation. In total, she has published 13 SCI papers.

EDUCATION:

2009-08 to 2013-12, National University of Singapore, Biology, Doctor of Philosophy 

2005-09 to 2009-06, Sichuan University, Biotechnology, Bachelor of Science

WOKRING EXPERIENCE:

2023-04 to present, Assistant Professor, Department of Pharmacology, School of Medicine, Southern University of Science and Technology, China

2022-07 to 2023-03. Senior Scientist, School of Medicine and Public Health, University of Wisconsin Madison, US

2019-09 to 2022-07 Associate Scientist, School of Medicine and Public Health, University of Wisconsin Madison, US

2017-07 to 2019-09 Research Associate, School of Medicine and Public Health, University of Wisconsin Madison, US

2014-01 to 2017-06 Research Fellow, National University of Singapore, Singapore

HONORS AND AWARDS:

2015 Excellent young investigator award from the Singapore Cardiac Society, Singapore

2009-2013 Award of full research scholarship to PhD program from National University of Singapore, Singapore

2009 Outstanding University Graduates of Sichuan Province, Sichuan, China

2007 National Scholarship, China

RESEARCH:

This research group will utilize various methods such as biochemistry, cell biology, and mass spectrometry to study the regulation of lipid metabolism signaling, lipid transport between organelles, lipid-protein complex formation and biological function, and to understand the localization and mechanisms of lipids in non-membrane structures within organelles. We aim to analyze abnormal lipid metabolism function in diseases and develop new therapeutics targeting these mechanisms.

PUBLICATIONS：

1. Chen, M., Choi, S., Wen, T., Chen, C., Thapa, N., Lee, J. H., Cryns, V. L. & Anderson, R. A. A p53-phosphoinositide signalosome regulates nuclear AKT activation. Nat Cell Biol 24, 1099-1113 (2022). https://doi.org:10.1038/s41556-022-00949-1

2. Thapa, N.#, Chen, M.# (#co-first author), Horn, H. T., Choi, S., Wen, T. & Anderson, R. A. Phosphatidylinositol-3 kinase signalling is spatially organized at endosomal compartments by microtubule-associated protein 4. Nat Cell Biol 22, 1357-1370 (2020). https://doi.org:10.1038/s41556-020-00596-4

3. Choi, S.#, Chen, M.# (#co-first author), Cryns, V. L. & Anderson, R. A. A nuclear phosphoinositide kinase complex regulates p53. Nat Cell Biol 21, 462-475 (2019). https://doi.org:10.1038/s41556-019-0297-2

4. Chen, M., Qiu, T., Wu, J., Yang, Y., Wright, G. D., Wu, M. & Ge, R. Extracellular anti-angiogenic proteins augment an endosomal protein trafficking pathway to reach mitochondria and execute apoptosis in HUVECs. Cell Death Differ 25, 1905-1920 (2018). https://doi.org:10.1038/s41418-018-0092-9

5. Chen, M., Zhang, Y., Yu, V. C., Chong, Y. S., Yoshioka, T. & Ge, R. Isthmin targets cell-surface GRP78 and triggers apoptosis via induction of mitochondrial dysfunction. Cell Death Differ 21, 797-810 (2014). https://doi.org:10.1038/cdd.2014.3

6. Chen, M., Horn, H. T., Wen, T., Cryns, V. L. & Anderson, R. A. Assessing In Situ Phosphoinositide-Protein Interactions Through Fluorescence Proximity Ligation Assay in Cultured Cells. Methods Mol Biol 2251, 133-142 (2021). https://doi.org:10.1007/978-1-0716-1142-5_9

7. Chen, M., Wen, T., Horn, H. T., Chandrahas, V. K., Thapa, N., Choi, S., Cryns, V. L. & Anderson, R. A. The nuclear phosphoinositide response to stress. Cell Cycle 19, 268-289 (2020). https://doi.org:10.1080/15384101.2019.1711316

8. Chen, M. #, Choi, S. #(#co-first author), Jung, O. et al. The Specificity of EGF-Stimulated IQGAP1 Scaffold Towards the PI3K-Akt Pathway is Defined by the IQ3 motif. Sci Rep 9, 9126 (2019). https://doi.org/10.1038/s41598-019-45671-5

9. Kumar, S. #, Chen, M.# (#co-first author),  Li, Y., Wong, F. H., Thiam, C. W., Hossain, M. Z., Poh, K. K., Hirohata, S., Ogawa, H., Angeli, V. & Ge, R. Loss of ADAMTS4 reduces high fat diet-induced atherosclerosis and enhances plaque stability in ApoE(-/-) mice. Sci Rep 6, 31130 (2016). https://doi.org:10.1038/srep31130

10. Kao, C., Chandna, R., Ghode, A., Dsouza, C., Chen, M., Larsson, A., Lim, S. H., Wang, M., Cao, Z., Zhu, Y., Anand, G. S. & Ge, R. Proapoptotic Cyclic Peptide BC71 Targets Cell-Surface GRP78 and Functions as an Anticancer Therapeutic in Mice. EBioMedicine 33, 22-32 (2018). https://doi.org:10.1016/j.ebiom.2018.06.004

11. Venugopal, S., Kao, C., Chandna, R., Sulochana, K. N., Subramanian, V., Chen, M., Kini, R. M. & Ge, R. Angio-3, a 10-residue peptide derived from human plasminogen kringle 3, suppresses tumor growth in mice via impeding both angiogenesis and vascular permeability. Angiogenesis 21, 653-665 (2018). https://doi.org:10.1007/s10456-018-9616-7

12. Venugopal, S., Chen, M., Liao, W., Er, S. Y., Wong, W. S. & Ge, R. Isthmin is a novel vascular permeability inducer that functions through cell-surface GRP78-mediated Src activation. Cardiovasc Res 107, 131-142 (2015). https://doi.org:10.1093/cvr/cvv142

13. Zhang, Y., Chen, M., Venugopal, S., Zhou, Y., Xiang, W., Li, Y. H., Lin, Q., Kini, R. M., Chong, Y. S. & Ge, R. Isthmin exerts pro-survival and death-promoting effect on endothelial cells through alphavbeta5 integrin depending on its physical state. Cell Death Dis 2, e153 (2011). https://doi.org:10.1038/cddis.2011.37