个人简介
Wang Min, Ph.D., received his B.S. degree in Microbiology from Wuhan University in 1984, his M.S degree in Cell Biology at Shanghai Institute of Cell Biology, Chinese Academy of Sciences, in 1989, and his Ph.D degree in Genetics at University of Wales, Swansea, U.K., in 1993. He then performed 4-year post-doctoral training in vascular biology and immunology at the Department of Pathology, Yale School of Medicine. He became a Senior Scientist and Project Leader at GeneMedicine, Inc., in 1997 and then an Assistant Professor at University of Rochester, NY, in 1999. In 2003, he was recruited back to Department of Pathology and Vascular Biology Program at Yale School of Medicine, where he was promoted to Professor with Tenure in 2013. Dr. Min is a member of NAVBO, AHA, Yale Stem Cell Center and Yale Cancer Center. Dr. Min is also a Guest Professor at Sun Yat-sen University and an Honorary Professor at Zhejiang University. The goal in Dr. Min's lab is to dissect the signaling pathways, establish mouse models, and define the fundamental mechanisms involved in vascular development, remodeling, and repair related to human diseases such as vascular malformation, ischemia, and stroke. Dr. Min's lab has extensively employed biochemical, cell biological, and mouse genetic approaches to define the critical molecules mediating vascular development, remodeling, and repair. Dr. Min serves on the editorial board of Arteriosclerosis, Thrombosis, and Vascular Biology, the Chinese Journal of Cell Biology, the Vascular Biology Publications Alert NAVBO (North American Vascular Biology Organization), World Journal of Experimental Medicine, and Frontiers in Physiology. Dr. Min has been the recipient of many awards, including the Irvine H. Page Young Investigator Research Award, the AHA Established Investigator Award, and the JACC Parmley Award.
PhD University of Wales, Swansea, UK (1993)
Postdoctoral Fellow Yale University School of Medicine
Postdoctoral Associate Yale University School of Medicine
近期论文
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Tumor-Associated Macrophages Drive Spheroid Formation During Early Transcoelomic Metastasis of Ovarian Cancer
Yin, M, Li, X, Tan S, Zhou HJ, Zhang HF, Ji, W, Bellone, S, Santin, A, Ge, L, Min, W* (2016) Tumor-Associated Macrophages Drive Spheroid Formation During Early Transcoelomic Metastasis of Ovarian Cancer. J Clin Invest. ePub on Oct 10.
Endothelial exocytosis of angiopoietin-2 resulting from CCM3-deficiency contributes to cerebral cavernous malformation.
Zhou HJ, Qin L, Zhang H, Tang, W, Ji, W, He Y, Liang, X, Wang Z, Yuan Q, Vortmeyer A, Toomre D, Fuh G, Yan M, Kluger MS, Wu D, Min W* (2016). Endothelial exocytosis of angiopoietin-2 resulting from CCM3-deficiency contributes to cerebral cavernous malformation. Nature Medicine 22(9):1033-42.
Leukaemia-associated Rho guanine nucleotide exchange factor (LARG) plays an agonist specific role in platelet function through RhoA activation.
Zou S, Teixeira AM, Yin M, Xiang Y, Xavier-Ferruccio J, Zhang PX, Hwa J, Min W, Krause DS. (2016) Leukaemia-associated Rho guanine nucleotide exchange factor (LARG) plays an agonist specific role in platelet function through RhoA activation. Thromb Haemost. 116(3). 116(3):506-16. Cover story at https://th.schattauer.de/en/contents/archive/issue/2392/manuscript/26004.html
The role of adipose-derived inflammatory cytokines in type 1 diabetes
Shao, L, Feng, B, Zhang, Y, Zhou, HJ, Ji, W, Min W* (2016) The role of adipose-derived inflammatory cytokines in type 1 diabetes. Adipocyte. 5(3):270-4.
SENP1-mediated NEMO deSUMOylation in the adipocyte limits inflammatory responses and type 1 diabetes progression.
Shao, L, Zhou HJ, Zhang H, Qin L, Hwa, J, Yun Z, Ji, W, Min W* (2015). SENP1-mediated NEMO deSUMOylation in the adipocyte limits inflammatory responses and type 1 diabetes progression. Nature Communications 6:8917. doi: 10.1038/ncomms9917.
AIP1/DAB2IP-mediated signaling in tumor niche suppresses tumor progression and metastasis.
Ji W, Li Y, He, Y., Yin M., Zhou, HJ., Boggon TJ., Zhang H., Min W.* (2015). AIP1/DAB2IP-mediated signaling in tumor niche suppresses tumor progression and metastasis. Cancer Res 75(17):3492-504.
AIP1-Mediated Stress Signaling in Atherosclerosis and Arteriosclerosis"
Zhang, JQ, Zhou, HJ, Ji, W, Min W.* (2015). AIP1-Mediated Stress Signaling in Atherosclerosis and Arteriosclerosis" Current Atherosclerosis Reports, 17(5):503.
Thioredoxin-2 inhibits mitochondrial ROS generation and ASK1 activity to maintain cardiac function.
Huang Q., Zhou HJ, Zhang H, Zhou HJ, Huang Y, Fan P., Yao L., Belardinelli L, Tellides T, Giordano FJ, Budas GR, Min W* (2015). Thioredoxin-2 inhibits mitochondrial ROS generation and ASK1 activity to maintain cardiac function. Circulation 131(12):1082-97.
AIP1 mediates VEGFR3-dependent angiogenic and lymphangiogenic responses.
Zhou, HJ, Chen, X, Huang, Q., Zhang, H, Wang, Y, Yu, J, Liu, R, Li, Y, Xu, Z, and Min, W.* (2014) AIP1 mediates VEGFR3-dependent angiogenic and lymphangiogenic responses. Arterioscler Thromb Vasc Biol. 34(3):603-15.
Important roles of the CCM3 and STK24 Complex in regulation of Ca2+-stimulated exocytosis.
Zhang, Y., Tang, W., Zhang, H., Niu, X., Xu, Y., Zhang, J., Gao, K., Boggon, TJ., Toomre, D., Min, W.*, Wu, D.* Important roles of the CCM3 and STK24 Complex in regulation of Ca2+-stimulated exocytosis. Dev Cell. 27(2):215-26. (*Min is co-corresponding author).
SOCS1 prevents graft arteriosclerosis by preventing endothelial cell function.
Qin, L., Huang, Q., Zhang, H., Liu, R., Tellides, G., Min, W*, Yu, L*. (2014). SOCS1 prevents graft arteriosclerosis by preventing endothelial cell function. J Amer Coll of Cardiol. 63(1):21-9 (*Min is contacting senior author). Also see commentary in this issue by Weger, RA Immune regulators regulated to prevent transplant reactions. This work was the winner for JACC Parmley Award in 2013.
H19 IncRNA acts as a natural sponge for let-7 miRNAs.
Kallen, AN., Xu, J., Qiao, C., Martinet, C., Lu, L., Ma, J., Zhou, XB., Yan, L., Liu, C., Yi, JS., Zhang, H., Min, W., Gregory, RI., Bennett, AM., Gabory, A., Dandolo, L., Huang, Y. (2013). H19 IncRNA acts as a natural sponge for let-7 miRNAs. Mol Cell. 52(1):101-12.
TNF, Acting through Inducibly Expressed TNFR2, Drives Activation and Cell Cycle Entry of c-kit+ Cardiac Stem Cells in Ischemic Heart Disease.