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Sei Yoshida(jitian zheng) |
Gender: male Department: 遗传学和细胞生物学系 Tel: Office Location: A402 Career: Professor Major: Cell Biology Email: seiyoshi@nankai.edu.cn Address: |
ResumeMy name is Sei Yoshida (吉田 整). I got my PhD at 東京大学, then spent more than 10 years at the University of Michigan in the US. I moved to 南开大学生命科学学院 to start my lab. If you are interested in Cell Biology (membrane trafficking, macrophage) and/or study in the US/Japan, please contact me.
Education2002 PhD. University of Tokyo, Japan
WorkExperience2002-2006: University of Tokyo
2006-2009: The University of Michigan
2009-2010: Univeristy of lIlinois at Chicago
2010-2020: The University of Mihigan
2020-: Nankai Univeristy, the School of Life Sciences
Research FieldsI got my PhD by studying host-pathogen interaction at the University of Tokyo, Japan, in 2002 (EMBO 2002; Trends in Microbiol 2003; and Science 2006, as first author). In 2006 I moved to the University of Michigan in to investigate PI3-mTORC1 pathway, one of the main signaling pathways of cell growth. I developed quantitative phase/fluorescence live-cell imaging techniques and identified that PI3K orchestrates macropinocytosis, a large-scale endocytosis (J Cell Sci 2009; and Front Physiol 2015a, as first author). My research also showed that macropinocytosis is a major mechanism for delivering extracellular amino acids into endolysosomal compartments in the activation of mTORC1 (J Biol Chem 2011 and J Cell Biol 2015b, as first author). In 2016 I was promoted to research faculty to establish independent projects (J Leuk Biol 2017; Cell Mol Life Sci 2018a; Phil Trans Royal Society B 2018b; and J Cell Sci 2018c; as corresponding author).The extensive breadth and diversity in my research areas (cell biology, biochemistry, microbiology, and immunology) have enabled me to make momentous contributions to the understanding of human health and disease. As a faculty of Nankai University, the College of Life Sciences, I am interested in the physiological/pathological functions of macropinocytosis in cancer development, immunology, and kidnye diseases. Achievement1. Swanson JA* and Yoshida S*. (2018). Macropinosomes as units of signal transduction. Philosophical Transactions of the Royal Society B. 374: 20180157 (review)
*Co-corresponding Author
2. Yoshida S*, Pacitto R, Sesi C, Kotula L, and Swanson J*. (2018). Dorsal Ruffles Enhance Activation of Akt by Growth Factors. Journal of Cell Science. 131: jcs220517 doi: 10.1242/jcs.220517
*Co-corresponding Author Highlighted in “First Person” (J Cell Sci 2018 131: jcs226373) Highlighted in “Research Highlight” (J Cell Sci 2018 131: e2201)
3. Rosselli-Murai LK, Yates JA, Yoshida S, Bourg J, HoKKY, White M, Prisby J, Tan X, Altemuc M, Bao L, Wu ZF, Veatch SL, Swanson JA, Merajver SD, and Liu AP. (2018). Loss of PTEN promotes formation of signaling-capable clathrin-caoted pits. Journal of Cell Science.131: jcs208926 doi: 10.1242/jcs.208926
4. Yoshida S, Pacitto R, Inoki K and Swanson J. (2018). Macropinocytosis, mTORC1 and Cellular Growth Control. Cellular and Molecular Life Sciences. 75: 1227-1239 doi: 10.1007/s00018-017-2710-7 (review)
5. Pacitto R, Gaeta I, Swanson JA and Yoshida S*. (2017). CXCL12-induced macropinocytosis modulates two distinct pathways to activate mTORC1 in macrophages. Journal of Leukocyte Biology. 101: 683-692 doi: 10.1189/jlb.2A0316-141RR
*Corresponding Author Highlighted on the cover
6. Yao Y, Wang J, Yoshida S, Nada S, Okada M and Inoki K. (2016). Role of Ragulator in the Regulation of Mechanistic Target of Rapamycin Signaling in Podocytes and Glomerular Function. Journal of American Society of Nephrology. 27: 3653-3665 doi: 10.1681/ASN2015010032
7. Swanson JA and Yoshida S. (2016). Macropinocytosis. Encyclopedia of Cell Biology. (R.A. Bradshaw and P. Stahl, Eds.). 2: 758-765. (Book chapter)
8. Yoshida S, Pacitto R, Yao Y, Inoki K and Swanson JA. (2015). Growth Factor Signaling to mTORC1 by Amino Acid-laden Macropinosomes. Journal of Cell Biology. 211: 159-172. doi: 10.1083/jcb.201504097
Highlighted in “Research Round-up” (J Cell Biol. 2015. 211: 1)
9. Yoshida S, Gaeta I, Pacitto R, Krienke L, Alge O, Gregorka B and Swanson JA. (2015). Differential signaling During Macropinocytosis in Response to M-CAF and PMA in Macrophages. Frontiers in Physiology. 6:8. doi: 10.3389/fphys.2015.00008.
10. Huber TB, Edelstein CL, Hartleben B, Inoki K, Jiang M, Koya D, Kume S, Lieberthal W, Pallet N, Quiroga A, Ravichandran K, Susztak K, Yoshida S and Dong Z. (2012). Emerging role of autophagy in kidney function, diseases and aging. Autophagy. 8: 1009-1031. (Review)
All authors contributed equally
11. Feliciano WD, Yoshida S, Straight SW, and Swanson JA. (2011). Coordination of the Rab5 cycle on macropinosomes. Traffic. 12:1911-1922. doi: 10.1111/j.1600-0854.2011.01280.x.
12. Yoshida S, Hong S, Suzuki T, Nada S, Mannan AM, Wang J, Okada M, Guan KL, and Inoki K. (2011). Redox regulates mTORC1 activity by modulating the TSC1/TSC2-Rheb pathway. Journal of Biological Chemistry. 286:32651-32660.
13. Inoki K, Mori H, Wang J, Suzuki T, Hong S, Yoshida S, Blattner SM, Ikenoue T, Ruegg MA, Hall MN, Kwiatkowski DJ, Rastaldi MP, Huber TB, Kretzler M, Holzman LB, Wiggins RC, Guan KL. (2011). mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice. Journal of Clinical Investigation.121:2181-2196.
14. Narita M, Young AR, Arakawa S, Samarajiwa SA, Nakashima T, Yoshida S, Hong S, Berry LS, Reichelt S, Ferreira M, Tavare S, Inoki K, Shimizu S, Narita M. (2011). Spatial coupling of mTOR and autophagy augments secretory phenotypes. Science. 332: 966-970.
15. Nagamatsu K, Kuwae A, Konaka T, Negal S, Yoshida S, Eguichi M, Watanabe M, Mimuro H, Koyasu S, Abe A. (2009). Bordetella evades the host immune system by inducing IL-10 through a type III effector, BopN. Journal of Experimental Medicine. 206:3073-3088.
16. Yoshida S, Hoppe AD, Araki N, and Swanson JA. (2009). Sequential signaling in plasma-membrane domains during macropinosome formation in macrophages. Journal of Cell Science. 122:3250-3261. doi: 10.1242/jcs.053207.
Highlighted in “In this issue” (J Cell Sci. 2009. 122)
17. Yoshida S, Handa Y, Suzuki T, Ogawa M, Suzuki M, Tamai A, Abe A, Katayama E, and Sasakawa C. (2006). Microtubule-severing activity of Shigella is pivotal for intercellular spreading. Science. 314:985-989.
Highlighted in “Perspectives” (Science, 2006. 314:931) Highlighted in “Research Highlights” (Nature, 2006. 444:246)
18. Matsuzawa T, Kuwae A, Yoshida S, Sasakawa C and Abe A. (2004). Enteropathogenic Escherichia coli activates the RhoA signaling pathway via the stimulation of GEF-H1. EMBO Joural. 23:3570-3582.
19. Yoshida S and Sasakawa C. (2003). Exploiting host microtubule dynamics: A new aspect of bacterial invasion. Trends in Microbiology. 11:139-143. (Review)
20. Yoshida S, Katayama E, Kuwae A, Mimuro H, Suzuki T, and Sasakawa C. (2002). Shigella delivers an effector protein to trigger host microtubule dynamic-instability, which promotes Rac1 activity and efficient bacterial internalization. EMBO Journal. 21:2923-2935.
Highlighted in “Research Round-up” (J Cell Biol. 2002. 158:10)
21. Kuwae A, Yoshida S, Tamano K, Mimuro H, Suzuki T, and Sasakawa C. (2001). Shigella invasion of macrophage requires the insertion of IpaC into the host plasma membrane. Journal of Biological Chemistry. 276:32230-32239.
Complete List of Published Work in My Bibliography: http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/49444569/?sort=date&direction=ascending
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