
Dr. Hajime Yurugi
PostDoc
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Hajime Yurugi was born and grew up in Kyoto, Japan. During his doctorate work, he studied the function of the protein prohibitin in immune cells.
He found that both prohibitin-1 and -2 are induced on the surface of T cells in response to activation and play a critical role in T cell signaling. In Sep 2013, he received Doctorate of Biotechnology from Kyoto Sangyo University, Kyoto, Japan.
In Nov 2013, he joined Dr. Krishnaraj Rajalingam's Group as a Postdoctoral Fellow.
EXPERIENCE
2013 - Present Postdoctoral Fellow, Rajalingam lab, MSU at the Institute for
Immunology, Unimedizin Mainz (previous: Institute for Biochemistry
II, Goethe-University, Frankfurt, Frankfurt-am-Main, Germany)
EDUCATION
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2009-2013 Doctorate of Biotechnology, Kyoto Sangyo University, Kyoto, Japan.
2007-2009 Master of Biotechnology, Kyoto Sangyo University, Kyoto, Japan.
2003-2007 Bachelor of Biotechnology, Kyoto Sangyo University, Kyoto, Japan.
PUBLICATIONS
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Yurugi H, Marini F, Weber C, David K, Zhao Q, Binder H, Désaubry L, Rajalingam K. Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours. Oncogene. 2017 Apr 17. doi: 10.1038/onc.2017.93.
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​Murali A, Shin J, Yurugi H, Krishnan A, Akutsu M, Carpy A, Macek B, Rajalingam K. Ubiquitin-dependent regulation of Cdc42 by XIAP. Cell Death Dis. 2017 Jun 29;8(6):e2900. doi: 10.1038/cddis.2017.305.
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H. Yurugi, K. Rajalingam, A Role For Prohibitin in Mast Cell Activation: Location Matters., Science Signaling. 292 (2013) pe29
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H. Yurugi, S. Tanida, A. Ishida, K. Akita, M. Toda, and H. Nakada, Prohibitins function as endogenous ligands for Siglec-9 and negatively regulate TCR signaling upon ligation., Biochemical and Biophysical Research Communications. 434 (2013) 376-381
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H. Yurugi, S. Tanida, A. Ishida, K. Akita, M. Toda, M. Inoue, and H. Nakada, Expression of prohibitins on the surface of activated T cells., Biochemical and Biophysical Research Communications. 420 (2012) 275-280.
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M. Toda, R. Hisano, H. Yurugi, K. Akita, K. Maruyama, M. Inoue, and H. Nakada, Ligation of tumour-produced mucins to CD22 dramatically impairs splenic marginal zone B-cells., The Biochemical Journal. 417 (2009) 673-83.