
Dr. Hajime Yurugi
PostDoc
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
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.


