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Žๅ‚ศŒค‹†‹ฦั

Honda, T., Morii, M., Nakayama, Y., Suzuki, K., Yamaguchi, N.-t., and Yamaguchi, N.: v-Src-driven transformation is due to chromosome abnormalities but not Src-mediated growth signaling. Sci. Rep., 8: 1063, (2018).

Morii, M., Kubota, S., Honda, T., Yuki, R., Morinaga, T., Kuga, T., Tomonaga, T., Yamaguchi, N.-t., and Yamaguchi, N.: Src acts as an effector for Ku70-dependent suppression of apoptosis through phosphorylation of Ku70 at Tyr-530. J. Biol. Chem., 292: 1648-1665, (2017).

Honda, T.*, Soeda, S.*, Tsuda, K., Yamaguchi, C., Aoyama, K., Morinaga, T., Yuki, R., Nakayama, Y., Yamaguchi, N.-t., and Yamaguchi, N. (*These authors contributed equally to this work.): Protective role for lipid modifications of Src-family kinases against chromosome missegregation. Sci. Rep., 6: 38751, (2016).

Makiyama, T., Nakamura, H., Nagasaka, N., Yamashita, H., Honda, T., Yamaguchi, N., Nishida, A., and Murayama, T.: Trafficking of acetyl-C16-ceramide-NBD with long-term stability and no cytotoxicity into the Golgi. Traffic, 16: 476-492, (2015).

Soeda, S., Nakayama, Y., Honda, T., Aoki, A., Tamura, N., Abe, K., Fukumoto, Y., and Yamaguchi, N. :v-Src causes delocalization of Mklp1, Aurora B, and INCENP from the spindle midzone during cytokinesis failure. Exp. Cell Res., 319: 1382-1397, 2013.


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