To assess the mechanical nature of the critical membrane sites and the mechanism by which the critical membrane site supports the resilience of life.
Yoshihiro Ujihara
Department of Electrical and Mechanical Engineering, Nagoya Institute of Technology
Selected publications
-
Y. Ogura, H. Ito, S. Sugita, M. Nakamura, Y. Ujihara*. Decrease in Ca2+ concentration in quail cardiomyocytes is faster than that in rat cardiomyocytes. Processes, 10: 508 (2022)
-
K. Hashimoto*, A. Kodama, M. Ohira, M. Kimoto, R. Nakagawa, Y. Usui, Y. Ujihara, A. Hanashima, S. Mohri. Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15, iScience, 25: 104337 (2022).
-
Y. Ujihara, M. Kanagawa, S. Mohri, S. Takatsu, K. Kobayashi, K. Naruse, Y. Katanosaka*. Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure. Nat Commun, 10: 5754 (2019)
-
Y. Ujihara, K. Iwasaki, S. Takatsu, K. Hashimoto, K. Naruse, S. Mohri, Y. Katanosaka*. Induced NCX1 overexpression attenuates pressure overload-induced pathological cardiac remodeling. Cardiovasc Res, 111:348-61 (2016)
-
Y. Katanosaka*, K. Iwasaki, Y. Ujihara, S. Takatsu, K. Nishitsuji, M. Kanagawa, A. Sudo, T. Toda, K. Katanosaka, S. Mohri, K. Naruse. TRPV2 is critical for cardiac function and compensatory hypertrophic response to hemodynamic stress. Nat Commun, 5: 3932 (2014)
Group A01 (Ujihara)
Mechanical quantification of critical membrane sites and evaluation of resilience dependent on unique membrane structures