K
Kiichiro Tomoda
Researcher at Osaka Medical College
Publications - 33
Citations - 24267
Kiichiro Tomoda is an academic researcher from Osaka Medical College. The author has contributed to research in topics: Induced pluripotent stem cell & Stem cell. The author has an hindex of 18, co-authored 30 publications receiving 21439 citations. Previous affiliations of Kiichiro Tomoda include University of California, San Francisco & Gladstone Institutes.
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Journal ArticleDOI
Calcium Transients Closely Reflect Prolonged Action Potentials in iPSC Models of Inherited Cardiac Arrhythmia
C. Ian Spencer,Shiro Baba,Kenta Nakamura,Ethan A. Hua,Marie A.F. Sears,Chi-cheng Fu,Jianhua Zhang,Sadguna Y. Balijepalli,Kiichiro Tomoda,Yohei Hayashi,Paweena Lizarraga,Julianne Wojciak,Melvin M. Scheinman,Katriina Aalto-Setälä,Jonathan C. Makielski,Craig T. January,Kevin E. Healy,Timothy J. Kamp,Shinya Yamanaka,Bruce R. Conklin +19 more
TL;DR: It is suggested that LQTS mutations act partly on cytosolic Ca2+ cycling, potentially providing a basis for functionally targeted interventions regardless of the specific mutation site.
Journal ArticleDOI
Derivation conditions impact X-inactivation status in female human induced pluripotent stem cells.
Kiichiro Tomoda,Kazutoshi Takahashi,Karen N. Leung,Aki Okada,Megumi Narita,N. Alice Yamada,Kirsten Eilertson,Peter Tsang,Shiro Baba,Mark P. White,Salma Sami,Deepak Srivastava,Bruce R. Conklin,Barbara Panning,Shinya Yamanaka,Shinya Yamanaka +15 more
TL;DR: It is shown here that X- inactivation status in female hiPSC lines depends on derivation conditions, and feeders are a significant factor affecting X-inactivation status.
Journal ArticleDOI
Myeloid leukemia factor 1 regulates p53 by suppressing COP1 via COP9 signalosome subunit 3
TL;DR: It is shown that MLF1 is a negative regulator of cell cycle progression functioning upstream of the tumor suppressor p53, and its involvement in leukemogenesis through a novel CSN3–COP1 pathway is suggested.
Journal ArticleDOI
The Jab1/COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase activity and facilitates cell-cycle progression.
Kiichiro Tomoda,Jun-ya Kato,Tatsumi E,Takayuki Takahashi,Yoshinobu Matsuo,Noriko Yoneda-Kato +5 more
TL;DR: It is shown that Bcr-Abl tyrosine kinase facilitates the down-regulation of p27 by modulating complex formation of Jab1/CSN through the mitogen-activated protein (MAP) kinase and phosphatidylinositol 3 (PI3) Kinase signaling pathways.
Journal ArticleDOI
Prognostic significance of localized p27Kip1 and potential role of Jab1/CSN5 in pancreatic cancer.
Akihisa Fukumoto,Naoya Ikeda,Masayuki Sho,Kiichiro Tomoda,Hiromichi Kanehiro,Michiyoshi Hisanaga,Yoshikazu Tsurui,Masahiro Tsutsumi,Jun-ya Kato,Yoshiyuki Nakajima +9 more
TL;DR: The results of this study suggested that the mislocalization as well as the downregulation of p27Kip1 had significant prognostic value in pancreatic cancer and that Jab1 might play an important role in carcinogenesis of pancreaticcancer.