Kiichiro Tomoda’s lab specializes in stem cell biology and regenerative medicine. His research focuses on how environmental signals impact the ability of human induced pluripotent stem (iPS) cells to grow and differentiate into specific cell types. He also studies fundamental aspects of cell biology, such as protein synthesis or the maintenance of specialized intracellular units called organelles, to improve the quality of iPS cells. One of Tomoda’s research goals is to model human disease using tissue generated from human iPS cells. These models are vital for studying the biological processes underlying conditions such as neurodegenerative diseases, heart diseases, and infectious diseases.
Disease Areas
Areas of Expertise
Lab Focus
Research Impact
Tomoda was part of Shinya Yamanaka’s lab when the team discovered ways to turn adult human cells into induced pluripotent stem cells. Human iPS cells provide the research community with an infinite source of stem cells that can be turned into any cell type in the body, without the technical and ethical limitations of stem cells derived from human embryos.
Since this seminal discovery, Tomoda’s work has focused on improving the quality of human iPS cells. He is particularly interested in the epigenetic modifications that restrict the differentiation potential of stem cells, thus limiting their applications for research or clinical uses. More recently, Tomoda has been investigating fundamental biological events, such as protein synthesis and the maintenance of a specialized intracellular unit known as small organelles, in iPS cells. Understanding these cell biology events, along with the epigenetic regulation of stem cells, helps Tomoda’s team harness stem cell technology toward applications such as regenerative medicine and disease modeling. In particular, Tomoda has combined CRISPR gene editing with human iPS cell technology to model human diseases and used these models for drug discovery.
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Professional Titles
Research Investigator, Gladstone Institutes
Associate Professor, Center for iPS Cell Research and Application, Kyoto University, Japan
Bio
Kiichiro Tomoda, PhD, is a research investigator at the Gladstone Institute of Cardiovascular Disease and associate professor at the Center for iPS Cell Research and Application, Kyoto University, Japan.
A native of Japan, Tomoda earned a bachelor’s degree at Osaka University and a PhD in molecular biology at the Nara Institute of Science and Technology in Nara, Japan, where he also conducted his postdoctoral training and became an assistant professor in 2003. Tomoda joined Gladstone as a research scientist in 2007 and trained for 3 years in stem cell biology as a California Institute for Regenerative Medicine Scholar, before becoming a staff research investigator at Gladstone in 2013. He became a junior associate professor in the department of pharmacology at Osaka Medical College in Osaka, Japan, in 2016, and an associate professor in 2019. In March 2020, he joined the Center for iPS Cell Research and Application, Kyoto University in Kyoto, Japan, where he is an associate professor.
Honors and Awards
2009–2012 CIRM Scholar Fellowship, California Institute for Regenerative Medicine
2000–2003 Postdoctoral Fellowship, Japan Society for the Promotion of Science
2000 NAIST Award, Nara Institute of Science and Technology, Japan
Publications
- Synthetic Embryology: Early Mammalian Embryo Modeling Systems from Cell Cultures. Tomoda K, Kime C. Dev Growth Differ. 2021 Feb 04.
- Fluctuation in O-GlcNAcylation inactivates STIM1 to reduce store-operated calcium ion entry via down-regulation of Ser621 phosphorylation. Nomura A, Yokoe S, Tomoda K, Nakagawa T, Martin-Romero FJ, Asahi M. J Biol Chem. 2020 Dec 11; 295(50):17071-17082.
- Fluctuation in O-GlcNAcylation inactivates STIM1 to reduce store-operated calcium ion entry via down-regulation of Ser621 phosphorylation. J Biol Chem. 2020 Dec 11; 295(50):17071-17082.
- Intravenously Injected Pluripotent Stem Cell-derived Cells Form Fetomaternal Vasculature and Prevent Miscarriage in Mouse. Daimon A, Morihara H, Tomoda K, Morita N, Koishi Y, Kanki K, Ohmichi M, Asahi M. Cell Transplant. 2020 Jan-Dec; 29:963689720970456.
- Overexpression of Na+/H+ exchanger 1 specifically induces cell death in human iPS cells via sustained activation of the Rho kinase ROCK. Wakabayashi S, Morihara H, Yokoe S, Nakagawa T, Moriwaki K, Tomoda K, Asahi M. J Biol Chem. 2019 12 20; 294(51):19577-19588.
- Induced 2C Expression and Implantation-Competent Blastocyst-like Cysts from Primed Pluripotent Stem Cells. Kime C, Kiyonari H, Ohtsuka S, Kohbayashi E, Asahi M, Yamanaka S, Takahashi M, Tomoda K. Stem Cell Reports. 2019 09 10; 13(3):485-498.
- BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence. Proc Natl Acad Sci U S A. 2016 11 15; 113(46):13057-13062.
- Autotaxin-mediated lipid signaling intersects with LIF and BMP signaling to promote the naive pluripotency transcription factor program. Proc Natl Acad Sci U S A. 2016 11 01; 113(44):12478-12483.
- Practical Integration-Free Episomal Methods for Generating Human Induced Pluripotent Stem Cells. Curr Protoc Hum Genet. 2015 Oct 06; 87:21.2.1-21.2.21.
- Structure-based discovery of NANOG variant with enhanced properties to promote self-renewal and reprogramming of pluripotent stem cells. Proc Natl Acad Sci U S A. 2015 Apr 14; 112(15):4666-71.
- Calcium transients closely reflect prolonged action potentials in iPSC models of inherited cardiac arrhythmia. Stem Cell Reports. 2014 Aug 12; 3(2):269-81.
- Derivation conditions impact X-inactivation status in female human induced pluripotent stem cells. Cell Stem Cell. 2012 Jul 06; 11(1):91-9.
- G(i)-coupled GPCR signaling controls the formation and organization of human pluripotent colonies. Nakamura K, Salomonis N, Tomoda K, Yamanaka S, Conklin BR. PLoS One. 2009 Nov 10; 4(11):e7780.
- Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Takahashi K, Tanabe K, Ohnuki M, Narita M, Ichisaka T, Tomoda K, Yamanaka S. Cell. 2007 Nov 30; 131(5):861-72.
- Preparation and characterization of monoclonal antibodies against mouse Jab1/CSN5 protein. Kato JY, Nakamae I, Tomoda K, Fukumoto A, Yoneda-Kato N. Hybridoma (Larchmt). 2006 Dec; 25(6):342-8.
- Depletion of Jab1 inhibits proliferation of pancreatic cancer cell lines. Fukumoto A, Tomoda K, Yoneda-Kato N, Nakajima Y, Kato JY. FEBS Lett. 2006 Oct 30; 580(25):5836-44.
- Myeloid leukemia factor 1 regulates p53 by suppressing COP1 via COP9 signalosome subunit 3. Yoneda-Kato N, Tomoda K, Umehara M, Arata Y, Kato JY. EMBO J. 2005 May 04; 24(9):1739-49.
- Small Jab1-containing subcomplex is regulated in an anchorage- and cell cycle-dependent manner, which is abrogated by ras transformation. Fukumoto A, Tomoda K, Kubota M, Kato JY, Yoneda-Kato N. FEBS Lett. 2005 Feb 14; 579(5):1047-54.
- The Jab1/COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase activity and facilitates cell-cycle progression. Tomoda K, Kato JY, Tatsumi E, Takahashi T, Matsuo Y, Yoneda-Kato N. Blood. 2005 Jan 15; 105(2):775-83.
- Multiple functions of Jab1 are required for early embryonic development and growth potential in mice. Tomoda K, Yoneda-Kato N, Fukumoto A, Yamanaka S, Kato JY. J Biol Chem. 2004 Oct 08; 279(41):43013-8.
- Prognostic significance of localized p27Kip1 and potential role of Jab1/CSN5 in pancreatic cancer. Fukumoto A, Ikeda N, Sho M, Tomoda K, Kanehiro H, Hisanaga M, Tsurui Y, Tsutsumi M, Kato JY, Nakajima Y. Oncol Rep. 2004 Feb; 11(2):277-84.
- The cytoplasmic shuttling and subsequent degradation of p27Kip1 mediated by Jab1/CSN5 and the COP9 signalosome complex. Tomoda K, Kubota Y, Arata Y, Mori S, Maeda M, Tanaka T, Yoshida M, Yoneda-Kato N, Kato JY. J Biol Chem. 2002 Jan 18; 277(3):2302-10.
Contact
Kiichiro Tomoda