Professor and Director, Medical Research Laboratory, Institute of Science Tokyo
EDUCATIONS
B.Sc. (1992)
Faculty of Pharmaceutical Sciences, The University of Tokyo, Japan
M.S. (1994)
Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan
Ph.D. (1997)
Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan
EXPERIENCES
1997-2000
Postdoctoral Fellow, Ontario Cancer Institute, The University of Toronto, Canada
2000-2003
Investigator, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
2003-2004
Research Leader, Akita University School of Medicine, Japan
2004-2009
Professor, Akita University School of Medicine, Japan
2009-2018
Professor, Akita University Graduate School of Medicine and Faculty of Medicine, Japan
2018-2024
Professor, Tokyo Medical and Dental University, Japan
(University merged into Institute of Science Tokyo in 2024)
2024-present
Professor, Institute of Science Tokyo, Japanof Medicine and Faculty of Medicine, Japan
2024-present
Director, Medical Research Laboratory, Institute of Science Tokyo, Japan
Visiting Professorships
2022–present
Visiting Professor, Kyushu University, Japan
2023–present
Visiting Professor, Kobe University, Japan
2024–present
Visiting Professor, Tokyo University of Science, Japan
MAJOR PUBLICATIONS
1. Morioka S. et al. A mass spectrometric method for in-depth profiling phosphoinositide regioisomers and their disease-associated regulation. Nature Commun. 13, 83, 2022
2. Kofuji S. et al. INPP4B is a PtdIns(3,4,5)P3 phosphatase that can act as a tumor suppressor. Cancer Discovery 5, 730-739, 2015
3. Sasaki J. et al. The PtdIns(3,4)P2-phosphatase INPP4A is a suppressor of excitotoxic neuronal death. Nature 465, 497-501. 2010
4. Nishio M. et al. Control of cell polarity and motility by the PI(3,4,5)P3 phosphatase SHIP1. Nature Cell Biol. 9, 36-44, 2007
5. Crackower M. et al. Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathway. Cell 110, 737-749, 2002
6. Clement S. et al. The lipid phosphatase SHIP2 controls insulin sensitivity. Nature 409, 92-97, 2001
7. Sasaki T. et al. Function of PI3K in thymocyte development, T cell activation, and neutrophil migration. Science 287, 1040-1046, 2000
8. Liu, Q. et al. SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activity and myeloid cell survival. Genes Dev. 13, 786-791, 1999
9. Suzuki, A. et al. High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice. Curr Biol. 8, 1169-1178, 1998
10. Stambolic V. et al. Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN. Cell 95, 29-39, 1998
RESEARCH FOCUS
Our laboratory focuses on the metabolism and signaling roles of phosphoinositides (PIPs), particularly D3-phosphorylated species such as PI(3,4,5)P₃, which are tightly regulated by the tumor suppressor PTEN.
In the late 1990s, we were among the first to demonstrate that PTEN deficiency leads to intracellular accumulation of PI(3,4,5)P₃, highlighting its critical role in growth and survival signaling.
To investigate the broader landscape of PIPs metabolism, governed by ~50 enzymes, we generate gene-targeted mouse models and apply advanced lipidomic technologies.
In particular, we have been developing mass spectrometry–based techniques for comprehensive and regioisomer-specific profiling of PIPs, including their fatty acyl variants (molecular species), applicable to both human cancer specimens and disease-model animals.
By integrating genetics and "PIPomics", we aim to elucidate lipid-driven mechanisms underlying cancer, inflammation, and neurodegeneration, and to identify therapeutic targets and diagnostic biomarkers relevant to PTEN-associated pathologies.
