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We focus on the molecular mechanisms controlling proliferation, differentiation, and death of mammalian cells, and studies the connection between cell cycle progression and oncogenesis, as well as differentiation, proliferation, and leukemogenesis in hematopoietic cells. The findings can be applied to regenerative medicine and cancer research. We use the following experimental systems: (1) an in vitro culture system using mouse and human cell lines, (2) an in vitro differentiation system using ES cells and primary cultures, and (3) a mouse model system using knockout mice and transgenic mice.
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- Cell cycle control and oncogenesis
- Cell cycle control: During the cell cycle, the decision on whether cells should proliferate or stop growing and prepare for differentiation is determined at the G1 phase. Therefore, we investigate the function of molecules that promote or inhibit the progression of G1 phase such as cyclins, Cdks, Cdk inhibitors, and Rb tumor suppressor gene products (Fig. 1).
- Checkpoint control: The checkpoint mechanism is a means of monitoring and controlling the progression of the cell cycle. The central role in this checkpoint mechanism is played by the tumor suppressor gene product, p53. Recently, members of the p53 gene family, p63 and p73, have been identified. We are interested in the role of these molecules not only in oncogenesis, but also in the developmental program including morphogenesis (Fig. 1).
- Cancer and the cell cycle: Since cancer cells grow abnormally, they generally have abnormalities in the cell cycle control. We are analyzing the key molecules involved in cell proliferation, G1 regulation, and checkpoint control, and investigating the mechanisms involved in the abnormal growth of cells and cellular oncogenesis.
- Leukemogenesis
We are investigating the molecular mechanisms underlying leukemogenesis, focusing on AML (acute myeloid leukaemia), MDS (myelodysplastic syndromes), and CML (chronic myeloid leukaemia).
- Hematopoietic stem cells
We are performing studies on hematopoietic stem cells, present in the bone marrow. We are aiming to develop in vitro amplification methods for hematopoietic stem cells. The results of these studies can be of benefit to regenerative medicine as well as leukemia research.
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- Kato J-Y. et al., 遺伝子医学別冊・遺伝子医学の入門書 これだけは知っておきたい遺伝子医学の基礎知識, p59-63, 2003
- Kato J-Y., Experimental Medicine, 13, 1588-1593, 1995
- Kato J-Y., Molecular Medicine, 32, 946-951, 1995
- Tomoda K. et al., Nature, 398, 160-165, 1999
- Kato J-Y. et al., Cell, 79, 487-496, 1994
- Kato J-Y. et al., Genes & Devel, 7, 331-342, 1993
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Fig. 1 Cell cycle and cyclin/Cdk complexes
Fig. 2 A group of erythrocytes and leukocytes (upper), neutrophils (lower left) and macrophages (lower right), which were induced to differentiate from ES cells in vitro.
Fig. 3 A chimeric mouse generated by infusion of genetically modified ES cells
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