Molecular Pharmaco-Biology (Cooperating field) - Molecular Pharmacology - Laboratories | Nagoya University GraduateSchool of Medicine


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Molecular PharmacologyMolecular Pharmaco-Biology (Cooperating field)


A myriad of lesions in DNA are caused by ubiquitous environmental and endogenous genotoxic agents. These DNA lesions can interfere with normal DNA metabolism including DNA replication, eventually resulting in mutations that leads to carcinogenesis, seneescence and/or cell death. To cope with DNA damagees, cells have multiple mechanisms such as Cell Cycle Checkpoint, DNA Repair and DNA Damage Tolerance which includes TlansLesion Synthesis (TLS). Dozens of inherited disesases are known or suspected to be caused by defects of these mechanisms. This department aims to elucidate molecular bases of cellular DNA damage resposes relating to the human disorders. We have identified human DNA polymerase eta (Polη) as the responsible gene product of Xeroderma Pigmentosum Variant (XPV) and shown that Polη catalyzes efficient and accurate TLS past unrepaired UV-induced pyrimidine dimers, therefore prevents UV-induced carcinogenesis.

Research Projects

  1. Regulatory mechanisms of TLS
  2. Unidentified DNA damage tolerance pathways
  3. Physiological relevance of DNA damage tolerance
  4. Crosstalk between multiple DNA damage response mechanisms
  5. Therapeutic targets for genome instability diseases

Faculty Members

Chikahide Masutani Professor Department of Genome Dynamics, Research Institute of Environmental Medicine
Yuji Masuda Associate Professor Department of Genome Dynamics, Research Institute of Environmental Medicine
Rie Kanao Assistant Professor Department of Genome Dynamics, Research Institute of Environmental Medicine


  • 2015
    1. Kashiwaba S, Kanao R, Masuda Y, Kusumoto-Matsuo R, Hanaoka F, Masutani C. USP7 Is a Suppressor of PCNA Ubiquitination and Oxidative-Stress-Induced Mutagenesis in Human Cells. Cell Reports, 2015; 13: 2072-2080.
    2. Masuda Y, Kanao R, Kaji K, Ohmori H, Hanaoka F, Masutani C. Different types of interaction between PCNA and PIP boxes contribute to distinct cellular functions of Y-family DNA polymerases. Nucleic Acids Research, 2015; 43: 7898-7910.
    3. Niimi A, Hopkins SR, Downs JA, Masutani C. The BAH domain of BAF180 is required for PCNA ubiquitination. Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis, 2015; 779: 16-23.
    4. Kanao R, Yokoi M, Ohkumo T, Sakurai Y, Dotsu K, Kura S, Nakatsu Y, Tsuzuki T, Masutani C, Hanaoka F. UV-induced mutations in epidermal cells of mice defective in DNA polymerase eta and/or iota. DNA Repair, 2015; 29: 139-146.
    5. Kanao R, Masuda Y, Deguchi S, Yumoto-Sugimoto M, Hanaoka F, Masutani C. Relevance of Simultaneous Mono-Ubiquitinations of Multiple Units of PCNA Homo-Trimers in DNA Damage Tolerance. Plos One, 2015; 10.
  • 2012
    1. Masuda Y, Suzuki M, Kawai H, Hishiki A, Hashimoto H, Masutani C, Hishida T, Suzuki F, Kamiya K. En bloc transfer of polyubiquitin chains to PCNA in vitro is mediated by two different human E2-E3 pairs. Nucleic Acids Research, 2012; 40: 10394-10407.

Research Keywords

DNA repair、 DNA replication、 DNA damage、 DNA damage tolerance、 translesion synthesis、 DNA polymerase eta

We are looking for highly motivated students of graduate school. (Doctoral course students are welcomed.)