Mikio Shimada

Assistant Professor

Tokyo Institute of Technology

Japan

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About

Mikio Shimada is an Assistant Professor at Tokyo Institute of Technology, Japan. His research focuses on DNA damage response, cell cycle progression, and the implications of antioxidants on neural differentiation and microcephaly in stem cells. Recent articles reflect his work on B-cell immunodeficiency, the role of DNA double-strand break repair, and the health effects associated with tritium exposure.

Articles (13)

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2025

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2025

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2025

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2025

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2024

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2022

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2021

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2021

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2021

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2021

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2021

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2021

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2020

Collaborators (3)

Yoshihisa Matsumoto

Associate Professor (PI)

Tokyo Institute of Technology

JAPAN

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Masaaki SUNAOSHI

National Institutes for Quantum and Radiological Science and Technology

JAPAN

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Junya Kobayashi

Professor

International University of Health and Welfare

JAPAN

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Mikio Shimada

Research Interests

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Articles (13)

Live-cell imaging of DNA damage and cell cycle progression uncovers distinct responses during neural differentiation of hiPSCs

B-cell immunodeficiency associated with polynucleotide kinase 3'-phosphatase (PNKP) deficiency.

Antioxidants Ameliorates Ionizing Radiation-Induced Microcephaly in Cerebral Organoid Derived from Human-induced Pluripotent Stem Cells.

CDK-mediated phosphorylation of PNKP is required for end-processing of single-strand DNA gaps on Okazaki fragments and genome stability

Dimethyl Sulfoxide Attenuates Ionizing Radiation-induced Centrosome Overduplication and Multipolar Cell Division in Human Induced Pluripotent Stem Cells.

THE ROLE OF DNA DOUBLE-STRAND BREAK REPAIR THROUGH NON-HOMOLOGOUS END JOINING IN THE DOSE-RATE EFFECT IN TERMS OF CLONOGENIC ABILITY

Health effects triggered by tritium: how do we get public understanding based on scientifically supported evidence?

Functional analysis of XRCC4 mutations in reported microcephaly and growth defect patients in terms of radiosensitivity

Diminished or inversed dose-rate effect on clonogenic ability in Ku-deficient rodent cells

The FHA domain of PNKP is essential for its recruitment to DNA damage sites and maintenance of genome stability

α-glucosyl-rutin activates immediate early genes in human induced pluripotent stem cells.

DNA-Dependent Protein Kinase Catalytic Subunit: The Sensor for DNA Double-Strand Breaks Structurally and Functionally Related to Ataxia Telangiectasia Mutated.

Linker region is required for efficient nuclear localization of polynucleotide kinase phosphatase

Collaborators (3)

Yoshihisa Matsumoto

Masaaki SUNAOSHI

Junya Kobayashi

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