Updated on 2023/09/11

写真a

 
MASUDA Yuji
 
Organization
Research Institute of Environmental Medicine Division of Stress Adaptation and Protection Associate professor
Graduate School
Graduate School of Medicine
Title
Associate professor
Contact information
メールアドレス

Degree 1

  1. 博士(農学) ( 1995.3   東京大学 ) 

Research Areas 1

  1. Others / Others  / 生化学

Research History 7

  1. 名古屋大学大学院医学研究科総合医学専攻・准教授           名古屋大学環境医学研究所・准教授

    2013.5

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    Country:Japan

  2. 名古屋大学環境医学研究所・准教授

    2011.10 - 2013.4

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    Country:Japan

  3. 広島大学原爆放射線医科学研究所・助教

    2007.4 - 2011.9

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    Country:Japan

  4. 広島大学原爆放射線医科学研究所・助手

    2002.4 - 2007.3

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    Country:Japan

  5. 広島大学原爆放射能医学研究所・助手

    1998.7 - 2002.3

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    Country:Japan

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Education 2

  1. The University of Tokyo

    - 1995.3

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    Country: Japan

  2. Saitama University   Faculty of Science

    1986.4 - 1990.3

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    Country: Japan

Professional Memberships 5

  1. 日本癌学会

  2. 日本放射線影響学会

  3. 日本分子生物学会

  4. 日本遺伝学会

  5. 環境変異原学会

Awards 4

  1. 日本遺伝学会第88回大会 ベストペーパー賞

    2017.3   日本遺伝学会  

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

  2. 日本遺伝学会第83回大会 ベストペーパー賞

    2012.3   日本遺伝学会  

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    Country:Japan

  3. 日本遺伝学会第82回大会 ベストペーパー賞

    2011.3   日本遺伝学会  

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    Country:Japan

  4. 日本遺伝学会奨励賞

    2008   日本遺伝学会  

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    Country:Japan

 

Papers 44

  1. Novel mechanisms for the removal of strong replication-blocking HMCES- and thiazolidine-DNA adducts in humans.

    Sugimoto Y, Masuda Y, Iwai S, Miyake Y, Kanao R, Masutani C

    Nucleic acids research   Vol. 51 ( 10 ) page: 4959 - 4981   2023.6

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    Language:English  

    DOI: 10.1093/nar/gkad246

    PubMed

  2. Stepwise multipolyubiquitination of p53 by the E6AP-E6 ubiquitin ligase complex. Reviewed

    Masuda Y, Saeki Y, Arai N, Kawai H, Kukimoto I, Tanaka K, Masutani C

    The Journal of biological chemistry   Vol. 294 ( 41 ) page: 14860-14875   2019.10

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.RA119.008374

    PubMed

  3. Spatiotemporal regulation of PCNA ubiquitination in damage tolerance pathways Invited Reviewed

    Masuda Yuji, Masutani Chikahide

    CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY   Vol. 54 ( 5 ) page: 418 - 442   2019.9

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

    DOI: 10.1080/10409238.2019.1687420

    Web of Science

    PubMed

  4. Preferential digestion of PCNA-ubiquitin and p53-ubiquitin linkages by USP7 to remove polyubiquitin chains from substrates Reviewed

    Masuda Yuji, Kanao Rie, Kawai Hidehiko, Kukimoto Iwao, Masutani Chikahide

    JOURNAL OF BIOLOGICAL CHEMISTRY   Vol. 294 ( 11 ) page: 4177 - 4187   2019.3

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.RA118.005167

    Web of Science

    PubMed

  5. Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway. Reviewed

    Masuda Y, Mitsuyuki S, Kanao R, Hishiki A, Hashimoto H, Masutani C

    Nucleic acids research   Vol. 46 ( 21 ) page: 11340 - 11356   2018.11

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

    DOI: 10.1093/nar/gky943

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Research Project for Joint Research, Competitive Funding, etc. 2

  1. チェックポイント機能を欠如したがん細胞特異的に化学療法の効果を増感させる薬剤の開発

    2011.12 - 2012.7

    研究成果最適展開支援プログラムA-STEPフィージビリティスタディステージ 探索タイプ 

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    Grant type:Competitive

  2. 哺乳類での突然変異誘発の分子機構の解明

    2003.4 - 2007.3

    特色ある大学教育支援プログラム 

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    Grant type:Competitive

KAKENHI (Grants-in-Aid for Scientific Research) 21

  1. 脱塩基部位-タンパク質クロスリンクにより開始する新規DNA損傷トレランス経路

    Grant number:23K11418  2023.4 - 2026.3

    科学研究費助成事業  基盤研究(C)

    増田 雄司

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

    DNA損傷はがん化や老化プロセスを促進する主要な原因の一つであり、内因性/外因性のDNA損傷に対する細胞応答機構の重要性が指摘されている。脱塩基損傷は主要な内因性のDNA損傷であり、動物組織の細胞では非常に多くの脱塩基損傷が定常的に存在している。脱塩基損傷は内/外因性の酸化反応に起因するだけではなく、生命現象さまざまな局面(APOBECによる副反応、免疫細胞での体細胞超突然変異、受精卵の初期化過程)で生じ、ある局面では突然変異を誘発する一方、別の局面では突然変異を抑制する未解明の制御機構の存在が示唆される。本研究では脱塩基損傷から細胞を保護するために必要な未解明の制御メカニズムを明らかにする。

  2. 誘発変異頻度を規定する損傷トレランス経路の時空間的制御の分子基盤の確立

    Grant number:18H03371  2018.4 - 2022.3

    科学研究費補助金  基盤研究(B)

    増田雄司

  3. Multiple mechanisms of post-replication repair pathway choice by deubiquitinases for ubiquitinated PCNA

    Grant number:16K12594  2016.4 - 2018.3

    MASUDA Yuji

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    Authorship:Principal investigator 

    Grant amount:\3770000 ( Direct Cost: \2900000 、 Indirect Cost:\870000 )

    The DNA damage tolerance pathways as the post-replication repair are regulated by ubiquitination of proliferating cell nuclear antigen (PCNA). Since mono- and poly-ubiquitination of PCNA stimulates the error-prone pathway, translesion DNA synthesis (TLS), and the error-free, in principle, pathway, template switch (TS), respectively. However, in humans, the regulatory mechanism is obscure because poly-ubiquitinated PCNA is only slightly detectable. In this study, we identified deubiquitinases for ubiquitinated PCNA and analyzed their functions in the damage tolerance pathways.

  4. Biochemical study of damage tolerance pathways to control the induced mutagenesis

    Grant number:15H02818  2015.4 - 2019.3

    Masuda Yuji

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    Authorship:Principal investigator 

    Grant amount:\12610000 ( Direct Cost: \9700000 、 Indirect Cost:\2910000 )

    Mutagenesis is one of the critical outcomes of exposure by radiation or environmental mutagens. The molecular mechanism of the induced mutagenesis, which is one of the most important issues in this field, remains to be elucidated. A significant fraction of the induced mutation is generated through a cellular process, so-called DNA damage tolerance. In humans, two sub-pathways are regulated by ubiquitination of PCNA, one of the auxiliary factors of DNA replication; one is the error-prone pathway, translesion DNA synthesis, inducing point mutations, and the other is template switch, which is the error-free, in principle, but has a risk of genomic rearrangements. Therefore the regulation of the choice of two pathways is a crucial step for the maintenance of genetic stability. In this study, we examined the molecular mechanisms of the pathway choice by analysis of factors involved in the PCNA ubiquitination.

  5. 誘発突然変異頻度を適切に制御する損傷トレランス経路の生化学的分子基盤の確立

    2015.4 - 2018.3

    科学研究費補助金  基盤研究(B)

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    Authorship:Principal investigator 

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