Updated on 2025/03/27

写真a

 
Nakamura Takanori
 
Organization
Premier Institute for Advanced Studies (PIAS) Proteo-Science Center (PROS) Assistant Professor
Title
Assistant Professor
Contact information
メールアドレス
Profile

大学学部生の時分にゲフィチニブ (EGFR阻害剤)、イマチニブ (BCR-ABL阻害剤)などの分子標的薬剤が脚光を集めていたこともあり生化学／分子生物学の中でもシグナル伝達（アポトーシス経路、MAPK経路等）に興味を持ちその研究を始めました。現在ではそこから派生した非膜型細胞内小器官（中心体、ストレス顆粒）にも興味が移行して研究しています。生化学的手法（ウェスタンブロット）、細胞生物学的手法（蛍光免疫染色、ライブイメージング）、数理解析などを取り入れて上記の細胞内情報伝達や非膜型細胞内オルガネラの生理機能や作動原理を包括的に理解することを目指しています。

更に上記の生体内メカニズムの破綻によって惹起される、がん、神経変性疾患、発育不全疾患の病態を理解して創薬に繋げることも目指して日々研究を続けています。

 

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Degree

  • Ph.D. ( 2013.4   The University of Tokyo )

Research Interests

  • post-translational modification

  • Growth failure

  • 個体形成

  • Tumorigenesis

  • Chromosomal instability

  • Centrosome

  • Cell cycle

  • Cell death

  • Mathematical analysis

  • Stress granules

  • Oxidative stress

  • Liquid-Liquid phase separation

  • neurodegenerative disease

  • BCR-ABL

  • mTOR

  • p38

  • JNK

  • ERK

  • MAPK

  • Signal transduction

  • Proximity dependent biotinylation

  • Phosphorylation

Research Areas

  • Life Science / Molecular biology

  • Life Science / Medical biochemistry

  • Life Science / Embryonic medicine and pediatrics

  • Natural Science / Mathematical analysis

  • Nanotechnology/Materials / Chemical biology

  • Life Science / Pathological biochemistry

  • Life Science / Tumor biology

  • Life Science / Cell biology

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Education

  • The University of Tokyo

    2008.4 - 2013.4

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    Country： Japan

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  • The University of Tokyo

    2006.4 - 2008.3

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    Country： Japan

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  • Tokyo University of Science   Faculty of Pharmaceutical Sciences   Department of Pharmacy

    2002.4 - 2006.3

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    Country： Japan

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Research History

  • 愛媛大学 プロテオサイエンスセンター   病理学部門（増本 純也 教授）   特定講師

    2024.4

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    Country：Japan

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  • Ehime University   Department of Pathology, Graduate School of Medicine   Senior Assistant Professorssor

    2024.4

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  • Ehime University   Division of Cell-Free Science, Proteo-Science Center   Senior Assistant Professor

    2023.4 - 2024.3

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    Country：Japan

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  • The University of Tokyo   The Institute of Medical Science   Assistant Professor

    2013.4 - 2023.3

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  • The University of Tokyo   The Institute of Medical Science   Research Associate

    2012.4 - 2013.3

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  • Nagoya University   Research Institute of Environmental Medicine   Research Associate

    2011.4 - 2012.3

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Committee Memberships

  • 日本生化学会中国四国支部例会   実行委員  

    2023.4 - 2023.5   

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    Committee type：Academic society

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  • Cancer Science誌   Peer Reviewer  

    2022.9   

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    Committee type：Academic society

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  • AIMS Bioengineering誌   Peer Reviewer  

    2021.12   

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    Committee type：Academic society

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  • 東京大学 医科学研究所   広報委員  

    2020.4 - 2023.3   

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  • American Society of Cell Biology (ASCB)   Ambassador  

    2017.9   

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    Committee type：Academic society

    https://info.ascb.org/net/ascbPortal/web/committeeRosterURL.aspx?groupid=committee/ambassadors

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Qualification acquired

  • 薬剤師免許

Papers

  • Formation of the NLRP3 inflammasome inhibits stress granule assembly by multiple mechanisms Reviewed International journal

    Daisuke Yoshioka, Takanori Nakamura, Yuji Kubota, Mutsuhiro Takekawa

    The Journal of Biochemistry   175 ( 6 )   629 - 641   2024.1

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

    Abstract

    Proper regulation of cellular response to environmental stress is crucial for maintaining biological homeostasis and is achieved by the balance between cell death processes, such as the formation of the pyroptosis-inducing NLRP3 inflammasome, and pro-survival processes, such as stress granule (SG) assembly. However, the functional interplay between these two stress-responsive organelles remains elusive. Here, we identified DHX33, a viral RNA sensor for the NLRP3 inflammasome, as a SG component, and the SG-nucleating protein G3BP as an NLRP3 inflammasome component. We also found that a decrease in intracellular potassium (K+) concentration, a key common step in NLRP3 inflammasome activation, markedly inhibited SG assembly. Therefore, when macrophages are exposed to stress stimuli with the potential to induce both SGs and the NLRP3 inflammasome, such as cytoplasmic poly(I:C) stimulation, they preferentially form the NLRP3 inflammasome but avoid SG assembly by sequestering G3BP into the inflammasome and by inducing a reduction in intracellular K+ levels. Thus, under such conditions, DHX33 is primarily utilized as a viral RNA sensor for the inflammasome. Our data reveal the functional crosstalk between NLRP3 inflammasome-mediated pyroptosis and SG-mediated cell survival pathways, and delineate a molecular mechanism that regulates cell-fate decisions and anti-viral innate immunity under stress.

    File： JB2024 Formation of the NLRP3 inflammasome inhibits stress granule assembly by multiple mechanisms.pdf

    DOI： 10.1093/jb/mvae009

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  • Stress granule formation inhibits stress-induced apoptosis by selectively sequestering executioner caspases Reviewed International journal

    Daichi Fujikawa, Takanori Nakamura, Daisuke Yoshioka, Zizheng Li, Hisashi Moriizumi, Mari Taguchi, Noriko Tokai-Nishizumi, Hiroko Kozuka-Hata, Masaaki Oyama, Mutsuhiro Takekawa

    Current Biology   33   1967 - 1981   2023.5

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    Cytoplasmic stress granules (SGs) are phase-separated membrane-less organelles that form in response to various stress stimuli. SGs are mainly composed of non-canonical stalled 48S preinitiation complexes. In addition, many other proteins also accumulate into SGs, but the list is still incomplete. SG assembly suppresses apoptosis and promotes cell survival under stress. Furthermore, hyperformation of SGs is frequently observed in various human cancers and accelerates tumor development and progression by reducing stress-induced damage of cancer cells. Therefore, they are of clinical importance. However, the precise mechanism underlying SG-mediated inhibition of apoptosis remains ill-defined. Here, using a proximity-labeling proteomic approach, we comprehensively analyzed SG-resident proteins and identified the executioner caspases, caspase-3 and -7, as SG components. We demonstrate that accumulation of caspase-3/7 into SGs is mediated by evolutionarily conserved amino acid residues within their large catalytic domains and inhibits caspase activities and consequent apoptosis induced by various stresses. Expression of an SG-localization deficient caspase-3 mutant in cells largely counteracted the anti-apoptotic effect of SGs, whereas enforced relocalization of the caspase-3 mutant to SGs restored it. Thus, SG-mediated sequestration of executioner caspases is a mechanism underlying the broad cytoprotective function of SGs. Furthermore, using a mouse xenograft tumor model, we show that this mechanism prevents cancer cells from apoptosis in tumor tissues, thereby promoting cancer progression. Our results reveal the functional crosstalk between SG-mediated cell survival and caspase-mediated cell death signaling pathways and delineate a molecular mechanism that dictates cell-fate decisions under stress and promotes tumorigenesis.

    DOI： 10.1016/j.cub.2023.04.012

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  • Stress-responsive MTK1 SAPKKK serves as a redox sensor that mediates delayed and sustained activation of SAPKs by oxidative stress Reviewed International journal

    Moe Matsushita, Takanori Nakamura, Hisashi Moriizumi, Hiroaki Miki, Mutsuhiro Takekawa

    Science Advances   6 ( 26 )   2020.6

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Association for the Advancement of Science (AAAS)  

    Cells respond to oxidative stress by inducing intracellular signaling, including stress-activated p38 and JNK MAPK
    (SAPK) pathways, but the underlying mechanisms remain unclear. Here, we report that the MAP three kinase 1
    (MTK1) SAPK kinase kinase (SAPKKK) functions as an oxidative-stress sensor that perceives the cellular redox state
    and transduces it into SAPK signaling. Following oxidative stress, MTK1 is rapidly oxidized and gradually reduced
    at evolutionarily conserved cysteine residues. These coupled oxidation-reduction modifications of MTK1 elicit
    its catalytic activity. Gene knockout experiments showed that oxidative stress–induced SAPK signaling is mediated
    by coordinated activation of the two SAPKKKs, MTK1 and apoptosis signal–regulating kinase 1 (ASK1), which
    have different time and dose-response characteristics. The MTK1-mediated redox sensing system is crucial for
    delayed and sustained SAPK activity and dictates cell fate decisions including cell death and interleukin-6 production.
    Our results delineate a molecular mechanism by which cells generate optimal biological responses under
    fluctuating redox environments.

    File： sciadv.aay9778.pdf

    DOI： 10.1126/sciadv.aay9778

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    Other Link： https://www.science.org/doi/epdf/10.1126/sciadv.aay9778

  • MCRIP1 promotes the expression of lung-surfactant proteins in mice by disrupting CtBP-mediated epigenetic gene silencing Reviewed International journal

    Jane S. Weng, Takanori Nakamura, Hisashi Moriizumi, Hiroshi Takano, Ryoji Yao, Mutsuhiro Takekawa

    Communications Biology   2 ( 1 )   2019.6

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Proper regulation of epigenetic states of chromatin is crucial to achieve tissue-specific gene expression during embryogenesis. The lung-specific gene products, surfactant proteins B (SP-B) and C (SP-C), are synthesized in alveolar epithelial cells and prevent alveolar collapse. Epigenetic regulation of these surfactant proteins, however, remains unknown. Here we report that MCRIP1, a regulator of the CtBP transcriptional co-repressor, promotes the expression of SP-B and SP-C by preventing CtBP-mediated epigenetic gene silencing. Homozygous deficiency of Mcrip1 in mice causes fatal respiratory distress due to abnormal transcriptional repression of these surfactant proteins. We found that MCRIP1 interferes with interactions of CtBP with the lung-enriched transcriptional repressors, Foxp1 and Foxp2, thereby preventing the recruitment of the CtBP co-repressor complex to the SP-B and SP-C promoters and maintaining them in an active chromatin state. Our findings reveal a molecular mechanism by which cells prevent inadvertent gene silencing to ensure tissue-specific gene expression during organogenesis.

    File： Commun Biol2019 MCRIP1.pdf

    DOI： 10.1038/s42003-019-0478-3

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    Other Link： https://www.nature.com/articles/s42003-019-0478-3

  • MCRIP1, an ERK Substrate, Mediates ERK-Induced Gene Silencing during Epithelial-Mesenchymal Transition by Regulating the Co-Repressor CtBP Reviewed International journal

    Kenji Ichikawa, Yuji Kubota, Takanori Nakamura, Jane S. Weng, Taichiro Tomida, Haruo Saito, Mutsuhiro Takekawa

    Molecular Cell   58 ( 1 )   35 - 46   2015.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    The ERK pathway not only upregulates growth-promoting genes, but also downregulates anti-proliferative and tumor-suppressive genes. In particular, ERK signaling contributes to repression of the E-cadherin gene during epithelial-mesenchymal transition (EMT). The CtBP transcriptional co-repressor is also involved in gene silencing of E-cadherin. However, the functional relationship between ERK signaling and CtBP is unknown. Here, we identified an ERK substrate, designated MCRIP1, which bridges ERK signaling and CtBP-mediated gene silencing. CtBP is recruited to promoter elements of target genes by interacting with the DNA-binding transcriptional repressor ZEB1. We found that MCRIP1 binds to CtBP, thereby competitively inhibiting CtBP-ZEB1 interaction. When phosphorylated by ERK, MCRIP1 dissociates from CtBP, allowing CtBP to interact with ZEB1. In this manner, the CtBP co-repressor complex is recruited to, and silences, the E-cadherin promoter by inducing chromatin modifications. Our findings reveal a molecular mechanism underlying ERK-induced epigenetic gene silencing during EMT and its dysregulation in cancer.

    File： Mol Cell 2015 MCRIP1.pdf

    DOI： 10.1016/j.molcel.2015.01.023

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    Other Link： https://www.sciencedirect.com/science/article/pii/S1097276515000465?via%3Dihub

  • SAPK pathways and p53 cooperatively regulate PLK4 activity and centrosome integrity under stress Reviewed International journal

    Takanori Nakamura, Haruo Saito, Mutsuhiro Takekawa

    Nature Communications   4 ( 1 )   2013.4

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Polo-like kinase 4 is essential for centrosome duplication, but its hyperactivation causes
    supernumerary centrosomes. Here we report that polo-like kinase 4 is directly phosphorylated and activated by stress-activated protein kinase kinase kinases (SAPKKKs). Stress-induced polo-like kinase 4 activation promotes centrosome duplication, whereas stress-induced SAPK activation prevents centrosome duplication. In the early phase of stress response, the balance of these opposing signals prevents centrosome overduplication. However, in the late phase of stress response, p53 downregulates polo-like kinase 4 expression, thereby preventing sustained polo-like kinase 4 activity and centrosome amplification. If both p53 and the SAPKK MKK4 are simultaneously inactivated, as is frequently found in cancer cells, persistent polo-like kinase 4 activity combined with the lack of SAPK-mediated inhibition of centrosome duplication conspire to induce supernumerarycentrosomes under stress. Indeed, tumour-derived MKK4 mutants induced centrosome amplification under genotoxic stress, but only in p53-negative cells. Thus, our results reveal a mechanism that preserves the numeral integrity of centrosomes, and an unexplored tumour-suppressive function of MKK4.

    File： ncomms2752.pdf

    DOI： 10.1038/ncomms2752

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    Other Link： https://www.nature.com/articles/ncomms2752

  • Mathematical analysis of the mechanism of how centriole biogenesis regulators are transported to mother centrioles

    Nakamura, Takanori, Tokai, Noriko, Nakazawa, Takashi, Mori, Tatsuki, Suzuki, Takashi, Takekawa, Mutsuhiro

    The 81st Annual Meeting of Japanese Cancer Association   113   E6-1   2022.9

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  • SAPK-regulated microRNA-X suppresses apoptosis in colorectal cancer

    Takanori Nakamura

    Cancer Science   2022

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    Publishing type：Research paper (scientific journal)  

    Web of Science

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  • Mathematical modeling of the molecular mechanism underlying the recruitment of centriole biogenesis regulators to mother centrioles

    Nakamura Takanori, Nishizumi-Tokai Noriko, Nakazawa Takashi, Mori Tatsuki, Suzuki Takashi, Takekawa Mutsuhiro

    The 80th Annual meeting of Japanese Cancer Association   2021.9

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  • ストレス顆粒形成による生命機能制御と疾患 Reviewed

    吉岡 大介、中村 貴紀、武川 睦寛

    実験医学 増刊 「相分離~メカニズムと疾患~」   39 ( 10 )   93 - 101   2021.6

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    Language：Japanese  

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  • Mathematical modeling of the recruitment of centriole biogenesis regulators to mother centrioles in the S-phase

    Takanori Nakamura, Noriko Nishizumi-Tokai, Takashi Nakazawa, Tatsuki Mori, Takashi Suzuki, Mutsuhiro Takekawa

    2020.10

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  • Mathematical modeling of the molecular mechanism that recruits centriole biogenesis regulators to mother centrioles

    Nakamura Takanori, Nishizumi-Tokai Noriko, Nakazawa Takashi, Mori Tatsuki, Suzuki Takashi, Takekawa Mutsuhiro

    The 78th Annual meeting of Japanese Cancer Association   2019.9

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  • 中心体複製初期に起こるPLK4の中心体輸送機構

    中村 貴紀, 西住(渡海) 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    第19回日本蛋白質科学年会・第71回日本細胞生物学会 合同年次大会   2019.6

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  • 数理解析を駆使した中心体複製開始を制御する分子機構の解明

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    第41回日本分子生物学会年会   2P-0255   2018.11

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  • 数理解析を用いた中心体複製の開始制御機構の解明

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    2018年日本応用数理学会年会   347 - 348   2018.9

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  • 中心体複製開始を司るPLK4中心体局在機構の解明

    中村貴紀, 西住(渡海)紀子, 中澤嵩, 鈴木貴, 武川睦寛

    2017年度生命科学系学会合同年次大会（第40回日本分子生物学会・第90回日本生化学会）   AT19-08 / 3P-384   2017.12

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  • The molecular mechanisms that maintain the numerical integrity of centrosomes under stress

    Nakamura Takanori, Mutsuhiro Takekawa

    EMBO Conference: Centrosomes and Spindle Pole bodies   146 - 146   2017.9

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    Authorship：Lead author   Language：English   Publishing type：Research paper (international conference proceedings)  

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  • The molecular mechanisms that maintain the numerical integrity of centrosomes under stress

    Nakamura Takanori, Mutsuhiro Takekawa

    Annual Meeting of the American-Society-for-Cell-Biology (ASCB)   27   P1045   2016.12

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  • Tumor suppressors MKK4 and p53 cooperatively maintain centrosome integrity and chromosomal stability

    Takanori Nakamura, Noriko Nishizumi-Tokai, Eriko Mikoshi, Moe Matsushita, Mutsuhiro Takekawa

    The 74th Annual meeting of Japanese Cancer Association   P-1123   2015.10

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  • 癌抑制遺伝子MKK4とp53による中心体数および染色体安定性の保持機構と癌におけるその 破綻

    中村 貴紀, 武川 睦寛

    第52回日本臨床分子医学会   2015.4

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  • Centrosome integrity under stress is maintained by a network of PLK4, p53 and SAPK pathways.

    Takanori Nakamura, Mutsuhiro Takekawa

    The 72nd Annual meeting of Japanese Cancer Association   2013.10

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  • Centrosome integrity under stress is maintained by a network of PLK4, p53 and SAPK pathways.

    Nakamura Takanori, Takekawa Mutsuhiro

    The 65th Japan Society for cell biology   2013.6

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  • Targeting the stress-responsive JNK/p38-AP1 pathway for therapeutic intervention Reviewed

    Nakamura Takanori, Takekawa Mutsuhiro

    Nihon Rinsho   Suppl 8   218 - 224   2012.11

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    Authorship：Lead author,　Corresponding author   Publishing type：Research paper (scientific journal)  

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  • 細胞内シグナル伝達と分子標的薬剤の作用機序 Reviewed

    中村 貴紀, 武川 睦寛

    メディカルサイエンス･ダイジェスト特集「分子標的薬」   38   150 - 153   2012.3

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    Authorship：Lead author,　Corresponding author   Language：Japanese  

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  • REGULATION OF STRESS-ACTIVATED MAP KINASE PATHWAYS DURING CELL FATE DECISIONS Reviewed

    Mutsuhiro Takekawa, Yuji Kubota, Takanori Nakamura, Kenji Ichikawa

    NAGOYA JOURNAL OF MEDICAL SCIENCE   73 ( 1-2 )   1 - 14   2011.2

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    Language：English   Publisher：NAGOYA UNIV, SCHOOL MED  

    Mammalian cells are frequently exposed to a variety of environmental stresses, such as ultraviolet rays, ionizing radiation, genotoxins, heat shock, and oxidative stress. In coping with the barrage of these and other stresses, multi-cellular eukaryotic organisms have developed a strategy as to how damaged cells will respond to stresses. In general, if the intensity of the damage is moderate, the cell will seek to repair the damage. If, however, the damage to a cell is too severe to be repaired, the affected cells are eliminated by apoptosis. This cell death reduces the risk to the organism as a whole, such as development of a cancer. Such a crucial decision between survival and death is, at least in part, mediated by the stress-activated MAP kinase (SAPK) pathways. SAPKs are a group of serine/threonine protein kinases that convert extracellular stress stimuli into diverse cellular responses, including cell cycle arrest, apoptotic cell death, and cytokine production, through phosphorylation of specific target proteins. Recent progress in the identification of molecules that participate in the SAPK pathways, such as GADD45 proteins and Wip1, has provided new insights, not only into the molecular basis of the cellular response to environmental stress, but also into the etiology of human diseases including cancer.

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  • REGULATION OF STRESS-ACTIVATED MAP KINASE PATHWAYS DURING CELL FATE DECISIONS Reviewed

    TAKEKAWA MUTSUHIRO, KUBOTA YUJI, NAKAMURA TAKANORI, ICHIKAWA KENJI

    Nagoya Journal of Medical Science   73 ( 1 )   1 - 14   2011.2

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    Language：English   Publisher：Nagoya University School of Medicine  

    Mammalian cells are frequently exposed to a variety of environmental stresses, such as ultraviolet rays, ionizing radiation, genotoxins, heat shock, and oxidative stress. In coping with the barrage of these and other stresses, multi-cellular eukaryotic organisms have developed a strategy as to how damaged cells will respond to stresses. In general, if the intensity of the damage is moderate, the cell will seek to repair the damage. If, however, the damage to a cell is too severe to be repaired, the affected cells are eliminated by apoptosis. This cell death reduces the risk to the organism as a whole, such as development of a cancer. Such a crucial decision between survival and death is, at least in part, mediated by the stress-activated MAP kinase (SAPK) pathways. SAPKs are a group of serine/threonine protein kinases that convert extracellular stress stimuli into diverse cellular responses, including cell cycle arrest, apoptotic cell death, and cytokine
    production, through phosphorylation of specific target proteins. Recent progress in the identification of molecules that participate in the SAPK pathways, such as GADD45 proteins and Wip1, has provided new insights, not only into the molecular basis of the cellular response to environmental stress, but also into the etiology of human diseases including cancer.

    File： v73n12p1_14.pdf

    DOI： 10.18999/nagjms.73.1-2.1

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    Other Link： http://search.jamas.or.jp/link/ui/2012123094

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Books

  • ストレス顆粒形成による生命機能制御と疾患

    吉岡 大介, 中村 貴紀, 武川 睦寛（ Role： Contributor）

    羊土社 実験医学 増刊「相分離-メカニズムと疾患-」  2021.6 

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  • JNK/p38-AP1経路とストレス反応系

    中村 貴紀, 武川 睦寛

    日本臨床増刊「分子標的薬：がんから他疾患までの治癒をめざして」  2012.11 

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MISC

  • Comprehensive understanding of BCR-ABL interactome in CML using proximity-dependent biotin labeling

    2P-828   2024.11

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  • Analysis of BCR-ABL drug-responsive interactions that induce chronic myeloid leukemia (CML)

    1P-818   2024.11

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  • Elucidation of the stress response mechanism through spatiotemporal regulation of SAPKK

    1P-462 (1MS-02-06)   2024.11

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  • Functional analysis of miRNA-X, whose expression is regulated by SAPK, in colorectal cancer

    1P-838   2024.11

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  • 近位依存性タンパク質間相互作用から迫る慢性骨髄性白血病 (CML) 病態の包括的理解と 新規創薬標的分子の探索

    中村 貴紀, 山内 陽生, 山田 航大, 小迫 英尊, 増本 純也, 澤崎 達也

    第20回 日本病理学会カンファレンス   P16   2024.7

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper, summary (national, other academic conference)  

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  • Exploring New Drug Targets for Chronic Myeloid Leukamia

    Yosei Yamauchi, Takanori Nakamura, Hidetaka Kosako, Mikihiko Naito, Tatsuya Sawasaki

    1P-818 (1SP-10-10)   2023.12

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  • Regulation of DNA damage-induced apoptosis by a tumor suppressor SAPKK

    Hisashi Moriizumi, Takanori Nakamura, Takashi Suzuki, Mutsuhiro Takekawa

    The 82nd Annual Meeting of The Japanese Cancer Association   P-3038   2023.9

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  • SAPK-regulated microRNA-X suppresses the expression of tumor suppressor miRNA in colorectal cancer

    Tokai Noriko, Nakamura Takanori, Takekawa Mutsuhiro

    The 82nd Annual Meeting of The Japanese Cancer Association   P-2060   2023.9

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  • 中心小体輸送の分子基盤と発育不全疾患におけるその破綻 Invited

    中村 貴紀, 西住 紀子, 河西 通, 中澤 崇, 森 竜樹, 武田 洋幸, 鈴木 貴, 武川 睦寛

    CREST 多細胞領域 第 4 回領域会議   2023.1

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  • Identification of novel core protein essential for stress granule formation under heat shock

    The 44th Annual Meeting of Molecular Biology Society of Japan   3P-0233   2021.12

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  • Mathematical modeling of the molecular mechanism underlying the recruitment of centriole biogenesis regulators to mother centrioles

    Nakamura Takanori, Nishizumi-Tokai Noriko, Nakazawa Takashi, Mori Tatsuki, Suzuki Takashi, Takekawa Mutsuhiro

    The 80th Annual meeting of Japanese Cancer Association   2021.9

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  • A novel analog-to-digital conversion system determines cell survival or death

    Hisashi ‌Moriizumi, Takanori‌ Nakamura, Youngmin‌ Cho, Toru‌ Kawanishi, Hiroyuki‌ Takeda, Takashi ‌Suzuki, Mutsuhiro‌Takekawa

    The 73rd Annual Meeting of the Japan Society for Cell biology   WS21-5   2021.7

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  • APEX2を用いた近位ビオチン標識法と質量分析を活用した熱刺激誘導性液-液相分離顆粒コアタンパク質の探索

    松田碧, 中村貴紀, 小迫英尊, 武川睦寛

    第72回日本電気泳動学会総会   2021.7

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  • Proteomic screening for novel stress granule components and their functional analysis

    Daisuke Yoshioka, Takanori Nakamura, Mitsuhiro Takekawa

    The 43rd Annual Meeting of Molecular Biology Society of Japan   2P-0067   2020.12

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  • ストレス顆粒形成を制御する分子機構の解析

    橋本 夏葉, 中村 貴紀, 武川 睦寛

    第42回日本分子生物学会   1P-0204   2019.12

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  • Mathematical modeling of the molecular mechanism that recruits centriole biogenesis regulators to mother centrioles Invited

    Nakamura Takanori, Nishizumi-Tokai Noriko, Nakazawa Takashi, Mori Tatsuki, Suzuki Takashi, Takekawa Mutsuhiro

    The 78th Annual meeting of Japanese Cancer Association   2019.9

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  • Stress-responsive MAP kinase pathways mediate apoptosis by downregulating the expression of an anti-apoptotic miRNA

    Tokai Noriko, Nakamura Takanori, Takekawa Mutsuhiro

    The 78th Annual meeting of Japanese Cancer Association   2019.9

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  • ストレス顆粒形成によるアポトーシス抑制機構の解明

    藤川 大地, 中村 貴紀, 武川 睦寛

    第41回日本分子生物学会年会   2P-0358   2018.11

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  • 数理解析を活用したSAPKシグナル時空間制御機構の解明

    森泉 寿士, 中村 貴紀, 曺 永旻, 鈴木 貴, 武川 睦寛

    第41回日本分子生物学会年会   1P-0317   2018.11

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  • 数理解析を駆使した中心体複製開始を制御する分子機構の解明

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    第41回日本分子生物学会年会   2P-0255   2018.11

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  • ストレス応答MAPキナーゼによるアポトーシス抑制性miRNAの発現制御

    渡海 紀子, 中村 貴紀, 武川 睦寛

    第41回日本分子生物学会年会   1P-0381   2018.11

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  • ストレス顆粒を構成する新規因子の同定とその機能解析

    田口 真梨, 中村 貴紀, 武川 睦寛

    第41回日本分子生物学会年会   3P-0244   2018.11

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  • 数理解析を用いた中心体複製の開始制御機構の解明 Invited

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    日本応用数理学会年会   347 - 348   2018.9

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  • Stress-activated p38 and JNK pathways downregulate an anti- apoptotic miRNA

    Noriko Tokai-Nishizumi, Takanori Nakamura, Mutuhiro Takekawa

    Cancer Science   P-1059   2018.9

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  • 新規ERK基質分子MCRIP1の生理機能解析

    Jane S. Weng, 中村 貴紀, 武川 睦寛

    2017年度生命科学系学会合同年次大会（第40回日本分子生物学会・第90回日本生化学会）   3P-0646   2017.12

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  • ストレス応答キナーゼMTK1による新たなストレス感知・応答機構

    松下萌恵, 中村 貴紀, 武川 睦寛

    2017年度生命科学系学会合同年次大会（第40回日本分子生物学会・第90回日本生化学会）   1P-0551   2017.12

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  • 中心体複製開始を司るPLK4中心体局在機構の解明

    中村貴紀, 西住(渡海)紀子, 中澤嵩, 鈴木貴, 武川睦寛

    2017年度生命科学系学会合同年次大会（第40回日本分子生物学会・第90回日本生化学会）   3P-384 (AT19-08)   2017.12

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  • ストレス応答MAPK経路によって制御されるmiRNAの機能解析

    渡海 紀子, 中村 貴紀, 武川 睦寛

    2017年度生命科学系学会合同年次大会（第40回日本分子生物学会・第90回日本生化学会）   2P-0481   2017.12

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  • Epigenetic regulation of pulmonary surfacetant protein expression by MCRIP1: a novel mouse model for respiratory distress syndrome

    Jane Weng, Takanori Nakamura, Mutsuhiro Takekawa

    12th International Symposium of the institute Network   2017.11

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  • Functional analysis of a novel ERK substrate, MCRIP1

    Jane Weng, Takanori Nakamura, Mutsuhiro Takekawa

    24th East Asia Joint Symposium on Biomedical Research   2017.10

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  • Feedback-phosphorylation of MKK4 by SAPKs promotes apoptosis

    Hisashi Moriizumi, Takanori Nakamura, Mutsuhiro Takekawa

    Cancer Science   P-2087   2017.9

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  • Comprehensive analysis of stress granule components

    Daichi Fujikawa, Takanori Nakamura, Mutsuhiro Takekawa

    CIMR(Cambridge Institute for Medical Research)-University of Tokyo Student Symposium   2017.9

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  • TheThe molecular mechanisms that maintain the numerical integrity of centrosomes under stress Reviewed

    Nakamura Takanori

    EMBO Conference: Centrosomes and Spindle Pole bodies   146 - 146   2017.9

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  • Functional analysis of feedback-phosphorylation of MKK4 by MAPKs

    Hisashi Moriizumi, Takanori Nakamura, Mutsuhiro Takekawa

    AACR Annual Meeting 2017   2017.4

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  • Functional analysis of feedback-phosphorylation of MKK4 by MAPKs

    Moriizumi Hisashi, Takanori Nakamura, Mutsuhito Takekawa

    IARU International Symposium on Aging, Longevity and Health   2016.11

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  • ストレス応答MAPK経路依存的に発現調節されるmiRNAの同定

    西住(渡海)紀子, 中村貴紀, 武川睦寛

    第39回日本分子生物学会年会   2016.11

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  • The molecular mechanisms that maintain the numerical integrity of centrosomes under stress

    T. Nakamura, M. Takekawa

    MOLECULAR BIOLOGY OF THE CELL   27   146   2016

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  • The molecular mechanisms that maintain the numerical integrity of centrosomes under stress

    T. Nakamura, M. Takekawa

    MOLECULAR BIOLOGY OF THE CELL   27   2016

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  • 新規ERK基質分子MCRIP1の生理機能解析

    Jane S. Weng, 中村 貴紀, 武川 睦寛

    BMB2015 (第38回日本分子生物学会・第88回日本生化学会 合同大会）   3P0724   2015.12

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  • Identification of a novel redox-sensor that mediates activation of stress-responsive MAPK pathways

    Moe Matsushita, Takanori Nakamura, Mutsuhito Takekawa

    22nd East Asia Joint symposium on Biomedical Research   2015.11

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  • TumoursuppressorsMKK4andp53cooperativelymaintain centrosome integrity and chromosomal stability

    Takanori Nakamura, Noriko Nishizumi-Tokai, Eriko Mikoshi, Moe Matsushita, Mutsuhiro Takekawa

    P-1123   2015.10

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  • ストレス応答MAPKK, MKK4のフィードバック・リン酸化と新規結合分子の同定および機能解析

    中村 貴紀, 武川 睦寛, 斎藤 春雄

    GCOE リトリート   PA-25   2009.3

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  • ストレス応答MAPKK, MKK4のフィードバック・リン酸化と新規結合分子の探索

    中村 貴紀, 武川 睦寛, 斎藤 春雄

    GCOE リトリート   PA-30   2008.10

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  • MAPKによるストレス応答MAPKK, MKK4のフィードバック・リン酸化とその機能解析

    中村 貴紀, 武川 睦寛, 斎藤 春雄

    東京大学生命科学研究ネットワークシンポジウム 2008   PA-002   2008.9

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  • MAPキナーゼによるストレス応答MAPKK, MKK4のフィードバック・リン酸化

    中村 貴紀, 武川 睦寛, 齋藤 春雄

    第30回日本分子生物学会年会・第80回日本生化学会大会合同大会   2P-0366   2007.12

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  • Molecular Dynamicsを用いたBcl-xLホットスポット領域の同定とアンタゴニスト設計

    高橋哲, 吉森篤史, 中村貴紀, 川西令紗, 高澤涼子, 田沼靖一

    第15回 日本アポトーシス研究会学術集会   2006.7

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  • コンピュータを用いた新規Bcl-xL阻害剤の設計

    中村貴紀, 高橋哲, 高澤涼子, 吉森篤史, 田沼靖一

    第78回 日本生化学会大会   4P-050   2005.10

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Presentations

  • 慢性骨髄性白血病のがん病態シグナル伝達を担う動的複合体の包括的理解~がん治療を目指 した新たな創薬標的分子の創出~ Invited

    中村 貴紀, 山内 陽生, 小迫 英尊, 内藤 幹彦, 増本 純也, 澤崎 達也

    2024年度【先端モデル動物支援プラットフォーム】成果発表会  2025.2 

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    Event date： 2025.2

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • SAPKKの時空間制御による生体ストレス応答機構の解明

    森泉 寿士, 中村 貴紀, 曺永 旻, 河西 通, 武田 洋幸, 鈴木 貴, 武川 睦寛

    第47回日本分子生物学会 1MS-02-06(1P-462)  2024.11 

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  • Mathematical model of mTORC1 pathway sensing intracellular amino-acids and glucose Invited International conference

    Takanori Nakamura, Shigeyuki Nada, Takashi Suzuki, Masato Okada

    10th International Congress on Industrial and Applied Mathematics (ICIAM2023 Tokyo) 0114-4D-04349  2023.8  International Congress on Industrial and Applied Mathematics (ICIAM)

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    Event date： 2023.8

    Language：English   Presentation type：Symposium, workshop panel (nominated)  

    Venue：Waseda University, Tokyo, Japan   Country：Japan  

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  • mTORC1経路 Invited

    中村貴紀, 名田茂之, 鈴木貴, 岡田雅人

    2022年度数理腫瘍学年末研究会  2022.12 

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    Event date： 2022.12

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  • Molecular basis of the recruitment of centriole-biogenesis regulators to mother centrioles Invited

    Takanori Nakamura, Noriko Tokai, Takashi Nakazawa, Tatsuki Mori, Takashi Suzuki, Mutsuhiro Takekawa

    The 81st Annual Meeting of the Japanese Cancer Association  2022.9 

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    Event date： 2022.9 - 2022.10

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  • SAPK down regulates miR-X expression through Sp1 phosphorylation

    Noriko Tokai, Takanori Nakamura, Mutsuhiro Takekawa

    The 81st Annual Meeting of the Japanese Cancer Associationhe 81  2022.10 

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    Event date： 2022.9 - 2022.10

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  • Mathematical analysis of the mechanism of how centriole biogenesis regulators are transported to mother centrioles Invited

    Takanori Nakamura, Noriko Tokai, Takashi Nakazawa, Tatsuki Mori, Takashi Suzuki, Mutsuhiro Takekawa

    The 80th Annual Meeting of the Japan Cancer Association  2021.9 

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    Event date： 2021.9 - 2021.10

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  • SAPK-regulated microRNA-X suppresses apoptosis in colorectal cancer Invited

    Noriko Tokai, Takanori Nakamura, Mutsuhiro Takekawa

    The 80th Annual Meeting of the Japan Cancer Associationf  2021.10 

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    Event date： 2021.9 - 2021.10

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  • Mathematical modeling of the recruitment of centriole biogenesis regulators to mother centrioles in the S-phase Invited

    Takanori Nakamura, Noriko Nishizumi-Tokai, Takashi Nakazawa, Tatsuki Mori, Takashi Suzuki, Mutsuhiro Takekawa

    JSPS Core-to-Core Program "Establishing International Research Network of Mathematical Oncology"  2020.10 

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    Event date： 2020.10

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  • 数理解析を活用したSAPKシグナル時空間制御機構の解明

    森泉 寿士, 中村 貴紀, 曺 永旻, 鈴木 貴, 武川 睦寛

    新学術領域「数理シグナル」第２回若手ワークショップ  2018.8 

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  • Mathematical modeling of the recruitment of centriole biogenesis regulators to mother centrioles in centriole duplication phase Invited

    Takanori Nakamura, Nishizumi-Tokai Noriko, Takashi Nakazawa, Tatsuki Mori, Takashi Suzuki, Mutsuhiro Takekawa

    JSPS Core-to-Core Program "Establishing International Research Network of Mathematical Oncology" @ Bordeaux  2019.3 

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  • 数理解析を用いた中心体複製の開始制御機構の解明 Invited International conference

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    日本応用数理学会  2018.9 

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  • Centrosome integrity under stress is maintained by a network of PLK4, p53 and SAPK pathways. Invited International conference

    Nakamura Takanori, Takekawa Mutsuhiro

    The 65th Japan Society for cell biology  2013.6 

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  • SAPK pathways and p53 cooperatively regulate PLK4 activity and centrosome integrity under stress.

    Nakamura Takanori, Takekawa Mutsuhiro

    7th Retreat Meeting of IMSUT & RCAST Global COE  2013.11 

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  • Centrosome integrity under stress is maintained by a network of PLK4, p53 and SAPK pathways. Invited International conference

    Takanori Nakamura, Mutsuhiro Takekawa

    72th Japanese Cancer Association  2013.10 

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  • 中心体複製開始を司るPLK4中心体局在機構の解明 International conference

    中村貴紀, 西住(渡海)紀子, 中澤嵩, 鈴木貴, 武川睦寛

    2017年度生命科学系学会合同年次会（第40回日本分子生物学会・第90回日本生化学会）4AT19-08  2017.12 

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  • 癌抑制遺伝子MKK4とp53による中心体数および染色体安定性の保持機構と癌におけるその 破綻 Invited

    中村 貴紀, 武川 睦寛

    第52回日本臨床分子医学会  2015.4 

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  • 発育不全疾患の発症メカニズムの解明と神経変性疾患治療を目指した取り組み Invited

    中村 貴紀

    PROS第1回合同教員会議 ショートセミナー  2023.4 

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  • 非膜型オルガネラを介した生体内恒常性の制御： その破綻に伴う癌および発育不全疾患の発症機構 Invited

    中村 貴紀

    愛媛大学プロテオサイエンスセンターPROSセミナー  2022.10 

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  • 中心体複製初期に起こるPLK4の中心体輸送機構 Invited International conference

    中村 貴紀, 西住(渡海) 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    第19回日本蛋白質科学年会・第71回日本細胞生物学会 合同年次大会  2019.6 

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  • Mathematical modeling of the molecular mechanism that recruits centriole biogenesis regulators to mother centrioles Invited International conference

    Nakamura Takanori, Nishizumi Noriko, Nakazawa Takashi, Mori Tatsuki, Suzuki Takashi, Takekawa Mutsuhiro

    The 78th annual meeting of Japan Cancer Association  2019.9 

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  • 非膜型細胞内小器官の観点から捉える生体内恒常性の維持機構 Invited

    中村 貴紀

    第301回 愛媛大学 応用化学セミナー  2023.11 

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  • 数理解析を用いた中心体複製の開始制御機構の解明

    中村 貴紀, 西住 紀子, 中澤 嵩, 森 竜樹, 鈴木 貴, 武川 睦寛

    新学術領域「数理シグナル」第２回若手ワークショップ  2018.9 

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Awards

  • 研究助成

    2024.2   高松宮妃癌研究基金  

    中村 貴紀

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  • Grant-in-aid for Research

    2020.12   Mochida Memorial Foundation for Medical and Pharmaceutical Research  

    Nakamura Takanori

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  • Grant-in-aid for Research

    2019.8   Takeda Science Foundation  

    Nakamura Takanori

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  • Young Scientist's Award

    2019.6   Japan Society for Cell Biology  

    Nakamura Takanori

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

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  • Grant-in-aid for Research

    2018.3   The Uehara Memorial Foundation  

    Nakamura Takanori

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    Award type：Award from publisher, newspaper, foundation, etc.  Country：Japan

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  • Grant for Japan-related Research Projects

    2016.11   The Sumitomo Foundation  

    Nakamura Takanori

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    Award type：Award from publisher, newspaper, foundation, etc.  Country：Japan

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  • Best Poster Award

    2015.6  

    Takanori Nakamura

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

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  • Young Investigator Award

    2015.4   Japanese Society of Molecular Medicine  

    Nakamura Takanori

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

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  • Excellent Presenter Award

    2013.11   7th Retreat Meeting of IMSUT & RCAST Global COE  

    Nakamura Takanori

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  • Best Discusser Award

    2013.10  

    Takanori Nakamura

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

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  • ベストポスター賞

    2012.9   文部科学省科学研究費補助金 新学術領域研究『がん研究分野の特性等を踏まえた支援活動』がん若手ワークショプ  

    中村 貴紀

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

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  • Outstanding Performance Award

    2012.6  

    Takanori Nakamura

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

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Research Projects

  • 中心体タンパク質の機能不全によって引き起こされる疾患の病態解明

    2025.1 - 2027.3

    文部科学省  学術変革領域研究 学術研究支援基盤形成 先端バイオイメージング支援プラットフォーム（ABiS) 

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    Authorship：Principal investigator 

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  • 中心体タンパク質の生理機能と疾患におけるその破綻

    2024.7 - 2027.3

    文部科学省  学術変革領域研究 学術研究支援基盤形成 先端モデル動物支援プラットフォーム (AdAMS) 

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  • 初期発生制御分子群の相互作用マップの創出~発育不全病態の包括的理解~

    2024.4 - 2027.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    中村 貴紀

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

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  • がん特有の多極分裂回避機構を標的とする抗がん剤の創出

    2024.3 - 2026.3

    高松宮妃癌研究基金  研究助成金 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\2000000

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  • 疾患発症機構の解明と新たな創薬標的の創出

    2023.12 - 2024.3

    愛媛大学 プロテオサイエンスセンター  社会実装促進支援プロジェクト 

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    Authorship：Principal investigator 

    Grant amount：\300000

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  • 中心体複製の開始機構と個体発生におけるその破綻

    2021.4 - 2024.3

    日本学術振興会 科学研究費  基盤研究(C) 

    中村 貴紀

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    Authorship：Principal investigator 

    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

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  • 中心体複製開始の基本原理と抗癌剤開発におけるその応用

    2020.12 - 2021.11

    持田記念医学薬学振興財団  研究助成 

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    Authorship：Principal investigator 

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  • ｢中心体複製開始の制御機構｣と癌診断／治療におけるその応用

    2019.8 - 2022.5

    武田科学振興財団  医学系研究助成 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\2000000

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  • 中心体複製開始の分子制御機構を利用した新たな抗癌剤開発

    2018.4 - 2021.3

    日本学術振興会 科学研究費  若手研究 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • 中心体複製開始制御機構と抗癌剤開発におけるその応用

    2017.12 - 2019.4

    上原記念生命科学財団  研究奨励 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • 中心体複製開始を制御する機構と癌におけるその破綻

    2017.7 - 2018.3

    小笠原財団  国際研究集会出張助成 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • 中心体複製開始を制御する分子機構と癌におけるその破綻

    2016.11 - 2017.11

    住友財団  基礎科学研究助成 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • 中心体複製制御機構の解明と癌におけるその破綻

    2016.7 - 2017.3

    小笠原財団  国際研究集会出張助成 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • SAPKおよびPLK4による中心体複製の開始と停止を制御する分子機構の解明

    2016

    文部科学省  新学術研究「学術研究支援基盤形成」先端モデル動物支援プラットフォーム (AdAMS) 

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    Authorship：Principal investigator 

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  • 新規MAPK基質分子による遺伝子発現制御機構と癌におけるその破綻

    2015.4 - 2018.3

    日本学術振興会 科学研究費  基盤研究 B 

    武川 睦寛

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    Grant type：Competitive

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  • SAPKおよびPLK4による中心体複製の開始と停止を制御する分子機構の解明

    2015.4 - 2017.3

    日本学術振興会 科学研究費  若手研究 B 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • SAPK新規標的分子の中心体複製抑制機構及びPLK4の中心体移行機構の解明

    2013.8 - 2015.3

    日本学術振興会 科学研究費  研究活動スタート支援 

    中村 貴紀

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    Authorship：Principal investigator  Grant type：Competitive

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  • MAPキナーゼ情報伝達経路による新たな細胞増殖制御機構と発癌

    2010.3 - 2013.5

    東レ科学振興会  東レ科学技術研究助成 

    武川 睦寛

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    Grant type：Competitive

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Teaching Experience (On-campus)

  • 2024年度第４クォーター / 先端研究入門B

  • 2024年度後期 / 学部共通PBL

  • 2024年度通年 / 病理学総論

  • 2024年度通年 / 病理学各論

  • 2024年度第２クォーター / 先端研究入門B

Teaching Experience

  • 病理学総論、病理学各論

    2024.4 Institution：愛媛大学医学部医学科

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  • 先端研究入門B

    2024.4 Institution：愛媛大学 共通教育

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  • 分子生物学、細胞生物学、生化学

    2023.4 - 2024.3 Institution：愛媛大学大学院理工学研究科 理工学専攻 応用化学講座

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  • 数理解析, 数理モデル, 数理シミュレーション

    2017.4 Institution：大阪大学 MMDSセンター

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  • 分子生物学, 細胞生物学, 生化学

    2013.4 - 2023.3 Institution：東京大学理学系研究科生物科学専攻

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Social Activities

  • 研究室体験

    Role(s)： Lecturer,　Demonstrator

    愛媛大学-松山南高校 (SSH)  愛媛大学研究室体験  2024.12

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    Type：Research consultation

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  • アウトリーチ活動：研究室見学

    Role(s)： Demonstrator

    2019.8

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    Type：Other

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  • アウトリーチ活動：研究室見学

    Role(s)： Demonstrator

    2018.3

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    Type：Other

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  • アウトリーチ活動：研究室見学

    Role(s)： Demonstrator

    2018.2

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    Type：Other

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  • アウトリーチ活動：研究室見学

    Role(s)： Demonstrator

    2017.9

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    Type：Other

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  • アウトリーチ活動：研究室見学

    Role(s)： Demonstrator

    2017.3

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    Type：Other

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