Updated on 2025/04/16

写真b

 
HIGUCHI Maiko
 
*Items subject to periodic update by Rikkyo University (The rest are reprinted from information registered on researchmap.)
Affiliation*
College of Science Department of Life Science
Graduate School of Science Doctoral Program in Life Science
Graduate School of Science Master's Program in Life Science
Title*
Associate Professor
Degree
博士(工学) ( 東京大学 )
Campus Career*
  • 4 2021 - Present 
    College of Science   Department of Life Science   Associate Professor
  • 4 2021 - Present 
    Graduate School of Science   Master's Program in Life Science   Associate Professor
  • 4 2021 - Present 
    Graduate School of Science   Doctoral Program in Life Science   Associate Professor
  • 11 2017 - 3 2021 
    College of Science   Assistant Professor
 

Research Areas

  • Life Science / Cell biology

Research History

  • 4 2021 - Present 
    Rikkyo University   College of Science

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  • 11 2017 - 3 2021 
    RIKKYO UNIVERSITY   College of Science   Assistant Professor

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  • 4 2014 - 10 2017 
    東京大学   薬学部   助教

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  • 1 2013 - 3 2014 
    Max Planck Institute for Heart and Lung Research   研究員

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  • 1 2012 - 12 2012 
    University of California, San Francisco   研究員

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Education

  • - 3 2003 
    The University of Tokyo   Graduate School, Division of Engineering

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    Country: Japan

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  • - 3 2000 
    The University of Tokyo   Graduate School, Division of Engineering

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    Country: Japan

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  • - 3 1998 
    The University of Tokyo   Faculty of Engineering

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    Country: Japan

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Papers

  • Maternal stress suppresses cell proliferation in the forebrain of zebrafish larvae Peer-reviewed

    Maiko Higuchi

    Genes to Cells25 ( 5 ) 350 - 357   2020

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

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  • PDK1-Akt pathway regulates radial neuronal migration and microtubules in the developing mouse neocortex Peer-reviewed

    Yasuhiro Itoh, Maiko Higuchi, Koji Oishi, Yusuke Kishi, Tomohiko Okazaki, Hiroshi Sakai, Takaki Miyata, Kazunori Nakajima, Yukiko Gotoh

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA113 ( 21 ) E2955 - E2964   5 2016

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATL ACAD SCIENCES  

    Neurons migrate a long radial distance by a process known as locomotion in the developing mammalian neocortex. During locomotion, immature neurons undergo saltatory movement along radial glia fibers. The molecular mechanisms that regulate the speed of locomotion are largely unknown. We now show that the serine/threonine kinase Akt and its activator phosphoinositide-dependent protein kinase 1 (PDK1) regulate the speed of locomotion of mouse neocortical neurons through the cortical plate. Inactivation of the PDK1-Akt pathway impaired the coordinated movement of the nucleus and centrosome, a microtubule-dependent process, during neuronal migration. Moreover, the PDK1-Akt pathway was found to control microtubules, likely by regulating the binding of accessory proteins including the dynactin subunit p150(glued). Consistent with this notion, we found that PDK1 regulates the expression of cytoplasmic dynein intermediate chain and light intermediate chain at a posttranscriptional level in the developing neocortex. Our results thus reveal an essential role for the PDK1-Akt pathway in the regulation of a key step of neuronal migration.

    DOI: 10.1073/pnas.1516321113

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  • The ASK family kinases differentially mediate induction of type I interferon and apoptosis during the antiviral response Peer-reviewed

    Tomohiko Okazaki, Maiko Higuchi, Kohsuke Takeda, Kiyoko Iwatsuki-Horimoto, Maki Kiso, Makoto Miyagishi, Hideyuki Yanai, Atsushi Kato, Mitsutoshi Yoneyama, Takashi Fujita, Tadatsugu Taniguchi, Yoshihiro Kawaoka, Hidenori Ichijo, Yukiko Gotoh

    SCIENCE SIGNALING8 ( 388 ) ra78   8 2015

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:AMER ASSOC ADVANCEMENT SCIENCE  

    Viral infection activates host defense mechanisms, including the production of type I interferon (IFN) and the apoptosis of infected cells. We investigated whether these two antiviral responses were differentially regulated in infected cells. We showed that the mitogen-activated protein kinase (MAPK) kinase kinase (MAPKKK) apoptosis signal-regulating kinase 1 (ASK1) was activated in cells by the synthetic double-stranded RNA analog polyinosinic: polycytidylic acid [poly(I:C)] and by RNA viruses, and that ASK1 played an essential role in both the induction of the gene encoding IFN-beta (IFNB) and apoptotic cell death. In contrast, we found that the MAPKKK ASK2, a modulator of ASK1 signaling, was essential for ASK1-dependent apoptosis, but not for inducing IFNB expression. Furthermore, genetic deletion of either ASK1 or ASK2 in mice promoted the replication of influenza A virus in the lung. These results indicated that ASK1 and ASK2 are components of the antiviral defense mechanism and suggested that ASK2 acts as a key modulator that promotes apoptosis rather than the type I IFN response. Because ASK2 is selectively present in epithelium-rich tissues, such as the lung, ASK2-dependent apoptosis may contribute to an antiviral defense in tissues with a rapid repair rate in which cells could be readily replaced.

    DOI: 10.1126/scisignal.aab1883

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  • NEDDylation controls the target specificity of E2F1 and apoptosis induction Peer-reviewed

    I. Aoki, M. Higuchi, Y. Gotoh

    ONCOGENE32 ( 34 ) 3954 - 3964   8 2013

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    The transcription factor E2F1 has pivotal roles in both cell proliferation and cell death, and is an important molecular target in cancer. Under proliferative conditions E2F1 induces the expression of genes that promote cell cycle progression, such as E2F2, whereas under proapoptotic conditions E2F1 induces expression of genes such as p73 that lead to apoptosis. The mechanism by which the apoptotic function of E2F1 is activated remains unclear, however. We now show that members of the E2F family are covalently conjugated with the ubiquitin-like modifier NEDD8. Overexpression of SENP8, a NEDD8-specific cysteine protease, resulted in deNEDDylation of E2F1 and promoted its transactivation activity at the p73 gene but not at the E2F2 gene. Knockdown of SENP8, on the other hand, attenuated p73 expression and apoptosis induced by E2F1 or by DNA damage. SENP8 also promoted the interaction between E2F1 and its cofactor Microcephalin 1, which is required for p73 induction. These results suggest that NEDDylation is a molecular trigger that modifies the target specificity of E2F1, and could have important implications for E2F1 regulation of apoptosis.

    DOI: 10.1038/onc.2012.428

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  • Mitochondrial localization of the antiviral signaling adaptor IPS-1 is important for its induction of caspase activation Peer-reviewed

    Tomohiko Okazaki, Maiko Higuchi, Yukiko Gotoh

    Genes to Cells18 ( 6 ) 493 - 501   6 2013

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

    The RIG-I-like receptor (RLR) family of intracellular receptors detects viral nucleic acids and transmits an antiviral signal through the adaptor IPS-1. IPS-1 activation triggers host defense mechanisms, including rapid production of type I interferon (IFN), such as IFN-β, and induction of apoptosis. IPS-1 is mainly localized to mitochondria, and this localization has been proposed to be essential for inducing production of type I IFN and IFN-stimulated genes (ISGs). However, the importance of this mitochondrial localization of IPS-1 in executing apoptosis has remained unclear. Here, using IPS-1 mutants that were directed to specific subcellular locations such as cytoplasm, plasma membrane and mitochondria, we found that IPS-1's localization to mitochondria is important to activate caspase, but not to signal for IFN-β gene induction. We also found that IPS-1 possesses a BH3-like motif, which is commonly found among members of the Bcl-2 family. Mutations within this motif promoted IPS-1-induced caspase activation, suggesting that this domain acts as an intrinsic inhibitor domain of apoptosis induction. These results establish that the mitochondrial location of IPS-1 is essential to its ability to induce apoptosis. © 2013 by the Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd.

    DOI: 10.1111/gtc.12052

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Misc.

  • Metatranscriptome analyses indicate resource partitioning between diatoms in the field (vol 112, pg E2182, 2015)

    Yasuhiro Itoh, Maiko Higuchi, Koji Oishi, Yusuke Kishi, Tomohiko Okazaki, Hiroshi Sakai, Takaki Miyata, Kazunori Nakajima, Yukiko Gotoh

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA113 ( 25 ) E3587 - E3587   6 2016

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    Language:English   Publishing type:Other   Publisher:NATL ACAD SCIENCES  

    DOI: 10.1073/pnas.1608043113

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  • PIキナーゼ-Akt経路 Invited

    樋口 麻衣子

    生体の科学   2015

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

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  • 新規翻訳後修飾による抗ウイルス応答分子IPS-1の機能の使い分け

    岡崎朋彦, 樋口麻衣子, 後藤由季子

    生化学   2011

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  • 新規翻訳後修飾による抗ウイルス応答分子IPS-1の機能の使い分け

    岡崎朋彦, 樋口麻衣子, 後藤由季子

    日本Cell Death学会学術集会プログラム抄録集20th   2011

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  • JNK/p38MAPK経路によるウイルス応答制御メカニズム

    岡崎朋彦, 樋口麻衣子, 武田弘資, 宮岸真, 加藤篤, 米山光俊, 藤田尚志, 一條秀憲, 後藤由季子

    生化学   2009

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Research Projects

  • Regulation of cell cycle-dependent microtubule dynamics by the Akt1-EB2/RP1 signaling pathway

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research 

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    4 2022 - 3 2025

    Grant number:22K06134

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

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  • Akt-EB2/RP1による微小管動態の新規制御メカニズムと細胞極性制御

    日本学術振興会  科学研究費助成事業 

    樋口 麻衣子

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    4 2018

    Grant type:Competitive

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  • 原癌遺伝子Aktによる微小管安定化を介した細胞極性制御メカニズムの解明

    日本学術振興会  科学研究費助成事業 

    樋口 麻衣子

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    4 2015 - 3 2018

    Grant type:Competitive

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  • スーパー制限酵素を用いたゲノム・マニュピュレーション工学の創成

    日本学術振興会  科学研究費助成事業 

    小宮山 真

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    4 2010 - 3 2015

    Grant type:Competitive

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  • 原癌遺伝子Aktによる細胞極性制御メカニズムの解明

    日本学術振興会  科学研究費助成事業 

    樋口 麻衣子

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    4 2011 - 3 2012

    Grant type:Competitive

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