Updated on 2022/11/04

写真a

 
WATANABE Takahiro
 
Organization
Graduate School of Medicine Program in Integrated Medicine Microbiology and Immunology Assistant Professor
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Assistant Professor
Contact information
メールアドレス

Degree 1

  1. 博士(医学) ( 2016.3   名古屋大学 ) 

Research Interests 3

  1. 口腔外科学

  2. ウイルス学

  3. 腫瘍ウイルス学

Research Areas 2

  1. Life Science / Surgical dentistry

  2. Life Science / Virology

Research History 6

  1. Nagoya University   Assistant

    2017.10

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    Country:Japan

  2. Aichi Gakuin University

    2017.1

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    Country:Japan

  3. Nagoya University

    2016.4 - 2017.9

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    Country:Japan

  4. Fujita Health University

    2013.4

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    Country:Japan

  5. Fujita Health University   Assistant

    2011.4 - 2013.3

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    Country:Japan

  6. 浜松医療センター   臨床研修歯科医師

    2009.4 - 2011.3

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    Country:Japan

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Education 1

  1. Nagoya University   Graduate School, Division of Medical Sciences

    - 2016.3

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    Country: Japan

Professional Memberships 5

  1. 日本有病者歯科医療学会   専門医

  2. 日本口腔外科学会   認定医

  3. 日本ウイルス学会

  4. 日本癌学会

  5. 日本臨床ウイルス学会

Committee Memberships 2

  1.   実験動物部門利用委員  

    2020.4   

  2.   個人情報取扱委員  

    2017.10   

Awards 2

  1. 優秀ポスター発表賞 第66回日本口腔外科学会総会学術大会

    2021.11   EBウイルス関連腫瘍のがん微小環境における炎症性細胞浸潤メカニズムの解析

  2. 優秀ポスター発表賞

    2017.10   第62回日本口腔外科学会総会学術大会  

    渡辺 崇広

 

Papers 34

  1. Comprehensive Analyses of Intraviral Epstein-Barr Virus Protein-Protein Interactions Hint Central Role of BLRF2 in the Tegument Network. International journal

    Yuya Hara, Takahiro Watanabe, Masahiro Yoshida, H M Abdullah Al Masud, Hiromichi Kato, Tomohiro Kondo, Reiji Suzuki, Shutaro Kurose, Md Kamal Uddin, Masataka Arata, Shouhei Miyagi, Yusuke Yanagi, Yoshitaka Sato, Hiroshi Kimura, Takayuki Murata

    Journal of virology   Vol. 96 ( 14 ) page: e0051822   2022.7

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

    Protein-protein interactions (PPIs) are crucial for various biological processes. Epstein-Barr virus (EBV) proteins typically form complexes, regulating the replication and persistence of the viral genome in human cells. However, the role of EBV protein complexes under physiological conditions remains unclear. In this study, we performed comprehensive analyses of EBV PPIs in living cells using the NanoBiT system. We identified 195 PPIs, many of which have not previously been reported. Computational analyses of these PPIs revealed that BLRF2, which is only found in gammaherpesviruses, is a central protein in the structural network of EBV tegument proteins. To characterize the role of BLRF2, we generated two BLRF2 knockout EBV clones using CRISPR/Cas9. BLRF2 knockout significantly decreased the production of infectious virus particles, which was partially restored by exogenous BLRF2 expression. In addition, self-association of BLRF2 protein was found, and mutation of the residues crucial for the self-association affected stability of the protein. Our data imply that BLRF2 is a tegument network hub that plays important roles in progeny virion maturation. IMPORTANCE EBV remains a significant public health challenge, causing infectious mononucleosis and several cancer types. Therefore, the better understanding of the molecular mechanisms underlying EBV replication is of high clinical importance. As protein-protein interactions (PPIs) are major regulators of virus-associated pathogenesis, comprehensive analyses of PPIs are essential. Previous studies on PPIs in EBV or other herpesviruses have predominantly employed the yeast two-hybrid (Y2H) system, immunoprecipitation, and pulldown assays. Herein, using a novel luminescence-based method, we identified 195 PPIs, most of which have not previously been reported. Computational and functional analyses using knockout viruses revealed that BLRF2 plays a central role in the EBV life cycle, which makes it a valuable target for drug development.

    DOI: 10.1128/jvi.00518-22

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  2. Epstein-Barr virus tegument protein BGLF2 in exosomes released from virus-producing cells facilitates de novo infection. International journal

    Yoshitaka Sato, Masahiro Yaguchi, Yusuke Okuno, Hanako Ishimaru, Ken Sagou, Somi Ozaki, Takeshi Suzuki, Tomoki Inagaki, Miki Umeda, Takahiro Watanabe, Masahiro Fujimuro, Takayuki Murata, Hiroshi Kimura

    Cell communication and signaling : CCS   Vol. 20 ( 1 ) page: 95 - 95   2022.6

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    BACKGROUND: Viruses must adapt to the environment of their host cells to establish infection and persist. Diverse mammalian cells, including virus-infected cells, release extracellular vesicles such as exosomes containing proteins and miRNAs, and use these vesicles to mediate intercellular communication. However, the roles of exosomes in viral infection remain unclear. RESULTS: We screened viral proteins to identify those responsible for the exosome-mediated enhancement of Epstein-Barr virus (EBV) infection. We identified BGLF2 protein encapsulated in exosomes, which were released by EBV-infected cells. BGLF2 protein is a tegument protein that exists in the space between the envelope and nucleocapsid, and it is released into the cytoplasm shortly after infection. BGLF2 protein-containing exosomes enhanced viral gene expression and repressed innate immunity, thereby supporting the EBV infection. CONCLUSIONS: The EBV tegument protein BGLF2 is encapsulated in exosomes and released by infected cells to facilitate the establishment of EBV infection. These findings suggest that tegument proteins support viral infection not only between the envelope and nucleocapsid, as well as in extraviral particles such as exosomes. Video abstract.

    DOI: 10.1186/s12964-022-00902-7

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  3. EBV Exploits RNA m6A Modification to Promote Cell Survival and Progeny Virus Production During Lytic Cycle. International journal

    Yusuke Yanagi, Takahiro Watanabe, Yuya Hara, Yoshitaka Sato, Hiroshi Kimura, Takayuki Murata

    Frontiers in microbiology   Vol. 13   page: 870816 - 870816   2022.6

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

    N6-methyladenosine (m6A) mediates various biological processes by affecting RNA stability, splicing, and translational efficiency. The roles of m6A modification in Epstein-Barr virus (EBV) infection in the lytic phase are unclear. Here, knockout of the m6A methyltransferase, N6-methyladenosine methyltransferase-like 3 (METTL3), or inhibition of methylation by DAA or UZH1a decreased the expression of viral lytic proteins and reduced progeny virion production. Interestingly, cell growth and viability were decreased by induction of the lytic cycle in METTL3-knockout or inhibitor-treated cells. Apoptosis was induced in those conditions possibly because of a decreased level of the anti-apoptotic viral protein, BHRF1. Therefore, m6A shows potential as a target of lytic induction therapy for EBV-associated cancers, including Burkitt lymphoma.

    DOI: 10.3389/fmicb.2022.870816

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  4. PD-L1 upregulation by lytic induction of Epstein-Barr Virus.

    Yanagi Y, Hara Y, Mabuchi S, Watanabe T, Sato Y, Kimura H, Murata T

    Virology   Vol. 568   page: 31 - 40   2022.3

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    Epstein-Barr virus (EBV) is an etiologic agent of infectious mononucleosis and several malignancies. Here, we found that reactivation of EBV resulted in increased programmed cell death-ligand 1 (PD-L1) expression in a cell type-dependent manner. Lytic induction in EBV-positive Akata, AGS, MutuI, and Jijoye cell lines increased PD-L1 levels, but cells such as EBV-negative Akata, MutuIII, and P3HR1 did not have increased PD-L1. EBV in the P3HR1 cell line has a deletion in the EBNA2 gene, while EBV in its parental cell line, Jijoye, has the complete EBNA2 gene. PD-L1 expression by lytic induction was reduced when EBNA2 was knocked down. In addition, pharmacological inhibition indicated involvement of nuclear factor kappa B, mitogen-activated protein kinase, and AKT signaling. These results suggest that EBV likely evades immunity by inducing PD-L1 upon reactivation, through the increased expression of EBNA2 and activation of signaling pathways.

    DOI: 10.1016/j.virol.2022.01.006

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  5. Molecular Basis of Epstein-Barr Virus Latency Establishment and Lytic Reactivation. International journal

    Takayuki Murata, Atsuko Sugimoto, Tomoki Inagaki, Yusuke Yanagi, Takahiro Watanabe, Yoshitaka Sato, Hiroshi Kimura

    Viruses   Vol. 13 ( 12 )   2021.12

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

    Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of cancer. Like other herpesviruses, it establishes an asymptomatic, life-long latent infection, with occasional reactivation and shedding of progeny viruses. During latency, EBV expresses a small number of viral genes, and exists as an episome in the host-cell nucleus. Expression patterns of latency genes are dependent on the cell type, time after infection, and milieu of the cell (e.g., germinal center or peripheral blood). Upon lytic induction, expression of the viral immediate-early genes, BZLF1 and BRLF1, are induced, followed by early gene expression, viral DNA replication, late gene expression, and maturation and egress of progeny virions. Furthermore, EBV reactivation involves more than just progeny production. The EBV life cycle is regulated by signal transduction, transcription factors, promoter sequences, epigenetics, and the 3D structure of the genome. In this article, the molecular basis of EBV latency establishment and reactivation is summarized.

    DOI: 10.3390/v13122344

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  6. A STING inhibitor suppresses EBV-induced B cell transformation and lymphomagenesis. International journal

    Shouhei Miyagi, Takahiro Watanabe, Yuya Hara, Masataka Arata, Md Kamal Uddin, Keisuke Mantoku, Ken Sago, Yusuke Yanagi, Takeshi Suzuki, H M Abdullah Al Masud, Jun-Ichi Kawada, Shigeo Nakamura, Yasuyuki Miyake, Yoshitaka Sato, Takayuki Murata, Hiroshi Kimura

    Cancer science     2021.10

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

    Epstein-Barr virus-associated lymphoproliferative disease (EBV-LPD) is frequently fatal. Innate immunity plays a key role in protecting against pathogens and cancers. The stimulator of interferon genes (STING) is regarded as a key adaptor protein allowing DNA sensors recognizing exogenous cytosolic DNA to activate the type I interferon signaling cascade. In terms of EBV tumorigenicity, the role of STING remains elusive. Herein we showed that treatment with the STING inhibitor, C-176, suppressed EBV-induced transformation in peripheral blood mononuclear cells. In an EBV-LPD mouse model, C-176 treatment also inhibited tumor formation and prolonged survival. Treatment with B cells alone did not affect EBV transformation, but suppression of EBV-induced transformation was observed in the presence of T cells. Even without direct B cell-T cell contact in a Transwell system, the inhibitor reduced the transformation activity, indicating that intercellular communication by humoral factors was critical to prevent EBV-induced transformation. These findings suggest that inhibition of STING signaling pathway with C-176 could be a new therapeutic target of EBV-LPD.

    DOI: 10.1111/cas.15152

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  7. Deletion of Viral microRNAs in the Oncogenesis of Epstein-Barr Virus-Associated Lymphoma

    Kimura Hiroshi, Okuno Yusuke, Sato Yoshitaka, Watanabe Takahiro, Murata Takayuki

    FRONTIERS IN MICROBIOLOGY   Vol. 12   page: 667968   2021.7

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    Language:Japanese   Publisher:Frontiers in Microbiology  

    Epstein–Barr virus (EBV), which encodes >80 genes and nearly 50 non-coding RNAs, is a double-stranded DNA virus. EBV is associated with various types of lymphomas and lymphoproliferative disorders not only of B-cell but also T/NK-cell origin. However, the oncogenic mechanism remains poorly understood, including the EBV receptors expressed on T/NK cells, relationship of EBV with host genes, and epigenetic regulation of EBV and host genes. The roles of host and viral non-coding RNAs during tumorigenesis have been elucidated. EBV encodes at least 49 mature microRNAs (miRNAs), of which 44 are located in BamHI-A rightward transcripts (BARTs) region, and the remaining five are located in BamHI-H rightward fragment 1. BART miRNAs modulate cell differentiation, proliferation, apoptosis, and the cell cycle, and they are considered positive regulators of oncogenesis. We and others have recently reported that EBV-positive lymphomas frequently possess large deletions in BART miRNA clusters, suggesting that some viral miRNAs have suppressive effects on oncogenesis, and that deletion of these miRNAs may aid lymphoma formation.

    DOI: 10.3389/fmicb.2021.667968

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  8. RNAseq analysis identifies involvement of EBNA2 in PD-L1 induction during Epstein-Barr virus infection of primary B cells. Reviewed International journal

    Yusuke Yanagi, Yusuke Okuno, Yohei Narita, H M Abdullah Al Masud, Takahiro Watanabe, Yoshitaka Sato, Teru Kanda, Hiroshi Kimura, Takayuki Murata

    Virology   Vol. 557   page: 44 - 54   2021.5

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    Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of malignancy. RNAseq of peripheral blood primary B cell samples infected with wild-type EBV revealed that expression of programmed cell death ligand-1 (PD-L1) is markedly induced by infection. This induction of PD-L1 was alleviated by knockout of the EBNA2 gene, but knockout of LMP1 had little effect. ChIPseq, ChIA-PET, and reporter assays further confirmed that EBNA2-binding sites in the promoter region and at 130 kb downstream of the PD-L1 gene played important roles in PD-L1 induction. Our results indicate that EBV mainly utilizes the EBNA2 gene for induction of PD-L1 and to evade host immunity on infection of primary B cells. Furthermore, pathway analysis revealed that genes involved in the cell cycle, metabolic processes, membrane morphogenesis, and vesicle regulation were induced by EBNA2, and that EBNA2 suppressed genes related to immune signaling.

    DOI: 10.1016/j.virol.2021.02.004

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  9. Anti-tumor effect of IL2-expressing HSV amplicon vector and oncolytic virus HF10 Reviewed International journal

    Esaki Shinichi, Goshima Fumi, Takano Gaku, Watanabe Takahiro, Sato Yoshitaka, Murata Takayuki, Kimura Hiroshi

    CANCER SCIENCE   Vol. 112   page: 394 - 394   2021.2

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  10. Role of Epstein-Barr Virus C Promoter Deletion in Diffuse Large B Cell Lymphoma. Reviewed International coauthorship International journal

    Seiyo Mabuchi, Fumiya Hijioka, Takahiro Watanabe, Yusuke Yanagi, Yusuke Okuno, H M Abdullah Al Masud, Yoshitaka Sato, Takayuki Murata, Hiroshi Kimura

    Cancers   Vol. 13 ( 3 ) page: 561 - 561   2021.2

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:{MDPI} {AG}  

    The Epstein-Barr virus (EBV) is the cause of several malignancies, including diffuse large B cell lymphoma (DLBCL). We recently found that EBV genomes in EBV-positive cancer specimens have various deletions (Okuno et al. Nat Microbiol. 2019). Here, we focus on the deletion of C promoter (Cp), which transcribes EBV nuclear antigen (EBNA) genes in type III latency. The Cp deletion found in a DLBCL patient (332 bp) was introduced into EBV-BAC of the B95-8 strain. Interestingly, the dCp virus transformed B cells more efficiently than WT and revertant strains. Deletion of Cp also promoted tumor formation and severe pathogenicity in a mouse xenograft model. RNA sequencing and qRT-PCR analyses revealed that Cp transcription was undetectable in the dCp cells. Instead, transcription from the W promoter (Wp), an alternative promoter for EBNA, was activated in the dCp mutant. We also found that the expression of latent membrane protein 2A (LMP2A) was somehow induced in the dCp mutant. Double knockout of Cp and LMP2A indicated that LMP2A is crucial for B cell transformation, but the increased transformation induced by Cp deletion cannot be explained by LMP2A alone. We also tested the effect of an anti-apoptotic viral BCL2 homolog, BHRF1, because its expression was reportedly induced more efficiently by that of Wp. However, increased growth transformation via Cp deletion was not due to the BHRF1 gene. Taken together, the results indicated that deletion of a specific region in Cp increased in vitro transformation and the rate of progression of EBV-positive lymphoproliferative disorders in vivo. Our data suggest that genomic alteration not only of the host but also the virus promotes EBV-positive tumor generation and expansion, although the molecular mechanism underlying this phenomenon is still unclear. However, LMP2A and BHRF1 are not involved.

    DOI: 10.3390/cancers13030561

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  11. Direct Evidence of Abortive Lytic Infection-Mediated Establishment of Epstein-Barr Virus Latency During B-Cell Infection Reviewed International journal

    Inagaki Tomoki, Sato Yoshitaka, Ito Jumpei, Takaki Mitsuaki, Okuno Yusuke, Yaguchi Masahiro, Al Masud H. M. Abdullah, Watanabe Takahiro, Sato Kei, Iwami Shingo, Murata Takayuki, Kimura Hiroshi

    FRONTIERS IN MICROBIOLOGY   Vol. 11   2021.1

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    DOI: 10.3389/fmicb.2020.575255

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  12. IL2発現HSVアンプリコンの抗腫瘍効果

    江崎 伸一, 五島 典, 高野 学, 渡辺 崇広, 佐藤 好隆, 村田 貴之, 木村 宏

    日本癌学会総会記事   Vol. 79回   page: OE12 - 7   2020.10

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  13. Oncolytic activity of HF10 in head and neck squamous cell carcinomas Reviewed International journal

    Shinichi Esaki, Fumi Goshima, Haruka Ozaki, Gaku Takano, Yoshimi Hatano, Daisuke Kawakita, Kei Ijichi, Takahiro Watanabe, Yoshitaka Sato, Takayuki Murata, Hiromitsu Iwata, Yuta Shibamoto, Shingo Murakami, Yukihiro Nishiyama, Hiroshi Kimura

    Cancer Gene Therapy   Vol. 27 ( 7-8 ) page: 585 - 598   2020.8

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

    DOI: 10.1038/s41417-019-0129-3

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  14. Antitumor activity of cyclin-dependent kinase inhibitor alsterpaullone in Epstein-Barr virus-associated lymphoproliferative disorders. Reviewed International journal

    Watanabe T, Sato Y, Masud HMAA, Takayama M, Matsuda H, Hara Y, Yanagi Y, Yoshida M, Goshima F, Murata T, Kimura H

    Cancer science   Vol. 111 ( 1 ) page: 279 - 287   2020.1

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    DOI: 10.1111/cas.14241

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  15. Epstein-Barr Virus BBRF2 Is Required for Maximum Infectivity. Reviewed International journal

    Masud HMAA, Yanagi Y, Watanabe T, Sato Y, Kimura H, Murata T

    Microorganisms   Vol. 7 ( 12 )   2019.12

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    DOI: 10.3390/microorganisms7120705

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  16. The BOLF1 gene is necessary for effective Epstein-Barr viral infectivity

    Al Masud H. M. Abdullah, Watanabe Takahiro, Sato Yoshitaka, Goshima Fumi, Kimura Hiroshi, Murata Takayuki

    VIROLOGY   Vol. 531   page: 114-125   2019.5

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    DOI: 10.1016/j.virol.2019.02.015

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  17. Initial Characterization of the Epstein-Barr Virus BSRF1 Gene Product

    Yanagi Yusuke, Al Masud H. M. Abdullah, Watanabe Takahiro, Sato Yoshitaka, Goshima Fumi, Kimura Hiroshi, Murata Takayuki

    VIRUSES-BASEL   Vol. 11 ( 3 )   2019.3

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    DOI: 10.3390/v11030285

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  18. Defective Epstein-Barr virus in chronic active infection and haematological malignancy

    Okuno Yusuke, Murata Takayuki, Sato Yoshitaka, Muramatsu Hideki, Ito Yoshinori, Watanabe Takahiro, Okuno Tatsuya, Murakami Norihiro, Yoshida Kenichi, Sawada Akihisa, Inoue Masami, Kawa Keisei, Seto Masao, Ohshima Koichi, Shiraishi Yuichi, Chiba Kenichi, Tanaka Hiroko, Miyano Satoru, Narita Yohei, Yoshida Masahiro, Goshima Fumi, Kawada Jun-Ichi, Nishida Tetsuya, Kiyoi Hitoshi, Kato Seiichi, Nakamura Shigeo, Morishima Satoko, Yoshikawa Tetsushi, Fujiwara Shigeyoshi, Shimizu Norio, Isobe Yasushi, Noguchi Masaaki, Kikuta Atsushi, Iwatsuki Keiji, Takahashi Yoshiyuki, Kojima Seiji, Ogawa Seishi, Kimura Hiroshi

    NATURE MICROBIOLOGY   Vol. 4 ( 3 ) page: 404-413   2019.3

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    DOI: 10.1038/s41564-018-0334-0

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  19. Oncolytic effect of HF10 for breast cancer lung metastasis

    Goshima Fumi, Esaki Shinichi, Takano Gaku, Watanabe Takahiro, Sato Yoshitaka, Murata Takayuki, Kimura Hiroshi

    CANCER SCIENCE   Vol. 109   page: 1038-1038   2018.12

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  20. Oncolytic activity of HF10 for head and neck squamous cell carcinomas International journal

    Esaki Shinichi, Goshima Fumi, Takano Gaku, Watanabe Takahiro, Sato Yoshitaka, Murata Takayuki, Kimura Hiroshi

    CANCER SCIENCE   Vol. 109   page: 275-275   2018.12

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  21. Oncolytic effect of HF10 for breast cancer lung metastasis

    Goshima Fumi, Esaki Shinichi, Takano Gaku, Watanabe Takahiro, Sato Yoshitaka, Murata Takayuki, Kimura Hiroshi

    CANCER SCIENCE   Vol. 109   page: 1038-1038   2018.12

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  22. マウス乳癌肺転移モデルへの抗腫瘍ウイルスHF10の効果(Oncolytic effect of HF10 for breast cancer lung metastasis)

    五島 典, 江崎 伸一, 高野 学, 渡辺 崇広, 佐藤 好隆, 村田 貴之, 木村 宏

    日本癌学会総会記事   Vol. 77回   page: 1718 - 1718   2018.9

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  23. 慢性活動性Epstein-Barrウイルス感染症における網羅的遺伝子解析(Comprehensive genetic analysis of chronic active Epstein-Barr virus infection) Reviewed

    奥野 友介, 村田 貴之, 佐藤 好隆, 村松 秀城, 伊藤 嘉規, 奥野 達矢, 村上 典寛, 吉田 健一, 澤田 明久, 井上 雅美, 河 敬世, 瀬戸 加大, 大島 孝一, 白石 友一, 千葉 健一, 田中 洋子, 宮野 悟, 成田 洋平, 吉田 全宏, 渡辺 崇広, 五島 典, 川田 潤一, 西田 徹也, 清井 仁, 加藤 省一, 中村 栄男, 森島 聡子, 藤原 成悦, 清水 則夫, 磯部 泰司, 野口 雅章, 菊田 敦, 岩月 啓氏, 高橋 義行, 小島 勢二, 小川 誠司, 木村 宏

    臨床血液   Vol. 59 ( 9 ) page: 1484 - 1484   2018.9

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  24. Antitumor effects of duvelisib on Epstein-Barr virus-associated lymphoma cells.

    Kawada JI, Ando S, Torii Y, Watanabe T, Sato Y, Ito Y, Kimura H

    Cancer medicine     2018.3

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    DOI: 10.1002/cam4.1311

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  25. Epstein-Barr Virus BKRF4 Gene Product Is Required for Efficient Progeny Production. Reviewed

    Masud HMAA, Watanabe T, Yoshida M, Sato Y, Goshima F, Kimura H, Murata T

    Journal of virology   Vol. 91 ( 23 )   2017.12

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    DOI: 10.1128/JVI.00975-17

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  26. The Epstein-Barr Virus BRRF1 Gene Is Dispensable for Viral Replication in HEK293 cells and Transformation. Reviewed

    Yoshida M, Watanabe T, Narita Y, Sato Y, Goshima F, Kimura H, Murata T

    Scientific reports   Vol. 7 ( 1 ) page: 6044   2017.7

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    DOI: 10.1038/s41598-017-06413-7

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  27. The C-Terminus of Epstein-Barr Virus BRRF2 Is Required for its Proper Localization and Efficient Virus Production. Reviewed

    Watanabe T, Sakaida K, Yoshida M, Masud HM, Sato Y, Goshima F, Kimura H, Murata T

    Frontiers in microbiology   Vol. 8   page: 125   2017

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    DOI: 10.3389/fmicb.2017.00125

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  28. Characterization of a Suppressive Cis-acting Element in the Epstein-Barr Virus LMP1 Promoter. Reviewed

    Yoshida M, Murata T, Ashio K, Narita Y, Watanabe T, Masud HMAA, Sato Y, Goshima F, Kimura H

    Frontiers in microbiology   Vol. 8   page: 2302   2017

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    DOI: 10.3389/fmicb.2017.02302

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  29. Tofacitinib induces G1 cell-cycle arrest and inhibits tumor growth in Epstein-Barr virus-associated T and natural killer cell lymphoma cells. Reviewed

    Ando S, Kawada JI, Watanabe T, Suzuki M, Sato Y, Torii Y, Asai M, Goshima F, Murata T, Shimizu N, Ito Y, Kimura H

    Oncotarget   Vol. 7 ( 47 ) page: 76793-76805   2016.11

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    DOI: 10.18632/oncotarget.12529

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  30. Induction of Epstein-Barr Virus Oncoprotein LMP1 by Transcription Factors AP-2 and Early B Cell Factor. Reviewed

    Murata T, Noda C, Narita Y, Watanabe T, Yoshida M, Ashio K, Sato Y, Goshima F, Kanda T, Yoshiyama H, Tsurumi T, Kimura H

    Journal of virology   Vol. 90 ( 8 ) page: 3873-3889   2016.4

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1128/JVI.03227-15

    PubMed

  31. The Epstein-Barr virus BRRF2 gene product is involved in viral progeny production. Reviewed

    Watanabe T, Tsuruoka M, Narita Y, Katsuya R, Goshima F, Kimura H, Murata T

    Virology   Vol. 484   page: 33-40   2015.10

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.virol.2015.05.010

    PubMed

  32. The Epstein-Barr Virus BDLF4 Gene Is Required for Efficient Expression of Viral Late Lytic Genes. Reviewed

    Watanabe T, Narita Y, Yoshida M, Sato Y, Goshima F, Kimura H, Murata T

    Journal of virology   Vol. 89 ( 19 ) page: 10120-10124   2015.10

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1128/JVI.01604-15

    PubMed

  33. Roles of Epstein-Barr virus BGLF3.5 gene and two upstream open reading frames in lytic viral replication in HEK293 cells. Reviewed

    Watanabe T, Fuse K, Takano T, Narita Y, Goshima F, Kimura H, Murata T

    Virology   Vol. 483   page: 44-53   2015.9

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.virol.2015.04.007

    PubMed

  34. A Herpesvirus Specific Motif of Epstein-Barr Virus DNA Polymerase Is Required for the Efficient Lytic Genome Synthesis. Reviewed

    Narita Y, Sugimoto A, Kawashima D, Watanabe T, Kanda T, Kimura H, Tsurumi T, Murata T

    Scientific reports   Vol. 5   page: 11767   2015.6

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/srep11767

    PubMed

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Books 1

  1. 最先端ナノライフシステム研究_電子版

    佐藤好隆、渡辺崇広、三宅康之、木村宏(重症ウイルス感染症/ウイルス関連腫瘍を制御するための宿主因子探索と創薬応用)

    2022.3 

Presentations 3

  1. 診療室における感染予防の 基本と実際 Invited

    公益社団法人 愛知県歯科衛生士会主催, 診療室における感染予防の 基本と実際, R2年度“卒後1~3年のための研修会”  2021.1.10 

  2. 新型コロナウイルスの最新知見から 歯科における対応を考える Invited

    2021年度名東区歯科医師会学術講演会  2021.3.25 

  3. 新型コロナウイルスについて −ウイルス学と歯科臨床の両方の視点で Invited

    愛知県歯科医学大会2021, (公社) 愛知県歯科衛生士会, 招待講演  2021.2.21 

Research Project for Joint Research, Competitive Funding, etc. 7

  1. Epstein-Barrウイルスが有する核酸認識受容体を介した自然免疫応答からの回避機構の解析

    2021

    堀科学芸術振興財団 

  2. EBウイルスにより細胞老化制御機構の解明

    2020

    共済団 医学研究奨励助成金 

  3. 遺伝子変異型EBVの造腫瘍性において果たす意義を解明する

    2019

    北村記念血液疾患研究基金 

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    Grant type:Competitive

  4. 網羅的プロテオーム解析で解くEBウイルス発癌の分子機構

    2019

    第44回がんその他の悪性新生物研究助成金 

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    Grant type:Competitive

  5. ヒト化マウスモデルを用いた EBV 関連リンパ増殖症に対する新たな標的治療の評価

    2018.4 - 2019.3

    那須基金 

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    Grant type:Competitive

  6. 平成30年度 海外学会等参加費用援助 (International Conference on EBV & KSHV 2018)

    2018

    第24回日本医学会総会記念医学振興基金 

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    Grant type:Competitive

  7. ヒト化マウスを用いたEpstein-Barr ウイルス感染症の病態解析

    2016.10 - 2018.3

    GSKジャパン研究助成 

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    Grant type:Competitive

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KAKENHI (Grants-in-Aid for Scientific Research) 4

  1. EBウイルスの病原体認識回避機構の解明

    Grant number:21K15449  2021.4 - 2024.3

    若手研究

    渡辺 崇広

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    Authorship:Principal investigator 

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

    Epstein-Barr virus (EBV) は、生体防御を担う免疫応答を巧みにコントロールし、免疫平衡の状態で生涯感染を維持することができる。この免疫平衡状態が何らかの理由で破綻すると、EBV関連がんを発症する。本研究では、EBV遺伝子発現ライブラリを用いて特に自然免疫制御機構に着目したスクリーニングを行い、この過程に関わるウイルス因子を同定する。さらに同定したウイルス因子を標的とした遺伝子組換えウイルスを構築し、EBVの造腫瘍性を再現したヒト化マウスモデルを用いたin vivoでの検証を実施し、生体におけるEBVと自然免疫との共進化および発がん機構の解明を推進する。

  2. 欠失EBVによるリンパ腫発生機構の解明

    Grant number:20H03493  2020.4 - 2023.3

    日本学術振興会  科学研究費助成事業 基盤研究(B)  基盤研究(B)

    木村 宏

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    Authorship:Coinvestigator(s) 

    我々は慢性活動性Epstein-Barr virus (EBV) 感染症に対して、網羅的遺伝子解析を行い、高率にEBV遺伝子の一部が欠失していることを発見した。本研究では、欠失ウイルスがEBV関連腫瘍で普遍的にみられる事象なのか、一部の疾患に限定しているのかを明らかにする。具体的には、様々なEBV関連腫瘍の腫瘍組織を集積し、Whole EBVシーケンシングを行う。この過程で、疾患特異的に欠失しているEBV遺伝子を同定する。次いで、それらのEBV遺伝子を欠失した変異ウイルスを再現・作成し、培養細胞を用いたin vitroおよびヒト化マウスを用いたin vivoモデルにより、当該遺伝子の役割を解明する。

  3. ヒト化マウスモデルを用いたEBV関連リンパ増殖症の病態解析と新たな標的治療の評価

    2018.4

    科学研究費補助金 

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    Authorship:Principal investigator 

  4. 遺伝子改変EBウイルスとヒト化マウスを用いたリンパ増殖性疾患の発症病理の解析

    2016.10 - 2018.3

    科学研究費補助金 

Industrial property rights 1

  1. Cyclin dependent kinase(CDK)阻害剤によるEpstein-Barrウイルスのウイルス産生抑制

    佐藤好隆、木村宏、渡辺崇広

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    Application no:特願2017-250093  Date applied:2017.12

    Country of applicant:Domestic  

 

Teaching Experience (On-campus) 3

  1. ウイルス学総論4

    2020

  2. ウイルス学総論6

    2020

  3. ウイルス学実習

    2020

Teaching Experience (Off-campus) 1

  1. DNAウイルスとヘルペスウイルス

    2021 Nagoya City University)

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    Level:Undergraduate (specialized) 

 

Academic Activities 1

  1. 名大MIRAI GSC

    2018

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    Type:Scientific advice/Review