Tokushima University / Educator and Researcher Directory --- Yamamoto, Kiyotake

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Tokushima University ⟩ Graduate School of Biomedical Sciences ⟩ 歯学域 ⟩ Oral Science ⟩ Basic Dentistry ⟩ Department of Oral Bioscience ⟩

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Research

Personal Web Page

https://researchmap.jp/kiyo-yama (researchmap)

https://orcid.org/0000-0002-5636-7130 (ORCID)

Field of Study

○	ライフサイエンス

Subject of Study

○	細胞生物学, 病態医化学, 分子生物学, 薬理学 (血管内皮細胞, diabetes, 分子細胞生物学)

Book / Paper

Academic Paper (Judged Full Paper):

1.	Kiyotake Yamamoto, Yuki Takagi, Koji Ando and Shigetomo Fukuhara : Rap1 Small GTPase Regulates Vascular Endothelial-Cadherin-Mediated Endothelial Cell-Cell Junctions and Vascular Permeability., Biological & Pharmaceutical Bulletin, 44, 10, 1371-1379, 2021. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b21-00504 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34602545 ● Search Scopus @ Elsevier (PMID): 34602545 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b21-00504 (DOI: 10.1248/bpb.b21-00504, PubMed: 34602545)
2.	Seung-Sik Rho, Eri Oguri-Nakamura, Koji Ando, Kiyotake Yamamoto, Yuki Takagi and Shigetomo Fukuhara : Protocol for analysis of integrin-mediated cell adhesion of lateral plate mesoderm cells isolated from zebrafish embryos, STAR Protocols, 2, 2, 100428, 2021. (Summary) Lateral plate mesoderm (LPM) cells differentiate into various cell types including endothelial and hematopoietic cells. In zebrafish embryos, LPM cells migrate toward the midline along the ventral surfaces of somites during which their cell fate specification depends upon efficient integrin-mediated cell adhesion and migration. Herein, we present a protocol for analysis of integrin-mediated cell adhesion of LPM cells isolated from zebrafish embryos. This allows the study of the molecular mechanisms underlying integrin activation required for LPM cell fate specification. For complete details on the use and execution of this protocol, please refer to Rho et al. (2019). (Link to Publication Site) ● Publication site (DOI): 10.1016/j.xpro.2021.100428 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33870229 ● Summary page in Scopus @ Elsevier: 2-s2.0-85103400102 (DOI: 10.1016/j.xpro.2021.100428, PubMed: 33870229, Elsevier: Scopus)
3.	Kiyotake Yamamoto, Hiroyuki Mizuguchi, Natsumi Tokashiki, Makoto Kobayashi, Motoyuki Tamaki, Youichi Sato, Hiroyuki Fukui and Aiko Yamauchi : Protein kinase C-δ signaling regulates glucagon secretion from pancreatic islets, The Journal of Medical Investigation : JMI, 64, 1,2, 122-128, 2017. (Summary) Accumulating evidence supports the "glucagonocentric hypothesis", in which antecedent -cell failure and inhibition of glucagon secretion are responsible for diabetes progression. Protein kinase C (PKC) is involved in glucagon secretion from -cells, although which PKC isozyme is involved and the mechanism underlying this PKC-regulated glucagon secretion remains unknown. Here, the involvement of PKC in the onset and progression of diabetes was elucidated. Immunofluorescence studies revealed that PKC was expressed and activated in -cells of STZ-induced diabetic model mice. Phorbol 12-myristate 13-acetate (PMA) stimulation significantly augmented glucagon secretion from isolated islets. Pre-treatment with quercetin and rottlerin, PKC signaling inhibitors, significantly suppressed the PMA-induced elevation of glucagon secretion. While Go6976, a Ca(2+)-dependent PKC selective inhibitor did not suppress glucagon secretion. Quercetin suppressed PMA-induced phosphorylation of Tyr(311) of PKC in isolated islets. However, quercetin itself had no effect on either glucagon secretion or glucagon mRNA expression. Our data suggest that PKC signaling inhibitors suppressed glucagon secretion. Elucidation of detailed signaling pathways causing PKC activation in the onset and progression of diabetes followed by the augmentation of glucagon secretion could lead to the identification of novel therapeutic target molecules and the development of novel therapeutic drugs for diabetes. J. Med. Invest. 64: 122-128, February, 2017. (Tokushima University Institutional Repository) ● Metadata: 2004288 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.122 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373608 ● Summary page in Scopus @ Elsevier: 2-s2.0-85016425921 (Tokushima University Institutional Repository: 2004288, DOI: 10.2152/jmi.64.122, PubMed: 28373608, Elsevier: Scopus)

Review, Commentary:

1.	石井智裕, Kiyotake Yamamoto and 福原茂朋 : 血管新生における内皮細胞の形態・運動を制御するシグナル機構, Inflammation & Immunology, 28, 5, 360-364, Aug. 2020.
2.	福原茂朋, 盧承湜, 小栗エリ, Kiyotake Yamamoto and 石井智裕 : 造血幹細胞がつくられる新たなしくみ, Science of the Living Body, 71, 4, 359-363, Aug. 2020. (Link to Publication Site) ● Publication site (DOI): 10.11477/mf.2425201190 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11477/mf.2425201190 (DOI: 10.11477/mf.2425201190)

Proceeding of Domestic Conference:

1.	Kiyotake Yamamoto, 渡邊-高野晴子, 堀上大貴, 石井智裕, 久保田義顕, 村田幸久, 大橋隆治, 望月直樹 and 福原茂朋 : Rap1低分子量Gタンパク質は肺における血管透過性制御に必須である, 日本薬学会第142年会, Mar. 2022.
2.	Kiyotake Yamamoto, 渡邊-高野晴子, 堀上大貴, 髙木夕希, 石井智裕, 大橋隆治, 久保田義顕, 村田幸久, 望月直樹 and 福原茂朋 : Rap1低分子量Gタンパク質による血管透過性制御とそれを標的とする血管透過性亢進がかかわる疾患の治療戦略, 日本薬学会第142年会, Mar. 2022.
3.	Kiyotake Yamamoto, 渡邊-高野晴子, 高木夕希, 堀上大貴, 安藤康史, 石井智裕, 久保田義顕, 村田幸久, 望月直樹 and 福原茂朋 : Rap1低分子量Gタンパク質は肺の血管バリア機能維持に必須である, 第94回日本生化学会大会, Nov. 2021.
4.	Kiyotake Yamamoto, Haruko Watanabe-Takano, Daiki Horikami, Koji Ando, Yuki Takagi, Tomohiro Ishii, Yoshiaki Kubota, Takahisa Murata, Naoki Mochizuki and Shigetomo Fukuhara : A small GTPase Rap1 is essential to maintain pulmonary endothelial barrier function mediated by vascular endothelial-cadherin in vivo, 第28回日本血管生物医学会学術集会, Mar. 2021.
5.	Kiyotake Yamamoto, Hiroyuki Mizuguchi, 渡嘉敷夏海, 小林誠, Youichi Sato, Hiromichi Fujino, Hiroyuki Fukui and Aiko Yamauchi : 膵α細胞からのグルカゴン分泌に関与するPKCアイソザイムの同定, 日本薬学会第137年会, Mar. 2017.
6.	Kiyotake Yamamoto, Hiroyuki Mizuguchi, 小林誠, Youichi Sato, Hiroyuki Fukui and Aiko Yamauchi : 膵α細胞からのグルカゴン分泌に対するquercetinの効果, 日本薬学会第136年会, Mar. 2016.
7.	Kiyotake Yamamoto, Hiroyuki Mizuguchi, 小林誠, Youichi Sato, Hiroyuki Fukui and Aiko Yamauchi : PKCδシグナル抑制化合物によるグルカゴン分泌抑制効果, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2015.
8.	Kiyotake Yamamoto, 米山雅紀 and 荻田喜代一 : 成体マウス海馬からのミクログリアの単離培養, 生体機能と創薬シンポジウム, Aug. 2012.

Et cetera, Workshop:

1.	Kiyotake Yamamoto : 血管透過性制御による疾患治療を目指して, 操薬シンポジウム「インタラクティブYAKUGAKUJIN」講演会, Feb. 2022.
2.	Kiyotake Yamamoto : Future planning, 第2回韓国・徳島大学薬学部学生交流シンポジウム, Feb. 2016.
3.	Kiyotake Yamamoto : PKCδシグナル抑制化合物によるグルカゴン分泌抑制効果 ∼新規糖尿病治療薬の開発∼, 第4回若手研究者シーズ発表会「医療・健康と化学」, Nov. 2015.
4.	Kiyotake Yamamoto : Pharmacist-Scientist, 第1回韓国・徳島大学薬学部学生交流シンポジウム, Feb. 2015.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

生活習慣病による毛細血管網障害を起点とした組織機能障害と病態形成機構の解明 (Project/Area Number: 24K18276 )
男性不妊症新規原因遺伝子の同定と治療法の開発研究 (Project/Area Number: 22K09528 )
Control of vascular permeability by Rap1 and elucidation of the pathology of ARDS due to failure of this control mechanism. (Project/Area Number: 21K15260 )
Search by Researcher Number (20866553)