Faculty Profiles - KANEMATSU TAKASHI

Information

写真a

KANEMATSU TAKASHI

Organization

Faculty of Dental Science Department of Dental Science Professor
Research Center for Education in Health Care System （Concurrent）
School of Dentistry Department of Dentistry（Concurrent）
Graduate School of Dental Science （Concurrent）
Graduate School of Dental Science Department of Dental Science（Concurrent）

Profile

— 新規イノシトール三リン酸結合タンパク質の発見— 　イノシトール1,4,5−三リン酸（Ins(1,4,5)P3）が細胞内の小胞体からCa2+を放出させる機構解明がなされ、Ins(1,4,5)P3の細胞内情報伝達物質としての重要性が認識されている。我々は、Ins(1,4,5)P3親和性レジンを作製し、この親和性レジンを使い、ラット大脳から新たに分子サイズが130kDaと85kDaの２種類のIns(1,4,5)P3結合タンパク質を見いだした。それぞれの部分アミノ酸配列を決定し、85kDa分子はホスホリパーゼＣ（PLC）のδ1型アイソザイムであり、一方130kDa分子は新規タンパク質であることをつきとめた。PLC-δ1（85kDa分子）に関しては、Ｎ末端の30番目から43番目までの領域がIns(1,4,5)P3結合ドメインであることを明らかにした。この領域は、プレックストリン相同領域（PHドメイン）に当たり、我々のこれらの一連の報告はIns(1,4,5)P3とその関連物質がPHドメインの共通性リガンドとして認知されるきかっけとなった。130kDa分子は、未知のタンパク質であったのでその全長遺伝子を単離した。クローン化した遺伝子から、本分子は85kDaのPLC-δ1よりひと回り大きいものの、全体的に38.2% のホモロジーでPLC-d1に類似していることが分かった。しかしこの分子にはPLC酵素活性は認められず、新しい機能タンパク質である可能性が示唆された。この分子をPLC Related Catalytically Inactive Protein （略してPRIP）と命名した。 — 新規タンパク質の機能解析から抑制性シナプス構築の分子メカニズム解明への展開 — 　130kDaもの分子サイズをもつこの新規Ins(1,4,5)P3結合性タンパク質の機能解明を目指して、２つのプロジェクト（１：相互作用分子の検索　２：ノックアウトマウス作製）を進めた。相互作用分子の検索からPRIP-1分子結合タンパク質を２つ同定した。一つはプロテインホスファターゼ１の活性サブユニット（PP1c）であった。PP1cはPRIP-1のPHドメイン直前部分に結合し、その複合体はPP1cの酵素活性（ホスファターゼ活性）を抑えた。もう一つの結合分子はGABA(A) receptor associated protein（GABARAP）であった。生化学的な結合実験から、PRIP-1がGABA(A)受容体のγ2サブユニットとGABARAPとの結合に競合することを示した。次に、PRIP-1 ノックアウトマウスを作製し、γ2サブユニットに作用点を持つ薬剤（ジアゼパム等）を作用させたところ、海馬細胞を用いた電気生理学的解析やマウス個体を用いた行動学的解析において、この薬理効果が無効であることをみいだした。即ちPRIP-1遺伝子を欠損させると、抑制性神経伝達物質である γ-アミノ絡酸(GABA)の受容体の機能異常が起こることを明らかにした。 —PRIPはGABA(A)受容体の一生を制御している — 　PRIPを介したGABA(A)受容体のγ2サブユニットの形質膜発現機構を解析した結果、PRIPがGABARAPをγ2サブユニットに適切なタイミングでトランスロケーションさせることでγ2サブユニットを含んだ（ジアゼパム感受性）受容体の膜発現調節をしていることを明らかにした。また、PRIPは相互作用分子であるプロテインホスファターゼ活性を制御して、形質膜に発現しているGABA(A)受容体のリン酸化/脱リン酸化制御を行なってチャネル活性を調節することを明らかにした。さらに、膜に発現しているGABA(A)受容体の数的調節には、受容体のリン酸化レベルに依存したエンドサイトーシス機構が関かわることが最近明らかになった。PRIPによる受容体の脱リン酸化調節は、受容体のエンドサイトーシスの制御にも重要な役割を持つことを明らかにした。 —今後の展望 — 　PRIPには二つのサブタイプが存在する。PRIP-1は中枢神経系に特異的な発現パターンを示すのに対し、PRIP-2は様々な臓器に発現している。そこで我々は、PRIP-1/2ダブルノックアウト(DKO)マウスを作製しその解析を進めている。PRIPは、これまでの結果からGABA(A)受容体の輸送に関わる重要な分子であることが分かっているが、このDKOマウスを解析した結果、PRIPはGABA(A)受容体の輸送のみならず普遍的な分泌現象にも関わる分子である可能性が出てきた。現在、PRIPと分泌小胞輸送との関係について解析を行なっている。

Homepage

http://www.dent.kyushu-u.ac.jp/sosiki/a04/index.html
Molecular & Cellular Biochemistry, Faculty of Dental Science, Kyushu University

External link

Research Areas

Life Science / Pharmacology
Life Science / Tumor biology
Life Science / Cell biology
Life Science / Oral biological science

Degree

Doctor of Dental Science

Research History

Kyushu University Professor

2019.4 - Present

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Country：Japan

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2009.2.1.-2019.3.31. 広島大学大学院医歯薬保健学研究科　教授　 2019.7.1.-2020.3.31. 広島大学大学院医系科学研究科特任教授

Research Interests・Research Keywords

Research theme：Functional analysis of M2 macrophages that regulates chronic inflammation

Keyword：macrophage

Research period： 2024.4 - 2027.3
Research theme：Functional analysis of a new anti-cancer molecule that promotes anti-tumor immune responses

Keyword：anti-tumor immune response

Research period： 2021.4 - 2024.3
Research theme：Studies on the connections between peripheral inflammation and type 2 diabetes

Keyword：obesity, diabetes, peripheral inflammation, miRNA

Research period： 2019.4 - 2022.3
Research theme：Studies on type 3 diabetes and Alzheimer's disease

Keyword：diabetes, Alzheimer's disease, brain inflammation, microglia

Research period： 2019.4 - 2022.3
Research theme：Studies on PRIP roles in insulin secretion machinery

Keyword：insulin secretion

Research period： 2005.4 - 2016.3
Research theme：肥満と新規分子PRIPの関わり

Keyword：肥満

Research period： 2005.4
Research theme：PRIP roles in autophagy signaling pathway

Keyword：autophagy

Research period： 2004.8 - 2015.3
Research theme：Studies on the intracellular signaling of GABA(A) receptor

Keyword：GABA(A) receptor

Research period： 2000.4 - 2017.3
Research theme：PRIP分子のイノシトール三リン酸情報伝達系における役割解明

Keyword：PRIP　イノシトール三リン酸

Research period： 2000.4 - 2004.3

Awards

第18回歯科基礎医学会ライオン学術賞

2018.9 歯科基礎医学会肥満を制御する新たな分子メカニズムの解明研究

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新規肥満抑制分子を見いだし、その解析を行なって新しい肥満抑制の分子基盤を明らかにした。
第１４回　歯科基礎医学会賞

2002.10 歯科基礎医学会「Role of the PLC-related, catalytically inactiove protein p130 in GABA(A) receptor function」 EMBO J 2002;21 1004-1011.
The Distinguished Poster Award

2002.5 The International Symposium on the Study of Brain Function 学内

Papers

miR-582-5p targets Skp1 and regulates NF-Kappa B signaling-mediated inflammation Invited Reviewed International journal

Li, Rongzhi; Sano, Tomomi; Mizokami, Akiko; Fukuda, Takao; Shinjo, Takanori; Iwashita, Misaki; Yamashita, Akiko; Sanui, Terukazu; Nakatsu, Yusuke; Sotomaru, Yusuke; Asano, Tomoichiro; Kanematsu, Takashi; Nishimura, Fusanori

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 734 109501 - 109501 2023.1 （ ISSN:0003-9861 eISSN:1096-0384 ）

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A well-tuned inflammatory response is crucial for an effective immune process. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammatory and innate immunity responses, and its dysregulation is closely associated with immune-related diseases. MicroRNAs (miRNAs) are important inflammation modulators. However, miRNA-regulated mechanisms that implicate NF-κB activity are not fully understood. This study aimed to identify a potential miRNA that could modulate the dysregulated NF-κB signaling during inflammation. We identified miR-582-5p that was significantly downregulated in inflamed murine adipose tissues and RAW264.7 cells. S-phase kinase-associated protein 1 (SKP1), a core component of an E3 ubiquitin ligase that regulates the NF-κB pathway, was proposed as a biological target of miR-582-5p by using TargetScan. The binding of miR-582-5p to a 3'-untranslated region site on Skp1 was confirmed using a dual-luciferase reporter assay; in addition, transfection with a miR-582-5p mimic suppressed SKP1 expression in RAW264.7 cells. Importantly, exogenous miR-582-5p attenuated the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 through suppressing the degradation of the NF-κB inhibitor alpha, followed by the nuclear translocation of NF-κB. Therefore, exogenously applied miR-582-5p can attenuate the NF-κB signaling pathway via targeting Skp1; this provides a prospective therapeutic strategy for treating inflammatory and immune diseases.

DOI： 10.1016/j.abb.2022.109501

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Imipramine prevents Porphyromonas gingivalis lipopolysaccharide- induced microglial neurotoxicity Invited Reviewed International journal

Yamawaki Yosuke, So Hiroki, Oue Kana, Asano Satoshi, Furusho Hisako, Miyauchi Mutsumi, Tanimoto Kotaro, Kanematsu Takashi

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 634 92 - 99 2022.12 （ ISSN:0006-291X eISSN:1090-2104 ）

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Porphyromonas gingivalis (P. gingivalis) is a Gram-negative anaerobe involved in the pathogenesis of chronic periodontitis, including local inflammation of the oral cavity. However, periodontal disease has recently been identified as a significant factor in the pathogenesis of neural diseases, including Alzheimer's disease. A virulence factor, P. gingivalis-lipopolysaccharide (LPS-PG), is involved in pro-inflammatory responses, not only in peripheral tissues but also in the brain. In this study, we examined whether P. gingivalis-induced brain inflammation could be ameliorated by pharmacotherapy, using in vivo and in vitro studies. In an animal experiment, peripheral administration of LPS-PG induced inflammation in the hippocampus via microglial activation, which was inhibited by pre-treatment with the antidepressant imipramine. Similarly, LPS-PG-induced inflammation in MG-6 cells, a mouse microglial cell line, was inhibited by pre-treatment with imipramine, which caused imipramine-induced inhibition of NF-κB signaling. Culture media obtained from LPS-PG-treated MG-6 cells induced neuronal cell death in Neuro-2A cells, a mouse neuroblastoma cell line, which was prevented by pre-treatment of MG-6 cells with imipramine. These results indicate that imipramine inhibits LPS-PG-induced inflammatory responses in microglia and ameliorates periodontal disease-related neural damage.

DOI： 10.1016/j.bbrc.2022.09.109

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Phospholipase C-related catalytically inactive protein enhances cisplatin-induced apoptotic cell death Invited Reviewed International journal

Asano Satoshi, Maetani Yuka, Ago Yukio, Kanematsu Takashi

EUROPEAN JOURNAL OF PHARMACOLOGY 933 175273 2022.10 （ ISSN:0014-2999 eISSN:1879-0712 ）

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DOI： 10.1016/j.ejphar.2022.175273

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RANKL elevation activates the NIK/NF-κB pathway, inducing obesity in ovariectomized mice Reviewed International journal

254 ( 1 ) 27 - 36 2022.5

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Menopausal women are susceptible to visceral obesity, which increases the risk of metabolic disorders. However, the mechanisms of menopause-induced visceral fat accumulation are not fully understood. Circulating levels of receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) are elevated in an animal model of menopause. RANKL, a multifunctional cytokine, activates the NF-κB pathway, which serves as a pivotal mediator of inflammatory responses. Here, we investigated whether RANKL-induced non-canonical NF-κB pathway activation induces inflammation and lipid accumulation in adipose tissues. RANKL induced Tnfa expression via the non-canonical NF-κB pathway in bone marrow cells. We therefore analyzed aly/aly mice, in which the non-canonical NF-κB pathway is not activated, owing to an inactive form of NF-κB-inducing kinase. A postmenopausal obesity model was generated by ovariectomy and subsequent high-fat and high-sucrose diet feeding. In aly/aly mice with postmenopausal obesity, serum RANKL levels were elevated, and hepatic lipid accumulation and adipocyte hypertrophy were suppressed, resulting in reduced macrophage infiltration and inflammatory cytokine mRNA expression in visceral adipose tissue. Furthermore, aly/aly mice showed protection from glucose intolerance and insulin resistance, which were observed in ovariectomized WT obese mice. These findings indicate that non-canonical NF-κB pathway activation via serum RANKL elevation contributes to postmenopausal obesity.

DOI： https://doi.org/10.1530/JOE-21-0424
Phospholipase C-related but catalytically inactive protein acts as a positive regulator of insulin signalling in adipocytes Reviewed International journal

Jing Gao, Akiko Mizokami, Hiroshi Takeuchi, Aonan Li, Fei Huang, Haruki Nagano, Takashi Kanematsu, Eijiro Jimi, Masato Hirata

Journal of Cell Science 135 ( 1 ) jcs258584 2022.1

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DOI： https://doi.org/10.1242/jcs.258584
Expression of PRIP, a phosphatidylinositol 4,5-bisphosphate binding protein, attenuates PI3K/AKT signaling and suppresses tumor growth in a xenograft mouse model Reviewed International journal

Yuka Maetani, Satoshi Asano, Akiko Mizokami, Yosuke Yamawaki, Tomomi Sano, Masato Hirata, Masahiro Irifune, Takashi Kanematsu

Biochemical and biophysical research communications 552 106 - 113 2021.5

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DOI： https://doi.org/10.1016/j.bbrc.2021.03.045
Phospholipase C-related catalytically inactive protein regulates cytokinesis by protecting phosphatidylinositol 4,5-bisphosphate from metabolism in the cleavage furrow Reviewed

Satoshi Asano, Yasuka Ikura, Mitsuki Nishimoto, Yosuke Yamawaki, Kozue Hamao, Keiju Kamijo, Masato Hirata, Takashi Kanematsu

Scientific reports 9 ( 1 ) 2019.12

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DOI： https://doi.org/10.1038/s41598-019-49156-3
Phospholipase C-related catalytically inactive protein regulates lipopolysaccharide-induced hypothalamic inflammation-mediated anorexia in mice Reviewed

Yosuke Yamawaki, Satomi Shirawachi, Akiko Mizokami, Kanako Nozaki, Hikaru Ito, Satoshi Asano, Kana Oue, Hidenori Aizawa, Shigeto Yamawaki, Masato Hirata, Takashi Kanematsu

Neurochemistry International 131 2019.12

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Poor Motor-Function Recovery after Spinal Cord Injury in Anxiety-Model Mice with Phospholipase C-Related Catalytically Inactive Protein Type 1 Knockout Reviewed

Taka Fujita, Gentaro Kumagai, Xizhe Liu, Kanichiro Wada, Toshihiro Tanaka, Hitoshi Kudo, Toru Asari, Tatsuhiro Fukutoku, Ayako Sasaki, Yohshiro Nitobe, Yoshikazu Nikaido, Ken Ichi Furukawa, Masato Hirata, Takashi Kanematsu, Shinya Ueno, Yasuyuki Ishibashi

Journal of Neurotrauma 35 ( 12 ) 1379 - 1386 2018.6

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DOI： 10.1089/neu.2017.5492
Suppression of cell migration by phospholipase C-related catalytically inactive protein-dependent modulation of PI3K signalling Reviewed

Satoshi Asano, Yuri Taniguchi, Yosuke Yamawaki, Jing Gao, Kae Harada, Hiroshi Takeuchi, Masato Hirata, Takashi Kanematsu

Scientific reports 7 ( 1 ) 2017.12

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DOI： 10.1038/s41598-017-05908-7
Propofol anesthesia is reduced in phospholipase c-related inactive protein type-1 knockout mices Reviewed

Yoshikazu Nikaido, Tomonori Furukawa, Shuji Shimoyama, Junko Yamada, Keisuke Migita, Kohei Koga, Tetsuya Kushikata, Kazuyoshi Hirota, Takashi Kanematsu, Masato Hirata, Shinya Ueno

Journal of Pharmacology and Experimental Therapeutics 361 ( 3 ) 367 - 374 2017.6

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DOI： 10.1124/jpet.116.239145
Phospholipase C-related Catalytically Inactive Protein Is a New Modulator of Thermogenesis Promoted by β-Adrenergic Receptors in Brown Adipocytes Reviewed

291 ( 8 ) 4185 - 4196 2016.2

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Phospholipase C-related catalytically inactive protein (PRIP) was first identified as an inositol 1,4,5-trisphosphate-binding protein, and was later found to be involved in a variety of cellular events, particularly those related to protein phosphatases. We previously reported that Prip knock-out (KO) mice exhibit a lean phenotype with a small amount of white adipose tissue. In the present study, we examined whether PRIP is involved in energy metabolism, which could explain the lean phenotype, using high-fat diet (HFD)-fed mice. Prip-KO mice showed resistance to HFD-induced obesity, resulting in protection from glucose metabolism dysfunction and insulin resistance. Energy expenditure and body temperature at night were significantly higher in Prip-KO mice than in wild-type mice. Gene and protein expression of uncoupling protein 1 (UCP1), a thermogenic protein, was up-regulated in Prip-KO brown adipocytes in ther-moneutral or cold environments. These phenotypes were caused by the promotion of lipolysis in Prip-KO brown adipocytes, which is triggered by up-regulation of phosphorylation of the lipolysis-related proteins hormone-sensitive lipase and perilipin, followed by activation of UCP1 and/or up-regulation of thermogenesis-related genes (e.g. peroxisome proliferator-activated receptor-γ coactivator-1α). The results indicate that PRIP negatively regulates UCP1-mediated thermogenesis in brown adipocytes.

DOI： 10.1074/jbc.M115.705723
Phospholipase C-related catalytically inactive protein (PRIP) controls KIF5B-mediated insulin secretion Reviewed

Satoshi Asano, Tomomi Nemoto, Tomoya Kitayama, Kae Harada, Jun Zhang, Kana Harada, Isei Tanida, Masato Hirata, Takashi Kanematsu

Biology Open 3 ( 6 ) 463 - 474 2014.6

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DOI： 10.1242/bio.20147591
Phospholipase C-related catalytically inactive protein (PRIP) regulates lipolysis in adipose tissue by modulating the phosphorylation of hormone-sensitive lipase Reviewed

Toshiya Okumura, Kae Harada, Kana Oue, Jun Zhang, Satoshi Asano, Masaki Hayashiuchi, Akiko Mizokami, Hiroto Tanaka, Masahiro Irifune, Nobuyuki Kamata, Masato Hirata, Takashi Kanematsu

PloS one 9 ( 6 ) 2014.6

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DOI： 10.1371/journal.pone.0100559
Phospholipase C-related catalytically inactive protein participates in the autophagic elimination of Staphylococcus aureus infecting mouse embryonic fibroblasts Reviewed

Kae Harada-Hada, Kana Harada, Fuminori Kato, Junzo Hisatsune, Isei Tanida, Michinaga Ogawa, Satoshi Asano, Motoyuki Sugai, Masato Hirata, Takashi Kanematsu

PloS one 9 ( 5 ) 2014.5

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DOI： 10.1371/journal.pone.0098285
Phospholipase C-related but catalytically inactive protein modulates pain behavior in a neuropathic pain model in mice Reviewed

Tomoya Kitayama, Katsuya Morita, Rizia Sultana, Nami Kikushige, Keisuke Mgita, Shinya Ueno, Masato Hirata, Takashi Kanematsu

Molecular Pain 9 ( 1 ) 2013.5

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DOI： 10.1186/1744-8069-9-23
Phospholipase C-related catalytically inactive protein, a novel microtubule-associated protein 1 light chain 3-binding protein, negatively regulates autophagosome formation Reviewed

Hisanori Umebayashi, Akiko Mizokami, Miho Matsuda, Kae Harada, Hiroshi Takeuchi, Isei Tanida, Masato Hirata, Takashi Kanematsu

Biochemical and Biophysical Research Communications 432 ( 2 ) 268 - 274 2013.3

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DOI： 10.1016/j.bbrc.2013.01.119
GABA_A receptor subunit alteration-dependent diazepam insensitivity in the cerebellum of phospholipase C-related inactive protein knockout mice Reviewed

Akiko Mizokami, Hiroto Tanaka, Hitoshi Ishibashi, Hisanori Umebayashi, Kiyoko Fukami, Tadaomi Takenawa, Keiichi I. Nakayama, Takeshi Yokoyama, Junichi Nabekura, Takashi Kanematsu, Masato Hirata

Journal of Neurochemistry 114 ( 1 ) 302 - 310 2010.7

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DOI： 10.1111/j.1471-4159.2010.06754.x
Phospholipase C-related but catalytically inactive protein is required for insulin-induced cell surface expression of γ-aminobutyric acid type A receptors Reviewed

285 ( 7 ) 4837 - 4846 2010.2

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The γ-aminobutyric acid type A (GABA_A) receptors play a pivotal role in fast synaptic inhibition in the central nervous system. One of the key factors for determining synaptic strength is the number of receptors on the postsynaptic membrane, which is maintained by the balance between cell surface insertion and endocytosis of the receptors. In this study, we investigated whether phospholipase C-related but catalytically inactive protein (PRIP) is involved in insulin-induced GABA_A receptor insertion. Insulin potentiated the GABA-induced Cl^- current (I_GABA) by about 30% in wild-type neurons, but not in PRIP1 and PRIP2 double-knock-out (DKO) neurons, suggesting that PRIP is involved in insulin-induced potentiation. The phosphorylation level of the GABA_A receptor β-subunit was increased by about 30% in the wild-type neurons but not in the mutant neurons, which were similar to the changes observed in I_GABA. We also revealed that PRIP recruited active Akt to the GABA_A receptors by forming a ternary complex under insulin stimulation. The disruption of the binding between PRIP and the GABA_A receptor β-subunit by PRIP interference peptide attenuated the insulin potentiation of I_GABA. Taken together, these results suggest that PRIP is involved in insulin-induced GABA_A receptor insertion by recruiting active Akt to the receptor complex.

DOI： 10.1074/jbc.M109.070045
Phospholipase C-related inactive protein is implicated in the constitutive internalization of GABA_A receptors mediated by clathrin and AP2 adaptor complex Reviewed

Takashi Kanematsu, Makoto Fujii, Akiko Mizokami, Josef T. Kittler, Junichi Nabekura, Stephen J. Moss, Masato Hirata

Journal of Neurochemistry 101 ( 4 ) 898 - 905 2007.5

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DOI： 10.1111/j.1471-4159.2006.04399.x
Phosholipase C-related inactive protein is involved in trafficking of γ2 subunit-containing GABA_A receptors to the cell surface Reviewed

27 ( 7 ) 1692 - 1701 2007.2

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The subunit composition of GABA_A receptors is known to be associated with distinct physiological and pharmacological properties. Previous studies that used phospholipase C-related inactive protein type 1 knock-out (PRIP-1 KO) mice revealed that PRIP-1 is involved in the assembly and/or the trafficking of γ2 subunit-containing GABA_A receptors. There are two PRIP genes in mammals; thus the roles of PRIP-1 might be compensated partly by those of PRIP-2 in PRIP-1 KO mice. Here we used PRIP-1 and PRIP-2 double knock-out (PRIP-DKO) mice and examined the roles for PRIP in regulating the trafficking of GABA_A receptors. Consistent with previous results, sensitivity to diazepam was reduced in electrophysiological and behavioral analyses of PRIP-DKO mice, suggesting an alteration of γ2 subunit-containing GABA_A receptors. The surface numbers of diazepam binding sites (α/γ2 subunits) assessed by [³H]flumazenil binding were reduced in the PRIP-DKO mice as compared with those of wild-type mice, whereas the cell surface GABA binding sites (α/β subunits, assessed by [³H]muscimol binding) were increased in PRIP-DKO mice. The association between GABA_A receptors and GABA_A receptor-associated protein (GABARAP) was reduced significantly in PRIP-DKO neurons. Disruption of the direct interaction between PRIP and GABA_A receptor β subunits via the use of a peptide corresponding to the PRIP-1 binding site reduced the cell surface expression of γ2 subunit-containing GABA_A receptors in cultured cell lines and neurons. These results suggest that PRIP is implicated in the trafficking of γ2 subunit-containing GABA_A receptors to the cell surface, probably by acting as a bridging molecule between GABARAP and the receptors.

DOI： 10.1523/JNEUROSCI.3155-06.2007
Modulation of GABA_A receptor phosphorylation and membrane trafficking by phospholipase C-related inactive protein/protein phosphatase 1 and 2A signaling complex underlying brain-derived neurotrophic factor-dependent regulation of GABAergic inhibition Reviewed

Takashi Kanematsu, Atsushi Yasunaga, Yoshito Mizoguchi, Akiko Kuratani, Josef T. Kittler, Jasmina N. Jovanovic, Kei Takenaka, Keiichi I. Nakayama, Kiyoko Fukami, Tadaomi Takenawa, Stephen J. Moss, Junichi Nabekura, Masato Hirata

Journal of Biological Chemistry 281 ( 31 ) 22180 - 22189 2006.8

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DOI： 10.1074/jbc.M603118200
GABA_A receptor phospho-dependent modulation is regulated by phospholipase C-related inactive protein type 1, a novel protein phosphatase 1 anchoring protein Reviewed

Miho Terunuma, Il Sung Jang, Sang Hoon Ha, Josef T. Kittler, Takashi Kanematsu, Jasmina N. Jovanovic, Keiichi I. Nakayama, Norio Akaike, Sung Ho Ryu, Stephen J. Moss, Masato Hirata

Journal of Neuroscience 24 ( 32 ) 7074 - 7084 2004.8

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DOI： 10.1523/JNEUROSCI.1323-04.2004
Role of the PLC-related, catalytically inactive protein p130 in GABA_A receptor function Reviewed

Takashi Kanematsu, Il Sung Jang, Taku Yamaguchi, Hiroyasu Nagahama, Kenji Yoshimura, Kiyoshi Hidaka, Miho Matsuda, Hiroshi Takeuchi, Yoshio Misumi, Keiko Nakayama, Tsuneyuki Yamamoto, Norio Akaike, Masato Hirata, Keiichi Nakayama

EMBO Journal 21 ( 5 ) 1004 - 1011 2002.3

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

DOI： 10.1093/emboj/21.5.1004
Interaction of p130 with, and Consequent Inhibition of, the Catalytic Subunit of Protein Phosphatase 1α Reviewed

276 ( 21 ) 17908 - 17913 2001.1

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The protein p130 was originally isolated from rat brain as an inositol 1,4,5-trisphosphate-binding protein with a domain organization similar to that of phospholipase C-δ1 but which lacks phospholipase C activity. Yeast two-hybrid screening of a human brain cDNA library for clones that encode proteins that interact with p130 has now led to the identification of the catalytic subunit of protein phosphatase 1α (PP1cα) as a p130-binding protein. The association between p130 and PP1cα was also confirmed in vitro by an overlay assay, a "pull-down" assay, and surface plasmon resonance analysis. The interaction of p130 with PP1cα resulted in inhibition of the catalytic activity of the latter in a p130 concentration-dependent manner. Immunoprecipitation and immunoblot analysis of COS-1 cells that stably express p130 and of mouse brain extract with antibodies to p130 and to PP1cα also detected the presence of a complex of p130 and PP1cα. The activity of glycogen phosphorylase, which is negatively regulated by dephosphorylation by PP1cα, was higher in COS-1 cells that stably express p130 than in control COS-1 cells. These results suggest that, in addition to its role in inositol 1,4,5-trisphosphate and Ca²⁺ signaling, p130 might also contribute to regulation of protein dephosphorylation through its interaction with PP1cα.

DOI： 10.1074/jbc.M009677200
Domain organization of p130, PLC-related catalytically inactive protein, and structural basis for the lack of enzyme activity Reviewed

Takashi Kanematsu, Kenji Yoshimura, Kiyoshi Hidaka, Hiroshi Takeuchi, Matilda Katan, Masato Hirata

European Journal of Biochemistry 267 ( 9 ) 2731 - 2737 2000.5

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DOI： 10.1046/j.1432-1327.2000.01291.x
Three amino acid residues determine selective binding of FK506-binding protein 12.6 to the cardiac ryanodine. Reviewed International journal

Xin H.B., Rogers K., Qi Y., Kanematsu T. & Fleischer S.

Journal of Biological Chemistry 1999.1

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Localization of a high-affinity inositol 1,4,5-trisphosphate/inositol 1,4,5,6-tetrakisphosphate binding domain to the pleckstrin homology module of a new 130 KDa protein Characterization of the determinants of structural specificity Reviewed

Hiroshi Takeuchi, Takashi Kanematsu, Yoshio Misumi, Hassan Bin Yaakob, Hitoshi Yagisawa, Yukio Ikehara, Yutaka Watanabe, Zheng Tan, Stephen B. Shears, Masato Hirata

Biochemical Journal 318 ( 2 ) 561 - 568 1996.9

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DOI： 10.1042/bj3180561
A new inositol 1,4,5-trisphosphate binding protein similar to phospholipase C-δ₁ Reviewed

313 ( 1 ) 319 - 325 1996.1

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We have reported that two inositol 1,4,5-trisphosphate binding proteins, with molecular masses of 85 and 130 kDa, were purified from rat brain; the former protein was found to be the δ₁-isoenzyme of phospholipase C (PLC-δ₁) and the latter was an unidentified novel protein [Kanematsu, Takeya, Watanabe, Ozaki, Yoshida, Koga, Iwanaga and Hirata (1992) J. Biol. Chem. 267, 6518-6525]. Here we describe the isolation of the full-length cDNA for the 130 kDa Ins(1,4,5)P₃ binding protein, which encodes 1096 amino acids. The predicted sequence of the 130 kDa protein had 38.2% homology to that of PLC-δ₁. Three known domains of PLC-δ₁ (pleckstrin homology and putative catalytic X and Y domains) were located at residues 110-222, 377-544 and 585-804 with 35.2%, 48.2% and 45.8% homologies respectively. However, the protein showed no PLC activity to phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol. The 130 kDa protein expressed by transfection in COS-1 cells bound Ins(1,4,5)P₃ in the same way as the molecule purified from brain. Thus the 130 kDa protein is a novel Ins(1,4,5)P₃ binding protein homologous to PLC-δ₁, but with no catalytic activity. The functional significance of the 130 kDa protein is discussed.

DOI： 10.1042/bj3130319
D-myo-inositol 1,4,5-trisphosphate-binding proteins in rat brain membranes Reviewed

Masako Yoshida, Takashi Kanematsu, Yutaka Watanabe, Toshitaka Koga, Shoichiro Ozaki, Sadaaki Iwanaga, Masato Hirata

Journal of biochemistry 115 ( 5 ) 973 - 980 1994.1

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DOI： 10.1093/oxfordjournals.jbchem.a124447
Putative inositol 1,4,5-trisphosphate binding proteins in rat brain cytosol Reviewed

T. Kanematsu, H. Takeya, Y. Watanabe, S. Ozaki, M. Yoshida, T. Koga, S. Iwanaga, M. Hirata

Journal of Biological Chemistry 267 ( 10 ) 6518 - 6525 1992.1

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Epicatechin: Potential Use as Anti-Obese and Anti-Periodontal Nutrient

Sano T., Elsheikh M., Kanematsu T.

Current Oral Health Reports 11 ( 4 ) 297 - 305 2024.12

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Purpose of Review: There is an increasing interest in the use of dietary supplements and natural products for the treatment and prevention of obesity and periodontitis. Epicatechin (EC), a flavonoid abundant in cocoa, green tea, and red wine, possesses excellent anti-inflammatory and antioxidant properties. This review summarizes preclinical and clinical findings on the effects of EC on obesity and periodontitis. Recent Findings: Obesity not only leads to weight gain but also causes chronic low-level inflammation in adipose tissue. Periodontitis is an infectious disease caused by periodontal pathogens that chronically destroy periodontal tissues. Chronic inflammation leads to lifestyle-related diseases, such as diabetes, hypertension, and arteriosclerosis. Current literature suggests that EC can reduce inflammatory responses and improve obesity-related complications and periodontal disease status. Summary: These findings highlight the potential use of EC in the management of obesity and periodontitis. However, direct evidence for the use of EC supplementation in the treatment of obesity and periodontitis in humans remains limited. Further well-designed controlled studies are required to confirm its efficacy.

DOI： 10.1007/s40496-024-00390-3

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Epicatechin suppresses the expression of C-C motif chemokine ligand 19 and ameliorates periodontitis

Sano T., Yuan M., Li R., Yasunaga A., Mizokami A., Nakatsu Y., Asano T., Kanematsu T.

Journal of Functional Foods 122 2024.11 （ ISSN:17564646 ）

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Periodontitis is a prevalent chronic inflammatory disease requiring the development of drug-based therapies. Epicatechin is a major polyphenol in cocoa extract and possesses numerous pharmacological properties. This study aimed to investigate the suppressive effect of epicatechin on C-C motif chemokine ligand 19 (CCL19)-mediated periodontitis using a mouse model. CCL19 expression was high in mouse gingiva with ligature-induced periodontitis. CCL19 expression was increased by lipopolysaccharide stimulation in murine gingival fibroblasts ESK-1 cells, and CCL19 induced the production of tumor necrosis factor alpha and interleukin-1 beta in mouse macrophage-like RAW264.7 cells. Importantly, lipopolysaccharide-enhanced CCL19 expression in ESK-1 cells was significantly suppressed by pretreatment with epicatechin. In addition, epicatechin administration significantly reduced alveolar bone resorption, and expression of Ccl19 and proinflammatory cytokines in the inflamed gingiva in high-fat diet-fed mice. These results demonstrate that epicatechin protects against periodontitis by reducing CCL19 levels, which may be a promising countermeasure for periodontitis in clinical practice.

DOI： 10.1016/j.jff.2024.106512

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Prolyl isomerase Pin1 in skeletal muscles contributes to systemic energy metabolism and exercise capacity through regulating SERCA activity. International journal

Yusuke Nakatsu, Yasuka Matsunaga, Mikako Nakanishi, Takeshi Yamamotoya, Tomomi Sano, Takashi Kanematsu, Tomoichiro Asano

Biochemical and biophysical research communications 715 150001 - 150001 2024.7 （ ISSN:0006-291X eISSN:1090-2104 ）

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The skeletal muscle is a pivotal organ involved in the regulation of both energy metabolism and exercise capacity. There is no doubt that exercise contributes to a healthy life through the consumption of excessive energy or the release of myokines. Skeletal muscles exhibit insulin sensitivity and can rapidly uptake blood glucose. In addition, they can undergo non-shivering thermogenesis through actions of both the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) and small peptide, sarcolipin, resulting in systemic energy metabolism. Accordingly, the maintenance of skeletal muscles is important for both metabolism and exercise. Prolyl isomerase Pin1 is an enzyme that converts the cis-trans form of proline residues and controls substrate function. We have previously reported that Pin1 plays important roles in insulin release, thermogenesis, and lipolysis. However, the roles of Pin1 in skeletal muscles remains unknown. To clarify this issue, we generated skeletal muscle-specific Pin1 knockout mice. Pin1 deficiency had no effects on muscle weights, morphology and ratio of fiber types. However, they showed exacerbated obesity or insulin resistance when fed with a high-fat diet. They also showed a lower ability to exercise than wild type mice did. We also found that Pin1 interacted with SERCA and elevated its activity, resulting in the upregulation of oxygen consumption. Overall, our study reveals that Pin1 in skeletal muscles contributes to both systemic energy metabolism and exercise capacity.

DOI： 10.1016/j.bbrc.2024.150001

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Retracing the rabbit's path: Effects of altering the second flash position in the visual saltation illusion

de Jesus, SAM; Ito, H; Kanematsu, T

I-PERCEPTION 15 ( 3 ) 20416695241254016 2024.5 （ ISSN:2041-6695 ）

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DOI： 10.1177/20416695241254016

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Perceived depth reversals of images on a concave screen

Gu, XY; Yu, H; Ito, H; Kanematsu, T

I-PERCEPTION 15 ( 3 ) 20416695241249945 2024.5 （ ISSN:2041-6695 ）

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DOI： 10.1177/20416695241249945

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The G protein-coupled receptor GPRC5C is a saccharide sensor with a novel 'off' response Reviewed International journal

Yuko Kawabata, Shingo Takai, Keisuke Sanematsu, Shusuke Iwata, Fuminori Kawabata, Takashi Kanematsu, Eijiro Jimi, Noriatsu Shigemura

FEBS Letters 597 ( 15 ) 2006 - 2016 2023.8 （ ISSN:0014-5793 eISSN:1873-3468 ）

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DOI： 10.1002/1873-3468.14695

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Preface

Aoki Kazuhiro, Kanematsu Takashi

Folia Pharmacologica Japonica 158 ( 3 ) 246 - 246 2023.5 （ ISSN:00155691 eISSN:13478397 ）

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Language：Japanese Publisher：The Japanese Pharmacological Society

DOI： 10.1254/fpj.23016

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miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress International journal

Hayashi Chikako, Fukuda Takao, Kawakami Kentaro, Toyoda Masaaki, Nakao Yuki, Watanabe Yukari, Shinjo Takanori, Sano Tomomi, Iwashita Misaki, Yotsumoto Karen, Shida Miyu, Taketomi Takaharu, Sanui Terukazu, Uchiumi Takeshi, Kanematsu Takashi, Nishimura Fusanori

Frontiers in Cell and Developmental Biology 10 1061216 - 1061216 2022.11 （ ISSN:2296-634X eISSN:2296634X ）

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The expression profiles of exosomal microRNAs (miRNAs) are regulated by the microenvironment, and appropriate priming with mesenchymal stem cells (MSCs) is one of the strategies to enhance the paracrine potency of MSCs. Our previous work demonstrated that exosomes from tumor necrosis factor (TNF)-α-primed human gingiva-derived MSCs (GMSCs) could be a therapeutic tool against periodontitis, and that TNFα-inducible exosomal miR-1260b is essential for the inhibition of alveolar bone loss. However, the precise molecular mechanism underlying miR-1260b-mediated inhibition of osteoclastogenesis is not yet fully understood. Here, we found that the activating transcription factor (ATF)-6β, a novel miR-1260b-targeting gene, is critical for the regulation of osteoclastogenesis under endoplasmic reticulum (ER) stress. An experimental periodontal mouse model demonstrated that induction of ER stress was accompanied by enhanced ATF6β expression, and local administration of miR-1260b and ATF6β siRNA using polyethylenimine nanoparticles (PEI-NPs) significantly suppressed the periodontal bone resorption. In periodontal ligament (PDL) cells, the ER stress inducer, tunicamycin, enhanced the expression of the receptor activator of NF-κB ligand (RANKL), while miR-1260b-mediated downregulation of ATF6β caused RANKL inhibition. Furthermore, the secretome from miR-1260b/ATF6β-axis-activated PDL cells inhibited osteoclastogenesis in human CD14^+ peripheral blood-derived monocytes. These results indicate that the miR-1260b/ATF6β axis mediates the regulation of ER stress, which may be used as a novel therapeutic strategy to treat periodontal disease.

DOI： 10.3389/fcell.2022.1061216

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miR-1260b inhibits periodontal bone loss by targeting ATF6 beta mediated regulation of ER stress Invited Reviewed International journal

Hayashi, Chikako; Fukuda, Takao; Kawakami, Kentaro; Toyoda, Masaaki; Nakao, Yuki; Watanabe, Yukari; Shinjo, Takanori; Sano, Tomomi; Iwashita, Misaki; Yotsumoto, Karen; Shida, Miyu; Taketomi, Takaharu; Sanui, Terukazu; Uchiumi, Takeshi; Kanematsu, Takashi; Nishimura, Fusanori

FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY 10 2022.11 （ ISSN:2296-634X ）

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DOI： 10.3389/icell.2022.1061216

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Phospholipase C-related catalytically inactive protein enhances cisplatin-induced apoptotic cell death Reviewed

Satoshi Asano, Yuka Maetani, Yukio Ago, Takashi Kanematsu

European Journal of Pharmacology 933 175273 2022.10

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DOI： 10.1016/j.ejphar.2022.175273.

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閉経後骨粗鬆症モデルマウスの味覚行動の変化(The behavioral taste responses of postmenopausal osteoporosis in mice)

川端由子, 尾池麻未, 高井信吾, 岩田周介, 實松敬介, 重村憲徳, 兼松隆, 自見英治郎

Journal of Oral Biosciences Supplement 2022 317 - 317 2022.9 （ ISSN:2187-2333 eISSN:2187-9109 ）

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RANKL elevation activates the NIK/NF-κB pathway, inducing obesity in ovariectomized mice. Reviewed International journal

Kayo Mori, Akiko Mizokami, Tomomi Sano, Satoru Mukai, Fumitaka Hiura, Yasunori Ayukawa, Kiyoshi Koyano, Takashi Kanematsu, Eijiro Jimi

The Journal of endocrinology 254 ( 1 ) 27 - 36 2022.7 （ ISSN:0022-0795 eISSN:1479-6805 ）

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Menopausal women are susceptible to visceral obesity, which increases the risk of metabolic disorders. However, the mechanisms of menopause-induced visceral fat accumulation are not fully understood. Circulating levels of receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) are elevated in an animal model of menopause. RANKL, a multifunctional cytokine, activates the NF-κB pathway, which serves as a pivotal mediator of inflammatory responses. Here, we investigated whether RANKL-induced non-canonical NF-κB pathway activation induces inflammation and lipid accumulation in adipose tissues. RANKL induced Tnfa expression via the non-canonical NF-κB pathway in bone marrow cells. We therefore analyzed aly/aly mice, in which the non-canonical NF-κB pathway is not activated, owing to an inactive form of NF-κB-inducing kinase. A postmenopausal obesity model was generated by ovariectomy and subsequent high-fat and high-sucrose diet feeding. In aly/aly mice with postmenopausal obesity, serum RANKL levels were elevated, and hepatic lipid accumulation and adipocyte hypertrophy were suppressed, resulting in reduced macrophage infiltration and inflammatory cytokine mRNA expression in visceral adipose tissue. Furthermore, aly/aly mice showed protection from glucose intolerance and insulin resistance, which were observed in ovariectomized WT obese mice. These findings indicate that non-canonical NF-κB pathway activation via serum RANKL elevation contributes to postmenopausal obesity.

DOI： 10.1530/JOE-21-0424

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Pentobarbital may protect against neurogenic inflammation after surgery via inhibition of substance P release from peripheral nerves of rats Reviewed International journal

Chiori Onizuka, Masahiro Irifune, Akari Mukai, Yoshitaka Shimizu, Mitsuru Doi, Kana Oue, Mitsuhiro Yoshida, Takahiro Kochi, Eiji Imado, Takashi Kanematsu, Yoki Nakamura, Norimitsu Morioka, Yoshihiro Nakata, Norio Sakai

Neuroscience Letters 771 136467 - 136467 2022.2 （ ISSN:0304-3940 eISSN:1872-7972 ）

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The inflammatory response related to surgery is considered surgical inflammation. Most anesthetic agents directly or indirectly suppress the immune response. However, the intravenous anesthetics pentobarbital and ketamine were reported to inhibit the lipopolysaccharide-induced inflammatory response such as cytokines formation. Neurogenic inflammation is inflammation originating from the local release of inflammatory mediators, such as substance P (SP), by primary afferent neurons after noxious stimuli like surgery. Thus, in this study, we examined whether pentobarbital and ketamine suppress SP release from cultured dorsal root ganglion (DRG) neurons. DRG cells were dissected from male Wistar rats. Released SP was measured by radioimmunoassay. We demonstrated that higher concentrations of pentobarbital (100-1,000 μM) significantly inhibited capsaicin (100 nM)-induced, but not high K+ (50 mM)-induced, SP release from DRG cells, although a high concentration of ketamine (1 mM) did not. This study revealed that pentobarbital functions between the activation of vanilloid receptor subtype 1 (TRPV1) receptors, to which capsaicin selectively binds, and the opening of voltage-operated Ca2+ channels (VOCC) in the nerve endings. Therefore, the anti-inflammatory action of pentobarbital is mediated through different mechanisms than those of ketamine. Thus, the inhibitory effect of pentobarbital on SP release from peripheral terminals may protect against neurogenic inflammation after surgery.

DOI： 10.1016/j.neulet.2022.136467

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Pentobarbital may protect against neurogenic inflammation after surgery via inhibition of substance P release from peripheral nerves of rats Reviewed International journal

Chiori Onizuka, Masahiro Irifune, Akari Mukai, Yoshitaka Shimizu, Mitsuru Doi, Kana Oue, Mitsuhiro Yoshida, Takahiro Kochi, Eiji Imado, Takashi Kanematsu, Yoki Nakamura, Norimitsu Morioka, Yoshihiro Nakata, Norio Sakai

Neuroscience Letters 771 136467 2022.2

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DOI： https://doi.org/10.1016/j.neulet.2022.136467
Phospholipase C-related but catalytically inactive protein acts as a positive regulator of insulin signalling in adipocytes. International journal

Jing Gao, Akiko Mizokami, Hiroshi Takeuchi, Aonan Li, Fei Huang, Haruki Nagano, Takashi Kanematsu, Eijiro Jimi, Masato Hirata

Journal of cell science 135 ( 1 ) 2022.1 （ ISSN:0021-9533 eISSN:1477-9137 ）

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Insulin signalling is tightly controlled by various factors, but the exact molecular mechanism remains incompletely understood. We have previously reported that phospholipase C-related but catalytically inactive protein (PRIP; used here to refer to both PRIP-1 and PRIP-2, also known as PLCL1 and PLCL2, respectively) interacts with Akt1, the central molecule in insulin signalling. Here, we investigated whether PRIP is involved in the regulation of insulin signalling in adipocytes. We found that insulin signalling, including insulin-stimulated phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1) and Akt, and glucose uptake were impaired in adipocytes from PRIP double-knockout (PRIP-KO) mice compared with those from wild-type (WT) mice. The amount of IR expressed on the cell surface was decreased in PRIP-KO adipocytes. Immunoprecipitation assays showed that PRIP interacted with IR. The reduced cell surface IR in PRIP-KO adipocytes was comparable with that in WT cells when Rab5 (Rab5a, -5b and -5c) expression was silenced using specific siRNA. In contrast, the dephosphorylation of IRS-1 at serine residues, some of which have been reported to be involved in the internalisation of IR, was impaired in cells from PRIP-KO mice. These results suggest that PRIP facilitates insulin signalling by modulating the internalisation of IR in adipocytes.

DOI： 10.1242/jcs.258584

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Spike firing attenuation of serotonin neurons in learned helplessness rats is reversed by ketamine Reviewed International journal

Kouichi Hashimoto, Yosuke Yamawaki, Kenji Yamaoka, Takayuki Yoshida, Kana Okada, Wanqin Tan, Miwako Yamasaki, Yoshiko Matsumoto-Makidono, Reika Kubo, Hisako Nakayama, Tsutomu Kataoka, Takashi Kanematsu, Masahiko Watanabe, Yasumasa Okamoto, Shigeru Morinobu, Hidenori Aizawa Shigeto Yamawaki

Brain Communications 3 ( 4 ) fcab285 2021.12

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DOI： https://doi.org/10.1093/braincomms/fcab285
Adipocyte-specific GPRC6A ablation promotes diet-induced obesity by inhibiting lipolysis Reviewed International journal

Satoru Mukai, Akiko Mizokami, Takahito Otani, Tomomi Sano, Miho Matsuda, Sakura Chishaki, Jing Gao, Tomoyo Kawakubo-Yasukochi, Ronghao Tang, Takashi Kanematsu, Hiroshi Takeuchi, Eijiro Jimi, Masato Hirata

The Journal of Biological Chemistry 296 100274 2021.1

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DOI： https://doi.org/10.1016/j.jbc.2021.100274
The indirect γ-aminobutyric acid (GABA) receptor agonist gabaculine-induced loss of the righting reflex may inhibit the descending analgesic pathway Reviewed International journal

198 173034 2020.11

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In the spinal cord, γ-aminobutyric acid (GABA) interneurons play an essential role in antinociception. However, not all actions of GABA favor antinociception at the supraspinal level. We previously reported that gabaculine, which increases endogenous GABA in the synaptic clefts, induces loss of the righting reflex (LORR) that is one indicator of hypnosis, but not immobility in response to noxious stimulus. A slow pain is transmitted to the spinal cord via C fibers and evokes substance P (SP) release from their terminals. However, the antinociceptive effects of gabaculine are still unknown. Our study examined whether the analgesic effects of the opioid morphine or the α2-adrenoceptor agonist dexmedetomidine, whose actions are mediated through facilitation of the descending analgesic pathway, are affected by gabaculine-induced LORR. We also explored the effects of GABA receptor agonists on SP release from cultured dorsal root ganglion (DRG) neurons. All drugs were administered systemically to mice. To assess antinociception, loss of nociceptive response (analgesia) and immobility were evaluated. DRG cells were dissected from rats. Gabaculine produced no analgesia. Either morphine or dexmedetomidine in combination with gabaculine induced immobility; however, the doses of each drug required to induce immobility were much higher than those required to induce analgesia. Capsaicin significantly increased SP release from DRG cells, but a high concentration (1 mM) of the GABA receptor agonist muscimol, propofol, gaboxadol, or baclofen did not inhibit the capsaicin-induced SP release, suggesting that their antinociceptive effects were not through this mechanism. Thus, the gabaculine-induced LORR may inhibit the descending analgesic pathway.

DOI： 10.1016/j.pbb.2020.173034.
IL-6 Induced by Periodontal Inflammation Causes Neuroinflammation and Disrupts the Blood-Brain Barrier Reviewed International journal

Daisuke Furutama, Shinji Matsuda, Yosuke Yamawaki, Saki Hatano, Ai Okanobu, Takumi Memida, Hiroshi Oue, Tsuyoshi Fujita, Kazuhisa Ouhara, Mikihito Kajiya, Noriyoshi Mizuno, Takashi Kanematsu, Kazuhiro Tsuga, Hidemi Kurihara

Brain sciences 10 ( 10 ) 679 2020.9

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DOI： 10.3390/brainsci10100679.
Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues Reviewed International journal

Taiki Sanada, Tomomi Sano, Yusuke Sotomaru, Rehab Alshargabi, Yosuke Yamawaki, Akiko Yamashita, Hiroaki Matsunaga, Misaki Iwashita, Takanori Shinjo, Takashi Kanematsu, Tomoichiro Asano, Fusanori Nishimura

Biochemistry and Biophysics Reports 22 100757 - 100757 2020.7

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DOI： https://doi.org/10.1016/j.bbrep.2020.100757
Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice Reviewed

Tomonori Furukawa, Yoshikazu Nikaido, Shuji Shimoyama, Yoshiki Ogata, Tetsuya Kushikata, Kazuyoshi Hirota, Takashi Kanematsu, Masato Hirata, Shinya Ueno

Journal of Anesthesia 33 ( 4 ) 531 - 542 2019.8

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DOI： 10.1007/s00540-019-02663-z
Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure Reviewed

Tomomi Sano, Taiki Sanada, Yusuke Sotomaru, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomoichiro Asano, Takashi Kanematsu, Fusanori Nishimura

Nutrition and Metabolism 16 ( 1 ) 2019.7

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DOI： 10.1186/s12986-019-0372-5
Phospholipase C-related catalytically inactive protein A novel signaling molecule for modulating fat metabolism and energy expenditure Reviewed

Takashi Kanematsu, Kana Oue, Toshiya Okumura, Kae Harada, Yosuke Yamawaki, Satoshi Asano, Akiko Mizokami, Masahiro Irifune, Masato Hirata

journal of oral biosciences 61 ( 2 ) 65 - 72 2019.6

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DOI： 10.1016/j.job.2019.04.002
Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16 Reviewed

Yusuke Nakatsu, Yasuka Matsunaga, Takeshi Yamamotoya, Koji Ueda, Masa ki Inoue, Yu Mizuno, Mikako Nakanishi, Tomomi Sano, Yosuke Yamawaki, Akifumi Kushiyama, Hideyuki Sakoda, Midori Fujishiro, Akihide Ryo, Hiraku Ono, Tohru Minamino, Shin Ichiro Takahashi, Haruya Ohno, Masayasu Yoneda, Kei Takahashi, Hisamitsu Ishihara, Hideki Katagiri, Fusanori Nishimura, Takashi Kanematsu, Tetsuya Yamada, Tomoichiro Asano

Cell Reports 26 ( 12 ) 3221 - 3230.e3 2019.3

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DOI： 10.1016/j.celrep.2019.02.066
Sodium butyrate abolishes lipopolysaccharide-induced depression-like behaviors and hippocampal microglial activation in mice Reviewed

Yosuke Yamawaki, Norika Yoshioka, Kanako Nozaki, Hikaru Ito, Keisuke Oda, Kana Harada, Satomi Shirawachi, Satoshi Asano, Hidenori Aizawa, Shigeto Yamawaki, Takashi Kanematsu, Hiroyuki Akagi

Brain Research 1680 13 - 38 2018.2

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DOI： 10.1016/j.brainres.2017.12.004
General anesthetic actions on GABA _A receptors in vivo are reduced in phospholipase C-related catalytically inactive protein knockout mice Reviewed

Masaki Hayashiuchi, Tomoya Kitayama, Katsuya Morita, Yosuke Yamawaki, Kana Oue, Taiga Yoshinaka, Satoshi Asano, Kae Harada, Youngnam Kang, Masato Hirata, Masahiro Irifune, Mitsugi Okada, Takashi Kanematsu

Journal of Anesthesia 31 ( 4 ) 531 - 538 2017.8

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DOI： 10.1007/s00540-017-2350-2
Phospholipase C-related catalytically inactive protein-knockout mice exhibit uncoupling protein 1 upregulation in adipose tissues following chronic cold exposure Reviewed

Kana Oue, Yosuke Yamawaki, Satoshi Asano, Akiko Mizokami, Masato Hirata, Masahiro Irifune, Takashi Kanematsu

journal of oral biosciences 59 ( 2 ) 108 - 112 2017.5

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DOI： 10.1016/j.job.2017.04.001
Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance Reviewed

Tomomi Sano, S. Nagayasu, S. Suzuki, Misaki Iwashita, Akiko Yamashita, T. Shinjo, Terukazu Sanui, A. Kushiyama, Takashi Kanematsu, T. Asano, Fusanori Nishimura

Nutrition, Metabolism and Cardiovascular Diseases 27 ( 3 ) 249 - 259 2017.3

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DOI： 10.1016/j.numecd.2016.11.008
Phospholipase C-related catalytically inactive protein can regulate obesity, a state of peripheral inflammation Reviewed

Yosuke Yamawaki, Kana Oue, Satomi Shirawachi, Satoshi Asano, Kae Harada, Takashi Kanematsu

Japanese Dental Science Review 53 ( 1 ) 18 - 24 2017.2

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DOI： 10.1016/j.jdsr.2016.06.001
New molecular basis in the regulation of lipolysis via dephosphorylation Reviewed

Kana Oue, Kae Harada-Hada, Takashi Kanematsu

Folia Pharmacologica Japonica 146 ( 2 ) 93 - 97 2015.8

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DOI： 10.1254/fpj.146.93
Enhanced lateral inhibition in the barrel cortex by deletion of phospholipase C-related catalytically inactive protein-1/2 in mice Reviewed

Hiroki Toyoda, Mitsuru Saito, Hajime Sato, Tsutomu Kawano, Shinpei Kawakami, Hirofumi Yatani, Takashi Kanematsu, Masato Hirata, Youngnam Kang

Pflugers Archiv European Journal of Physiology 467 ( 7 ) 1445 - 1456 2015.7

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DOI： 10.1007/s00424-014-1592-1
Selective blockade of N-methyl-D-aspartate channels in combination with dopamine receptor antagonism induces loss of the righting reflex in mice, but not immobility Reviewed

Nobuhito Kikuchi, Masahiro Irifune, Yoshitaka Shimizu, Keita Yoshida, Katsuya Morita, Takashi Kanematsu, Norimitsu Morioka, Yoshihiro Nakata, Norio Sakai

Psychopharmacology 232 ( 1 ) 39 - 46 2015.1

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DOI： 10.1007/s00213-014-3634-y
Palliation of bone cancer pain by antagonists of platelet-activating factor receptors Reviewed

Katsuya Morita, Seiji Shiraishi, Naoyo Motoyama, Tomoya Kitayama, Takashi Kanematsu, Yasuhito Uezono, Toshihiro Dohi

PloS one 9 ( 3 ) 2014.3

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DOI： 10.1371/journal.pone.0091746
Enhanced desensitization followed by unusual resensitization in GABA_A receptors in phospholipase C-related catalytically inactive protein-1/2 double-knockout mice Reviewed

Hiroki Toyoda, Mitsuru Saito, Hajime Sato, Takuma Tanaka, Takeo Ogawa, Hirofumi Yatani, Tsutomu Kawano, Takashi Kanematsu, Masato Hirata, Youngnam Kang

Pflugers Archiv European Journal of Physiology 467 ( 2 ) 267 - 284 2014.1

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DOI： 10.1007/s00424-014-1511-5
Relief of cancer pain by glycine transporter inhibitors Reviewed

Naoyo Motoyama, Katsuya Morita, Seiji Shiraishi, Tomoya Kitayama, Takashi Kanematsu, Yasuhito Uezono, Toshihiro Dohi

Anesthesia and Analgesia 119 ( 4 ) 988 - 995 2014.1

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DOI： 10.1213/ANE.0000000000000388
Pain-releasing action of Platelet-activating factor (PAF) antagonists in neuropathic pain animal models and the mechanisms of action Reviewed

N. Motoyama, K. Morita, T. Kitayama, S. Shiraishi, Y. Uezono, Fusanori Nishimura, Takashi Kanematsu, Toshihiro Dohi

European Journal of Pain (United Kingdom) 17 ( 8 ) 1156 - 1167 2013.9

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DOI： 10.1002/j.1532-2149.2013.00289.x
Phospholipase C-related but catalytically inactive protein, PRIP as a scaffolding protein for phospho-regulation Reviewed

Goro Sugiyama, Hiroshi Takeuchi, Takashi Kanematsu, Jing Gao, Miho Matsuda, Masato Hirata

Advances in Biological Regulation 53 ( 3 ) 331 - 340 2013.1

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DOI： 10.1016/j.jbior.2013.07.001
Dysfunction of extrasynaptic GABAergic transmission in phospholipase C-related, but catalytically inactive protein 1 knockout mice is associated with an epilepsy phenotype Reviewed

Gang Zhu, Shukuko Yoshida, Keisuke Migita, Junko Yamada, Fumiaki Mori, Masahiko Tomiyama, Koichi Wakabayashi, Takashi Kanematsu, Masato Hirata, Sunao Kaneko, Shinya Ueno, Motohiro Okada

Journal of Pharmacology and Experimental Therapeutics 340 ( 3 ) 520 - 528 2012.3

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DOI： 10.1124/jpet.111.182386
Phenotypes of pain behavior in phospholipase C-related but catalytically inactive protein type 1 knockout mice Reviewed

Keisuke Migita, Masahiko Tomiyama, Junko Yamada, Masashi Fukuzawa, Takashi Kanematsu, Masato Hirata, Shinya Ueno

Molecular Pain 7 2011.10

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DOI： 10.1186/1744-8069-7-79
Involvement of PRIP, phospholipase C-related, but catalytically inactive protein, in bone formation Reviewed

Koshiro Tsutsumi, Miho Matsuda, Miho Kotani, Akiko Mizokami, Ayako Murakami, Ichiro Takahashi, Yoshihiro Terada, Takashi Kanematsu, Kiyoko Fukami, Tadaomi Takenawa, Eijiro Jimi, Masato Hirata

Journal of Biological Chemistry 286 ( 35 ) 31032 - 31042 2011.9

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DOI： 10.1074/jbc.M111.235903
Genetic reduction of GABA_A receptor γ2 subunit expression potentiates the immobilizing action of isoflurane Reviewed

472 ( 1 ) 1 - 4 2010.3

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Potentiation of inhibitory γ-aminobutyric acid subtype A (GABA_A) receptor function is involved in the mechanisms of anesthetic action. The present study examined the immobilizing action of the volatile anesthetic isoflurane in mice with double knockout (DKO) of phospholipase C-related inactive protein (PRIP)-1 and -2. Both of these proteins play important roles in the expression of GABA_A receptors containing the γ2 subunit on the neuronal cell surface. Immunohistochemistry for GABA_A receptor subunits demonstrated reduced expression of γ2 subunits in the spinal cord of the DKO mice. Immunohistochemistry also revealed up-regulation of the α1 and β3 subunits even though there were no apparent differences in the immunoreactivities for the β2 subunits between wild-type and DKO mice. The tail-clamp method was used to evaluate the anesthetic/immobilizing effect of isoflurane and the minimum alveolar concentration (MAC) was significantly lower in DKO mice compared with wild-type controls (1.07 ± 0.01% versus 1.36 ± 0.04% atm), indicating an increased sensitivity to isoflurane in DKO mice. These immunohistochemical and pharmacological findings suggest that reduced expression of the GABA_A receptor γ2 subunit affects the composition and function of spinal GABA_A receptors and potentiates the immobilizing action of isoflurane.

DOI： 10.1016/j.neulet.2010.01.031
Orofacial movements in phospholipase C-related catalytically inactive protein-1/2 double knockout mice Effect of the GABAergic agent diazepam and the D₁ dopamine receptor agonist SKF 83959 Reviewed

Katsunori Tomiyama, Liqiu Song, Masayuki Kobayashi, Anthony Kinsella, Takashi Kanematsu, Masato Hirata, Noriaki Koshikawa, John L. Waddington

Synapse 64 ( 9 ) 714 - 720 2010.1

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DOI： 10.1002/syn.20798
Surface expression of gaba_A receptors Roles for the binding partners Reviewed

Takashi Kanematsu, Makoto Fujii, Hiroto Tanaka, Hisanori Umebayashi, Masato Hirata

journal of oral biosciences 52 ( 4 ) 322 - 329 2010.1

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DOI： 10.2330/joralbiosci.52.322
Involvement of phospholipase C-related inactive protein in the mouse reproductive system through the regulation of gonadotropin levels Reviewed

Miho Matsuda, Koushirou Tsutsumi, Takashi Kanematsu, Kiyoko Fukami, Yoshihiro Terada, Tadaomi Takenawa, Keiichi I. Nakayama, Masato Hirata

Biology of Reproduction 81 ( 4 ) 681 - 689 2009.12

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DOI： 10.1095/biolreprod.109.076760
Binding of phospholipase C-related but catalytically inactive protein to phosphatidylinositol 4,5-bisphosphate via the PH domain Reviewed

Jing Gao, Hiroshi Takeuchi, Zhao Zhang, Makoto Fujii, Takashi Kanematsu, Masato Hirata

Cellular Signalling 21 ( 7 ) 1180 - 1186 2009.7

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DOI： 10.1016/j.cellsig.2009.03.008
Regulation of GABA_A-receptor surface expression with special reference to the involvement of GABARAP (GABA_A receptor-associated protein) and PRIP (phospholipase C-related, but catalytically inactive protein) Reviewed

Takashi Kanematsu, Akiko Mizokami, Keiko Watanabe, Masato Hirata

Journal of Pharmacological Sciences 104 ( 4 ) 285 - 292 2007.9

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DOI： 10.1254/jphs.CP0070063
Early changes in KCC2 phosphorylation in response to neuronal stress result in functional downregulation Reviewed

Hiroaki Wake, Miho Watanabe, Andrew J. Moorhouse, Takashi Kanematsu, Shoko Horibe, Noriyuki Matsukawa, Kiyofumi Asai, Kosei Ojika, Masato Hirata, Junichi Nabekura

Journal of Neuroscience 27 ( 7 ) 1642 - 1650 2007.2

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DOI： 10.1523/JNEUROSCI.3104-06.2007
Identification of a Novel Signaling Molecule and Elucidation of Its Cellular Functions —Development of an Interface between Neuroscience and Oral Health Science— Reviewed

49 ( 4 ) 244 - 258 2007.1

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The investigation of chemically synthesized inositol 1,4,5-trisphosphate [Ins(1,4,5)P₃] analogs has led to the isolation of a novel protein with a molecular size of 130 kDa, characterized as a molecule with a domain organization similar to phospholipase C (PLC)-δ1 but lacking enzymatic activity. Two isoforms of the molecule were subsequently identified, the molecule has been named PRIP (PLC-related, but catalytically inactive protein), with the two isoforms named PRIP-1 and-2. Regarding its ability to bind Ins (1,4,5)-P₃ via the pleckstrin homology domain, the involvement of PRIP-1 in Ins(1,4,5)P₃-mediated Ca²⁺ signaling was first examined. Yeast two-hybrid screening of a brain cDNA library identified GABARAP (GABA_A receptor-associated protein) and PP1 (protein phosphatase 1), which led us to examine the possible neurological involvement of PRIP, particularly in GABA_A receptor signaling. PRIP-1 and-2 double knock-out (DKO) mice were analyzed for GABA_A receptor function with special reference to the action of benzodiazepines whose target is the γ subunit of the receptors; sensitivity to benzodiazepine was reduced, as assessed by biochemical, electrophysiological, and behavioral analyses of DKO mice, suggesting the dysfunction of γ2 subunit-containing GABA_A receptors. The mesencephalic trigeminal nucleus, which mediates perceptions from periodontal mechanoreceptors and jaw-closer muscle spindles, receives many synaptic inputs, including those from GABA_A receptors, indicating that PRIP might indirectly be involved in rhythmical jaw movement. In the present article, we summarize our current research and the functional significance of PRIP.

DOI： 10.2330/joralbiosci.49.244
Roles of PRIP in GABA_A Receptor Signaling Reviewed

Akiko Mizokami, Takashi Kanematsu, Masato Hirata

journal of oral biosciences 49 ( 2 ) 105 - 112 2007.1

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DOI： 10.2330/joralbiosci.49.105
Lysosomal turnover of GABARAP-phospholipid conjugate is activated during differentiation of C2C12 cells to myotubes without inactivation of the mTor kinase-signaling pathway Reviewed

Isei Tanida, Mika Wakabayashi, Takashi Kanematsu, Naoko Minematsu-Ikeguchi, Yu Shin Sou, Masato Hirata, Takashi Ueno, Eiki Kominami

Autophagy 2 ( 4 ) 264 - 271 2006.1

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DOI： 10.4161/auto.2871
Protein phosphatase regulation by PRIP, a PLC-related catalytically inactive protein-Implications in the phospho-modulation of the GABA_A receptor Reviewed

Satoko Yanagihori, Miho Terunuma, Kiyoshi Koyano, Takashi Kanematsu, Sung Ho Ryu, Masato Hirata

Advances in Enzyme Regulation 46 ( 1 ) 203 - 222 2006

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DOI： 10.1016/j.advenzreg.2006.01.006
PRIP, a novel Ins(1,4,5)P₃ binding protein, functional significance in Ca²⁺ signaling and extension to neuroscience and beyond Reviewed

Takashi Kanematsu, Hiroshi Takeuchi, Miho Terunuma, Masato Hirata

Molecules and cells 20 ( 3 ) 305 - 314 2005.12

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The inhibitory effect of alendronate, a nitrogen-containing bisphosphonate on the PI3K-Akt-NFκB pathway in osteosarcoma cells Reviewed

146 ( 5 ) 633 - 641 2005.11

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1. Bisphosphonates are inhibitors of tumor cell growth as well as of bone resorption by inducing cell apoptosis. However, little is known regarding the mechanisms by which the drug induces cell apoptosis. The aim of the present study was to determine the effect of alendronate, one of the nitrogen-containing bisphosphonates on the phoshoinositide 3-kinase (PI3K)-Akt-NFκB pathway, the major cell survival pathway. 2. The PI3K-Akt-NFκB pathway was activated in the osteosarcoma cell line MG-63 treated with tumor necrosis factor-α or insulin. Saos-2 was also used in some experiments. This was assessed by the production of phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P ₃), increased PI3K activity, phosphorylation of Akt at serine 473 and threonine 308, increase in activity of the inhibitor of nuclear factor κB (IκB) kinase (IKK) and finally phosphorylation of IκB and its subsequent degradation. 3. Pretreatment with alendronate at 100 μM for 24 h prior to the stimulation with tumor necrosis factor-α or insulin partially inhibited the IκB phosphorylation and degradation. These events were more clearly observed in the presence of inhibitors of proteasomes, which are responsible for the degradation of IκB. The drug also partially inhibited the activity of IKK, but almost fully inhibited the phosphorylation of Akt and the production of PtdIns(3,4,5)P ₃. 4. The inhibitory effect of alendronate on IκB phosphorylation and degradation was not attenuated by the exogenous addition of geranylgeraniol to replenish the cytosolic isoprenyl lipid substrate. 5. The present findings demonstrate that alendronate inhibited the PI3K-Akt-NFκB cell survival pathway at the point of PI3K activation, thus indicating the presence of new targets of alendronate.

DOI： 10.1038/sj.bjp.0706373
Direct interaction of N-ethylmaleimide-sensitive factor with GABA _A receptor β subunits Reviewed

30 ( 2 ) 197 - 206 2005.10

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GABA_A receptors mediate most of the fast inhibitory neurotransmission in the brain, and are believed to be composed mainly of α, β, and γ subunits. It has been shown that GABA_A receptors interact with a number of binding partners that act to regulate both receptor function and cell surface stability. Here, we reveal that GABA _A receptors interact directly with N-ethylmaleimide-sensitive factor (NSF), a critical regulator of vesicular dependent protein trafficking, as measured by in vitro protein binding and co-immunoprecipitation assays. In addition, we established that NSF interacts with residues 395-415 of the receptor β subunits and co-localizes with GABA_A receptors in hippocampal neurons. We also established that NSF can regulate GABA_A receptor cell surface expression depending upon residues 395-415 in the β3 subunit. Together, our results suggest an important role for NSF activity in regulating the cell surface stability of GABA_A receptors.

DOI： 10.1016/j.mcn.2005.07.006
Solution structure of microtubule-associated protein light chain 3 and identification of its functional subdomains Reviewed

Takahide Kouno, Mineyuki Mizuguchi, Isei Tanidal, Takashi Uenol, Takashi Kanematsu, Yoshihiro Mori, Hiroyuki Shinoda, Masato Hirata, Eiki Kominami, Keiichi Kawano

Journal of Biological Chemistry 280 ( 26 ) 24610 - 24617 2005.7

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DOI： 10.1074/jbc.M413565200
Role of PRIP-1, a novel Ins(1,4,5)P₃ binding protein, in Ins(1,4,5)P₃-mediated Ca²⁺ signaling Reviewed

Kae Harada, Hiroshi Takeuchi, Masahiro Oike, Miho Matsuda, Takashi Kanematsu, Hitoshi Yagisawa, Kei Ichi I. Nakayama, Katsumasa Maeda, Christophe Erneux, Masato Hirata

Journal of cellular physiology 202 ( 2 ) 422 - 433 2005.2

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DOI： 10.1002/jcp.20136
Hypersensitivity to pentylenetetrazol-induced convulsion in mice lacking the PLC-related inactive protein-1 Reviewed

Taku Yamaguchi, Takashi Kubota, Takashi Kanematsu, Keiichi Nakayama, Masato Hirata, Tsuneyuki Yamamoto

Brain Research 1025 ( 1-2 ) 237 - 240 2004.10

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DOI： 10.1016/j.brainres.2004.08.009
The life cycle of the GABA_A receptor and its regulating molecules Reviewed

Takashi Kanematsu, Miho Terunuma, Hidefumi Goto, Akiko Kuratani, Masato Hirata

Folia Pharmacologica Japonica 123 ( 2 ) 105 - 112 2004.2

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DOI： 10.1254/fpj.123.105
A Rapid Increase in the Total Number of Cell Surface Functional GABA _A Receptors Induced by Brain-derived Neurotrophic Factor in Rat Visual Cortex Reviewed

Yoshito Mizoguchi, Takashi Kanematsu, Masato Hirata, Junichi Nabekura

Journal of Biological Chemistry 278 ( 45 ) 44097 - 44102 2003.11

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DOI： 10.1074/jbc.M305872200
The importance to chondrocyte differentiation of changes in expression of the multiple inositol polyphosphate phosphatase Reviewed

Kiyoshi Hidaka, Takashi Kanematsu, James J. Caffrey, Hiroshi Takeuchi, Stephen B. Shears, Masato Hirata

Experimental Cell Research 290 ( 2 ) 254 - 264 2003.11

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DOI： 10.1016/S0014-4827(03)00337-9
PRIP-1 involved in GABAA receptor trafficking Reviewed

Takashi Kanematsu, Masato Hirata

Seikagaku. The Journal of Japanese Biochemical Society 75 ( 5 ) 378 - 382 2003.1

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Molecules interacting with PRIP-2, a novel Ins(1,4,5)P₃ binding protein type 2 Comparison with PRIP-1 Reviewed

Ayako Uji, Miho Matsuda, Toshio Kukita, Katsumasa Maeda, Takashi Kanematsu, Masato Hirata

Life Sciences 72 ( 4-5 ) 443 - 453 2002.12

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DOI： 10.1016/S0024-3205(02)02275-0
TNF inhibited the apoptosis by activation of Akt serine/threonine kinase in the human head and neck squamous cell carcinoma Reviewed

Ferry Sandra, Nori Aki Matsuki, Hiroshi Takeuchi, Tetsuro Ikebe, Takashi Kanematsu, Masamichi Ohishi, Masato Hirata

Cellular Signalling 14 ( 9 ) 771 - 778 2002.6

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DOI： 10.1016/S0898-6568(02)00025-6
The analysis of protein-protein interaction with special reference to PRIP-1 Reviewed

Takashi Kanematsu, Masato Hirata

Folia Pharmacologica Japonica 119 ( 4 ) 241 - 246 2002.5

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DOI： 10.1254/fpj.119.241
The role of MDM2 in the proliferative activity of ameloblastoma Reviewed

F. Sandra, N. Nakamura, Takashi Kanematsu, Masato Hirata, M. Ohishi

Oral Oncology 38 ( 2 ) 153 - 157 2002.3

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DOI： 10.1016/S1368-8375(01)00036-7
Letter to the editor ¹H, ¹³C and ¹⁵N resonance assignments of GABARAP, GABA_A receptor associated protein [4] Reviewed

Takahide Kouno, Kazunori Miura, Takashi Kanematsu, Masahiro Shirakawa, Masato Hirata, Keiichi Kawano

Journal of Biomolecular NMR 22 ( 1 ) 97 - 98 2002.2

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DOI： 10.1023/A:1013884402033
Involvement of the phosphoinositide 3-kinase/protein kinase B signaling pathway in insulin/IGF-I-induced chondrogenesis of the mouse embryonal carcinoma-derived cell line ATDC5 Reviewed

Kiyoshi Hidaka, Takashi Kanematsu, Hiroshi Takeuchi, Minoru Nakata, Ushio Kikkawa, Masato Hirata

International Journal of Biochemistry and Cell Biology 33 ( 11 ) 1094 - 1103 2001.9

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DOI： 10.1016/S1357-2725(01)00067-X
Role of the pleckstrin homology domain of PLC-related catalytically inactive protein, p130 in Ca2+ signaling. Reviewed International journal

Matsuki N., Takeuchi H., Oike M., Lia J., Sandra F., Ohishi M., Kanematsu T. & Hirata M.

Curr. Top. Biochem. 2001.1

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Hyperinsulinemia in PRIP-1 gene deleted mice Reviewed

Naoko Doira, Takashi Kanematsu, Miho Matsuda, Hiroshi Takeuchi, Hito O. Nakano, Yushi Ito, Keiko Nakayama, Kei Ichi Nakayama, Masato Hirata

Biomedical Research 22 ( 3 ) 157 - 165 2001.1

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DOI： 10.2220/biomedres.22.157
Inhibition of Ca²⁺ signalling by p130, a phospholipase-C-related catalytically inactive protein Critical role of the p130 pleckstrin homology domain Reviewed

Hiroshi Takeuchi, Masahiro Oike, Hugh F. Paterson, Victoria Allen, Takashi Kanematsu, Yushi Ito, Christophe Erneux, Matilda Katan, Masato Hirata

Biochemical Journal 349 ( 1 ) 357 - 368 2000.7

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DOI： 10.1042/0264-6021:3490357
Novel Ins(1,4,5)P3 binding protein and GABA-A receptor signaling Reviewed

Takashi Kanematsu, Masato Hirata

Fukuoka igaku zasshi = Hukuoka acta medica 91 ( 7 ) 159 - 164 2000.1

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Studies on new ins(1,4,5)P₃ binding proteins with reference to the pH domains Reviewed

Takashi Kanematsu, Hiroshi Takeuchi, Masato Hirata

ACS Symposium Series 718 55 - 78 1999.12

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Involvement of EF hand motifs in the Ca²⁺-dependent binding of the pleckstrin homology domain to phosphoinositides Reviewed

Tada Aki Yamamoto, Hiroshi Takeuchi, Takashi Kanematsu, Victoria Allen, Hitoshi Yagisawa, Ushio Kikkawa, Yutaka Watanabe, Akihiko Nakasima, Matilda Katan, Masato Hirata

European Journal of Biochemistry 265 ( 1 ) 481 - 490 1999.10

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DOI： 10.1046/j.1432-1327.1999.00786.x
Antibodies against the PH domain of phospholipase C-δ1 inhibit Ins(1,4,5)P₃-Mediated Ca²⁺ release from the endoplasmic reticulum Reviewed

260 ( 1 ) 42 - 47 1999.6

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The pleckstrin homology domain (PH domain) is now well known as a structural module for the binding of inositol compounds. In the present study, polyclonal antibodies against the peptide KVKSSSWRRERFYK, derived from the N-terminal of the PH domain of phospholipase C-δ1 (PLC-δ1), were raised in rabbits. These were then tested for their ability to inhibit the binding of inositol 1,4,5-trisphosphate [Ins(1,4,5)P₃] to the binding proteins including the receptor molecule. The Fab fragment of the antibodies but not the whole molecule inhibited the binding of Ins(1,4,5)P₃ not only to PLC-δ1 but also to the Ins(1,4,5)P₃ receptor, indicating that the antibodies raised recognized the binding site for Ins(1,4,5)P₃ in the receptor. Rat basophilic leukemic cells were permeabilized with saponin and assayed for Ins(1,4,5)P₃mediated Ca²⁺ release. Pretreatment of permeabilized RBL cells with the Fab fragment of the antibodies diminished the release of Ca²⁺ caused by Ins(1,4,5)P₃, and further absorption experiments using a variety of synthetic peptides suggested that the tripeptide KVK is the epitope of the antibodies. Structural information about KVK will help in screening for Ins(1,4,5)P₃ antagonists.

DOI： 10.1006/bbrc.1999.0869
Membrane association of a new inositol 1,4,5-trisphosphate binding protein, p130 is not dependent on the pleckstrin homology domain Reviewed

Hiroshi Takeuchi, Takashi Kanematsu, Yoshio Misumi, Masato Hirata

Chemistry and Physics of Lipids 98 ( 1-2 ) 35 - 47 1999.4

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DOI： 10.1016/S0009-3084(99)00016-X
Intrinsic inhibitor of inositol 1,4,5-trisphosphate binding Reviewed

Masato Hirata, Masako Yoshida, Takashi Kanematsu, Hiroshi Takeuchi

Molecular and Cellular Biochemistry 190 ( 1-2 ) 179 - 184 1999

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Localization of a novel inositol 1,4,5-trisphosphate binding protein, p130 in rat brain Reviewed

Miho Matsuda, Takashi Kanematsu, Hiroshi Takeuchi, Toshio Kukita, Masato Hirata

Neuroscience Letters 257 ( 2 ) 97 - 100 1998.11

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DOI： 10.1016/S0304-3940(98)00810-6
PTB domain of insulin receptor substrate-1 binds inositol compounds Reviewed

Hiroshi Takeuchi, Miho Matsuda, Tada Aki Yamamoto, Takashi Kanematsu, Ushio Kikkawa, Hitoshi Yagisawa, Yutaka Watanabe, Masato Hirata

Biochemical Journal 334 ( 1 ) 211 - 218 1998.8

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DOI： 10.1042/bj3340211
Pleckstrin homology domain as an inositol compound binding module Reviewed

Masato Hirata, Takashi Kanematsu, Hiroshi Takeuchi, Hitoshi Yagisawa

Japanese Journal of Pharmacology 76 ( 3 ) 255 - 263 1998.3

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DOI： 10.1254/jjp.76.255
Distinct specificity in the binding of inositol phosphates by pleckstrin homology domains of pleckstrin, RAC-protein kinase, diacylglycerol kinase and a new 130 kDa protein Reviewed

Hiroshi Takeuchi, Takashi Kanematsu, Yoshio Misumi, Fumio Sakane, Hiroaki Konishi, Ushio Kikkawa, Yutaka Watanabe, Matilda Katan, Masato Hirata

Biochimica et Biophysica Acta - Molecular Cell Research 1359 ( 3 ) 275 - 285 1997.12

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DOI： 10.1016/S0167-4889(97)00109-2
Both PTB domain and PH domain of IRS-1 bind inositol polyphosphates with distinct specificity Reviewed

H. Takeuchi, Miho Matsuda, Takashi Kanematsu, M. Hirata

FASEB Journal 11 ( 9 ) 1997

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d-myo-Inositol 1,4,5-trisphosphate analogues substituted at the 3-hydroxyl group Reviewed

Masato Hirata, Yutaka Watanabe, Takashi Kanematsu, Shoichiro Ozaki, Toshitaka Koga

BBA - General Subjects 1244 ( 2-3 ) 404 - 410 1995.6

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DOI： 10.1016/0304-4165(95)00043-B
Expression and characterization of an inositol 1,4,5-trisphosphate binding domain of phosphatidylinositol-specific phospholipase C-δ₁ Reviewed

269 ( 31 ) 20179 - 20188 1994.8

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

It was previously found that the 85-kDa protein purified from rat brain using an inositol 1,4,5-trisphosphate (Ins(1,4,5)P₃)-immobilized matrix was the δ₁ isoform of phosphatidylinositol-specific phospholipase C (PLC). We expressed rat PLC-δ₁ in Escherichia coli as a fusion protein with glutathione S-transferase, and found that the bacterial lysate shows a significant amount of Ins(1,4,5)P₃ binding. The lysate was applied to Ins(1,4,5)P₃-immobilized column chromatography and the eluate with 2 M NaCl solution containing only a 100-kDa protein showed high Ins(1,4,5)P₃ binding. The lysate was also purified to near homogeneity using a glutathione- Sepharose 4B affinity system. Bacterially-expressed enzyme thus purified showed essentially the same inositol phosphate binding characteristics as the brain-derived enzyme. PLC-δ₁ consists of the amino-terminal nonconserved region and two well-conserved regions among isozymes, designated as X and Y, which are thought to constitute a catalytic core of the enzyme. Using a combination of deletion mutants and proteolytic products of the enzyme, we were able to locate an Ins(1,4,5)P₃ binding domain in the molecule. Deletion of 223 residues from the amino terminus completely abolished the binding activity, while deletion of X region only partially inhibited the binding and deletion of Y region did not affect the binding. A 76-kDa proteolytic product of the expressed PLC-δ₁ which lacked 60 amino acids at the amino terminus showed a minimal Ins(1,4,5)P₃ binding activity. A peptide consists of 14 amino acids corresponding to residues 30-43 of PLC-δ₁, which contains 6 basic amino acids, binds to an Ins(1,4,5)P₃-immobilized matrix. Moreover, Ins(1,4,5)P₃ binding was blocked by phospholipid vesicles containing phosphatidylinositol 4,5-bisphosphate. These results, taken together, indicate that the amino-terminal domain of PLC-δ₁ is important for the binding of both Ins(1,4,5)P₃ and phosphatidylinositol 4,5-bisphosphate.
DL-myo-inositol 1,2,4,5-tetrakisphosphate, a potent analog of D-myo- inositol 1,4,5-trisphosphate Reviewed

M. Hirata, N. Narumoto, Y. Watanabe, T. Kanematsu, T. Koga, S. Ozaki

Molecular Pharmacology 45 ( 2 ) 271 - 276 1994.3

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D-myo-inositol 1,4,5-trisphosphate binding domain of phospholipase C-δ1 Reviewed

205 ( 3 ) 1563 - 1571 1994.1

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D-myo-Inositol 1,4,5-trisphosphate (Ins(1,4,5)P₃) binding domain of phospholipase C-δ1 (PLC-δ1) was determined by examining binding activity of the synthetic peptide corresponding to residues 30-43 of PLC-δ1. The peptide coupled with carrier proteins such as keyhole limpet hemocyanin or bovine serum albumin bound Ins(1,4,5)P₃, whereas a scrambled peptide with the same amino acids did not do so. Polyclonal antibody against the peptide was examined to determine whether it would cause inhibition of the Ins(1,4,5)P₃ binding to PLC-δ1. Fab fragment of antibody to the peptide did inhibit binding to PLC-δ1, in a dose-dependent manner. Thus it seems likely that the region of residues 30-43 of PLC-δ1 is responsible for the binding of Ins(1,4,5)P₃.

DOI： 10.1006/bbrc.1994.2845
Synthesis and biological properties of 2-substituted myo-inositol 1,4,5-trisphosphate analogues directed toward affinity chromatography and photoaffinity labeling Reviewed

Shoichiro Ozaki, Yutaka Watanabe, Tomio Ogasawara, Masato Hirata, Takashi Kanematsu

Carbohydrate Research 234 ( C ) 189 - 206 1992.10

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DOI： 10.1016/0008-6215(92)85048-5
Synthetic inositol 1,3,4,5-tetrakisphosphate analogs and their effect on the binding to microsomal fraction of rat cerebellum Reviewed

Yuichi Kimura, Takashi Kanematsu, Yutaka Watanabe, Shoichiro Ozaki, Toshitaka Koga, Masato Hirata

BBA - Biomembranes 1069 ( 2 ) 218 - 222 1991.11

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DOI： 10.1016/0005-2736(91)90127-T

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Books

現代歯科薬理学　第７版（１刷）

監修・編集：鈴木邦明、戸苅彰史、青木和広、兼松隆、筑波隆幸、八田光世（ Role： Edit）

医歯薬出版株式会社 2024.1

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ポイントがよくわかる　シンプル歯科薬理学　第３版

大浦清 (監修), 戸苅彰史 (監修), 笠原正貴 (編集), 兼松隆 (編集), 三枝禎 (編集), 十川紀夫 (編集), 高橋俊介 (編集), 八田光世 (編集)（ Role： Edit）

永末書店 2023.2

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DOI： 978-4816014154
疾病の成り立ち及び回復過程の促進３　薬理学

兼松隆　　編集：鈴木邦明、眞木吉信、升井一朗、山田小枝子（ Role： Joint author）

医歯薬出版株式会社 2023.1

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DOI： ISBN978-4-263-42611-1
歯科衛生学シリーズ　疾病の成り立ち及び回復過程の促進３　薬理学　第１版　（１刷）

兼松隆（分担）　編集：鈴木邦明、眞木吉信、升井一朗、山田小枝子（ Role： Joint author）

医歯薬出版株式会社 2023.1

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現代歯科薬理学　第６版（６刷）改

兼松隆　　　監修：大谷啓一　　編集：鈴木邦明、戸苅彰史、青木和広、兼松隆、筑波隆幸（ Role： Edit）

医歯薬出版株式会社 2021.10

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ポイントがよくわかる　シンプル歯科薬理学　第２版

兼松隆：　　編集-大浦清，兼松隆，戸苅彰史，二藤彰（ Role： Edit）

永末書店 2019.3

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薬理学　第２版　　疾病の成り立ち及び回復過程の促進３

兼松隆　　編集：鈴木邦明、眞木吉信、升井一朗、山田小枝子（ Role： Joint author）

医歯薬出版株式会社 2018.2

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ポイントがよくわかる　シンプル歯科薬理学

兼松隆，山脇洋輔：　　編集-大浦清，坂上宏，戸苅彰史，二藤彰，山﨑純（ Role： Joint author）

永末書店 2017.1

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歯科衛生学シリーズ　疾病の成り立ち及び回復過程の促進３　薬理学　第１版　（２刷）

兼松隆（分担）　編集：鈴木邦明、眞木吉信、升井一朗、山田小枝子（ Role： Joint author）

医歯薬出版株式会社 2024.1

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現代歯科薬理学

戸苅彰史, 青木和広, 兼松隆, 筑波隆幸, 八田光世, 鈴木邦明

医歯薬出版 2024 （ ISBN:9784263456774 ）

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Language：Japanese

CiNii Books
ポイントがよくわかるシンプル歯科薬理学第３版

笠原正貴、兼松隆、三枝禎、十川紀夫、高橋俊介、八田光世（ Role： Joint editor）

永末書店 2023.2 （ ISBN:9784816014154 ）

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Total pages：ix, 173p Language：Japanese

CiNii Books

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疾病の成り立ち及び回復過程の促進薬理学

鈴木, 邦明, 全国歯科衛生士教育協議会（ Role： Contributor）

医歯薬出版 2023.1 （ ISBN:9784263426111 ）

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Total pages：xiv, 215p Language：Japanese

CiNii Books

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現代歯科薬理学　第６版

兼松隆　　　監修：大谷啓一　　編集：鈴木邦明、戸苅彰史、青木和広、兼松隆、筑波隆幸（ Role： Edit）

医歯薬出版株式会社 2018.2

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Clinical Neuroscience：GABA(A)受容体の構造と機能

北山友也、兼松隆（ Role： Joint author）

中外医学社 2012.12

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Mechanisms of phase-dependent pain-relief activity of glycine transporter inhibitors after nerve injury. in MEDIMOND; Monduzzi Editore International Proceeding Division, 3rd International Congress on Neuropathic Pain NeuPSIG, Athens (Greece), 2010. International　Association for the Study of Pain (IASP) Working together for pain relief. (Christopher D Wells, Editors)

Morita　K, Motoyama N, Kitayama T, Kanemastu T, Dohi T.（ Role： Joint author）

Editografica・Bologna 2010.6

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ブレインサイエンスレビュー2009 新規分子を介したGABAA受容体輸送調節の分子基盤

兼松隆編：伊藤正男・川合述史（ Role： Joint author）

クバプロ 2009.6

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Interface Oral Health Science 2007 Involvement of PRIP, a new signaling molecule, in neuroscience and beyond oral health science (Makoto Watanabe, Osamu Okuno, Eds.)

Masato Hirata, Takashi Kanematsu, Akiko Mizokami（ Role： Joint author）

Springer 2007.11

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Responsible for pages：pp129-137 Language：English Book type：Scholarly book
GABA受容体機能に関わる新しい分子ブレインサイエンスレビュー 2004 （伊藤正男・川合述史　編）

平田雅人、兼松　隆、照沼美穂（ Role： Joint author）

クバプロ 2004.1

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Responsible for pages：pp83-94 Language：Japanese Book type：Scholarly book
GABAシグナリングに関わる新しい分子「脳機能の解明」- 生命科学の主潮流 - （赤池紀扶、東　英穂、阿部康二、久保千春　編）

兼松　隆、照沼美穂、平田雅人（ Role： Joint author）

ガイア出版会, 福岡 2002.1

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Responsible for pages：pp.49-56 Language：Japanese Book type：Scholarly book
Studies on new Ins(1,4,5)P3 binding proteins with reference to the PH domains. In ACS Symposium Series Advances in Phosphoinositide (Bruzik K S. ed)

Kanematsu T., Takeuchi H. & Hirata M.（ Role： Joint author）

Oxford University Press, Washington DC 1999.1

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Responsible for pages：pp55-78 Language：English Book type：Scholarly book

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Presentations

The role of microglial testosterone signaling in the sex-related differences in Alzheimer's disease

Akiko Mizokami, Haiyan Du, Tomomi Sano, Yosuke Yamawaki, Eijiro Jimi, Takashi Kanematsu

2023.12

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Event date： 2023.12

Language：Japanese

Country：Japan
腫瘍関連マクロファージにおけるPLCL欠失は腫瘍微小環境を制御し癌の悪性化に関与する

佐野朋美、Malaz Elsheikh、溝上顕子、兼松隆

第97回　日本薬理学会年会 2023.12

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Event date： 2023.12

Language：Japanese

Venue：神戸国際会議場 Country：Japan
リン脂質代謝変調による細胞の癌化機構

兼松隆

第96回日本生化学会大会 2023.10

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Event date： 2023.10 - 2023.11

Language：Japanese Presentation type：Symposium, workshop panel (public)

Venue：福岡国際会議場・マリンメッセ福岡 Country：Japan

加齢による細胞機能の低下や器質的変化は、細胞内情報伝達機構の変調を起こし、細胞の癌化を引き起こす。我々は、イノシトールリン脂質代謝に重要な酵素であるphospholipase C (PLC)に相同性はあるがPLC酵素活性を有しない分子をクローニングし、PLC-related catalytically inactive protein (PRIP)と命名した。PRIPのヒト遺伝子はPLCL（PLC like)と命名されているが、最近、腎臓癌でPLCL遺伝子の有無と生存率には相関があることが示された。我々は、PRIP遺伝子欠損マウスを解析して、PRIP欠損で細胞分裂に異常が起こること、細胞移動能が亢進すること、また、癌細胞にPRIP を発現させることによって癌転移が抑制できることなどを明らかにした。本シンポジウムでは、癌の増悪化にPRIP (PLCL)を介したリン脂質代謝シグナルがどの様に関わるかを紹介する。また、腫瘍微小環境が腫瘍の進行に深く関わることが明らかとなっているが、マクロファージにおけるPRIP (PLCL)遺伝子欠失と腫瘍周囲の腫瘍関連マクロファージ（TAM）との集積の関係についても紹介する。
The functional analysis of GPRC5C as a saccharide sensor

Shingo Takai, Yuko Kawabata, Keisuke Sanematsu, Shusuke Iwata, Fuminori Kawabata, Takashi Kanematsu, Eijiro Jimi, Noriatsu Shigemura

2024.3

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Country：Japan
閉経後骨粗鬆症モデルマウスにおける金属味感受性の変化

川端由子、髙井信吾、岩田周介、實松敬介、川端二功、兼松隆、自見英治郎、重村憲德

第101回　日本生理学会大会 2024.3

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Event date： 2024.3

Language：Japanese

Venue：福岡国際会議場・マリンメッセ福岡 Country：Japan
Role of microRNA-3535 in modulating microglial fatty acid synthesis and inflammatory response: testosterone as a modulator

Zheng Haolin, Akiko Mizokami, Yosuke Yamawaki, Tomomi Sano, Eijiro Jimi, Takashi Kanematsu

2023.10

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Event date： 2023.10 - 2023.11

Language：English

Country：Japan
エピカテキンはCCL19の発現抑制を介して歯周病に抗炎症効果を示す

佐野朋美、#李栄智、西村英紀、兼松隆

第96回日本生化学会大会 2023.10

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Event date： 2023.10 - 2023.11

Language：Japanese

Venue：福岡国際会議場・マリンメッセ福岡 Country：Japan
GPRC6A-mediated testosterone signaling induces microglial autophagy

#Haiyan Du, Akiko Mizokami, Tomomi Sano, @Yosuke Yamawaki, Eijiro Jimi, Takashi Kanematsu

2023.10

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Event date： 2023.10 - 2023.11

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Activation of YAP signaling promote fibrosis in Prip deficient mice

#Meiqun Yuan, Tomomi Sano, Akiko Mizokami, Jing Gao, Takashi Kanematsu

2023.10

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Country：Japan
RAW264.7においてmiR-15b-5pはCcr7を標的とし、M1マクロファージへの分化を抑制する

佐野朋美、溝上顕子、兼松隆

第76回　日本薬理学会西南部会 2023.10

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Language：Japanese

Venue：神戸国際会議場 Country：Japan
PRIPがM1 / M2マクロファージの分極化に与える影響についての検討

佐野朋美、#Malaz Elsheikh、溝上顕子、清島保、兼松隆

第65回歯科基礎医学会学術大会 2023.9

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Language：Japanese

Venue：パシフィコ横浜 Country：Japan
閉経後骨粗鬆症モデルマウスの味覚変調とその分子機構の解明

川端由子，高井信吾，岩田周介，實松敬介，兼松隆，自見英治郎，重村憲徳

第65回歯科基礎医学会学術大会 2023.9

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Event date： 2023.9

Language：Japanese

Venue：日本大学歯学部（東京都千代田区） Country：Japan
Elucidating the role of microglia in molecular basis of sex differences in Alzheimer's disease

2023.9

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Language：English Presentation type：Oral presentation (general)

Country：Japan
Testosterone, FASN, and Neuroinflammation: Unraveling Sex Differences in Microglial-Mediated Protection in Alzheimer's Disease

#Haolin Z, Mizokami A, Yamawaki Y, Sano T, Kanematsu T

2023.9

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Identification of a novel microRNA involving in apoptosis signaling

#Elsheikh M, Sano T, Mizokami A, Kanematsu T

2023.9

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PRIP, a regulatory molecule for AKT signaling, negatively modulates renal fibrosis progression

#Yuan M, Sano T, Mizokami A, Gao J, Kanematsu T

2023.9

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P.gingivalis由来LPSが誘導する炎症に対するリコピンとキシリトールの抑制効果

#桂淑格、#高間立、#上野功騎、#五十野貴大、#行圓元朗、武洲、兼松隆

第65回歯科基礎医学会学術大会 2023.9

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Venue：日本大学歯学部（東京都千代田区） Country：Japan
三環系抗うつ薬イミプラミンは歯周病原細菌由来LPSが誘導するミクログリアによる神経障害を抑制する

山脇　洋輔、兼松　隆

第53回日本精神神経薬理学会年会 2023.9

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Language：Japanese

Venue：福岡国際会議場・マリンメッセ福岡 Country：Japan
An anti-inflammatory miRNA, miR-582-5p targets Skp1 and regulates NF-κB signaling-mediated inflammation

佐野朋美、#李栄智、溝上顕子、西村英紀、兼松隆

第96回日本薬理学会年会/第43回日本臨床薬理学会学術総会 2022.11

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Event date： 2022.11 - 2022.12

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Venue：パシフィコ横浜 Country：Japan
Phospholipase C like protein PRIP1 PH-domain-containing liposomes enhance apoptotic cell death in cisplatin resistant breast cancer cells

2022.11

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Event date： 2022.11 - 2022.12

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Country：Japan
腫瘍微小環境における腫瘍随伴マクロファージの制御機構

佐野朋美，#Du Haiyan，溝上顕子，兼松隆

第64回歯科基礎医学会学術大会 2022.9

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Venue：徳島大学蔵本キャンパス（徳島県徳島市） Country：Japan
Testosterone signaling enhances autophagic activity in microglia

2022.9

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Language：English Presentation type：Oral presentation (general)

Country：Japan
Identification and characterization of a microRNA regulating adipocyte inflammation

2022.9

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Language：English

Country：Japan
ミクログリアにおけるmiRNA 発現の性差

溝上顕子，佐野朋美，@山脇洋輔，自見英治郎，兼松隆

第64回歯科基礎医学会学術大会 2022.9

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Language：Japanese

Venue：徳島大学蔵本キャンパス（徳島県徳島市） Country：Japan
閉経後骨粗鬆症モデルマウスの味覚行動の変化

川端由子，#尾池麻未，高井信吾，岩田周介，實松敬介，重村憲徳，兼松隆，自見英治郎

第64回歯科基礎医学会学術大会 2022.9

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Event date： 2022.9

Language：Japanese

Venue：徳島大学蔵本キャンパス（徳島県徳島市） Country：Japan
Soluble RANKL exacerbates menopause-associated obesity via non-canonical NF-κB signaling pathway International conference

KOB・OBT 合同国際シンポジウム 2021.11

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Language：English Presentation type：Oral presentation (general)

Venue：ハイブリッド開催 Country：Japan
Role of G-protein coupled receptor GPRC6A in regulating adipose tissue metabolism Invited International conference

Akiko Mizokami, @Takahito Otani, Takashi Kanematsu, Eijiro Jimi, Masato Hirata

JAOB-KAOS Symposium 2021.10

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Event date： 2021.10

Language：English Presentation type：Oral presentation (general)

Country：Japan
脂肪組織炎症でCCL19-CCR7経路が制御するmicroRNAの同定

佐野朋美，#Elsheikh Malaz，溝上顕子，兼松隆

第63回歯科基礎医学会学術大会 2021.10

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Language：Japanese

Venue：web開催 Country：Japan
閉経による血清RANKL 濃度の上昇はNF-κBの非古典的経路を活性化し肥満を引き起こす

#森馨代，溝上顕子，佐野朋美，兼松隆，自見英治郎

第63回歯科基礎医学会学術大会 2021.10

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Language：Japanese Presentation type：Oral presentation (general)

Venue：web開催 Country：Japan

肥満で増大した脂肪組織は、炎症性サイトカインを分泌し、脂肪組織や肝臓などに慢性炎症を引き起こす。この肥満による慢性炎症反応は、生活習慣病の病態の基盤となる。閉経後の女性は、内臓脂肪型肥満をきたしやすく生活習慣病リスクが増大するが、その発症機序には未だ解明の余地がある。さて、炎症反応で中心的な役割を担う転写因子のNF-Bは、receptor activator of NF-B ligand (RANKL)によっても活性化される。我々は、閉経後にRANKLの血中濃度が上昇することに着目し、RANKL-NF-B経路の活性化が閉経後の脂肪蓄積の一因ではないかとの仮説を立て、本研究を行った。
　野生型マウスの骨髄細胞をRANKLで刺激すると、TNFのmRNA発現は２相性に上昇した。このTnfaの発現変化は、第１相が古典的経路に第２相が非古典的経路に依存することをNF-B古典的経路阻害剤を用いて確認し、経路依存的に炎症反応が制御される可能性を示した。本研究ではNF-Bの非古典的経路に焦点をあて、閉経後肥満の発症機構を解析するために、非古典的経路の活性化が障害されているaly/alyマウスを用いて実験を行なった。野生型およびaly/alyマウスの卵巣を摘出（OVX）した閉経モデルマウスを高脂肪・高ショ糖食の自由摂餌下で飼育した。野生型マウスでは、OVX後10週の間に脂肪細胞の肥大、脂肪組織の炎症、肝臓への異所性脂肪蓄積が起こり、インスリン抵抗性、耐糖能異常を示した。一方、OVX施行で野生型同様にaly/alyマウスの血清RANKL濃度は上昇したにも関わらず、野生型で認めた脂肪蓄積・炎症は抑制され、全身の糖代謝の異常も抑制された。これらの結果は、RANKL-NF-B の非古典的経路の活性化が、閉経後の肥満を引き起こす要因となることを示している。
肥満病態下における歯周病感染が引き起こす認知機能障害の機序の検討

@大植香菜，@山脇洋輔，兼松隆

第63回歯科基礎医学会学術大会 2021.10

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Event date： 2021.10

Language：Japanese

Venue：web開催 Country：Japan
歯科基礎医学会：学会活動における国際交流 Invited

兼松　隆

フォーラム「歯学領域における国際的人材育成と学会活動」　一般社団法人日本歯科医学会連合主催 2021.1

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Event date： 2021.1

Language：Japanese Presentation type：Oral presentation (general)

Venue：web開催 Country：Japan
三環系抗うつ薬イミプランの歯周病原細菌由来LPSが誘導するミクログリアによ神経障害抑制効果

山脇洋輔、兼松隆

第62回歯科基礎医学会学術大会 2020.9

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Event date： 2020.9 - 2020.10

Language：Japanese

Venue：鹿児島大学（Web開催） Country：Japan
PRIP regulates talin1 dimerization by binding to its dimerization domain, and controls fibronectin/integrin-mediated cell adhesion

Satoshi Asano, Takashi Kanematsu

2019.10

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Event date： 2019.10

Language：Japanese Presentation type：Oral presentation (general)

Country：Japan
細胞接着に関与する新規タンパク質の発見と機能解析

浅野智志、兼松隆

第14回細胞運動研究会 2019.9

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Event date： 2019.9

Language：Japanese Presentation type：Oral presentation (general)

Venue：広島大学 Country：Japan
Mechanism linking periodontitis to Alzheimer’s disease: Critical roles of cathepsin B in neuroinflammation

第1回JRSDOF 2019.8

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Event date： 2019.8

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

Venue：東京医科歯科大学 Country：Japan
Regulation of cell adhesion by phospholipase C-related catalytically inactive protein (PRIP); PRIP directly binds to talin1 and promotes talin1 dimerization

Satoshi Asano, Takashi Kanematsu

2019.6

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Event date： 2019.6

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

Country：Japan
Phospholipase C-related catalytically inactive protein modulates cytokinesis progression

Kanematsu Takashi, Asano Satoshi

2019.3

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Event date： 2019.3

Language：Japanese Presentation type：Oral presentation (general)

Country：Japan

Phospholipase C-related catalytically inactive protein modulates cytokinesis progression
PRIP (phospholipase C-related inactive protein) is implicated in the clathrin mediated GABA(A) receptor endocytosis. International conference

Kanematsu T., Hirata M.

20th IUBMB International Congress of Biochemistry and Molecular Biology 2006.6

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Country：Japan
PRIP (phospholipase C-related inactive protein) is involved in trafficking of gamma in the clathrin mediated GABA(A) receptor endocytosis. International conference

Kuratani A., Kanematsu T., Hirata M.

20th IUBMB International Congress of Biochemistry and Molecular Biology 2006.6

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Country：Japan
GABA(A)受容体のインターナリゼーションにおける新規分子（PRIP）の関わり

兼松　隆、平田雅人

第48回歯科基礎医学会 2006.9

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Venue：横浜市 Country：Japan
The regulation of GABA(A) receptor endocytosis via PRIP, a phospholipase C-related but catallytically inactive protein International conference

Kanematsu T., Yasunaga A., Hirata M.

The 5th Asian-Pacific Organization for Cell Biology 2006.10

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Country：China
Cell-surface expression of GABA(A) receptor is regulated by PRIP, a phospholipase C-related inactive protein International conference

Mizokami A., Kanematsu T., Hirata M.

The 5th Asian-Pacific Organization for Cell Biology 2006.10

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Country：China
The clathrin/AP2 dependent endocytosis of GABA(A) receptor is facilitated by PRIP

Fujii M., Kanematsu T., Hirata M.

2006.12

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Country：Japan
新規情報伝達タンパク質の発見と機能解への奮闘 Invited

兼松　隆

口腔医科学フロンティア研究会 2007.2

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Venue：仙台市 Country：Japan
PRIP facilitates trafficking of gamma2 subunit-containing GABA(A) receptor to cell-surface

M. Hirata, T. Kanematsu, A. Mizokami

2007.3

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Country：Japan
Intramolecular regulation in membrane localization of pleckstrin homology domain of PRIP International conference

Jing Gao, Hiroshi Takeuchi, Takashi Kanematsu and Masato Hirata

The 5th Korea-Japan Conference on Cellular Signaling for Young Scientists 2007.7

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Country：Korea, Republic of
PRIP regulates the cell surface expression of GABAA receptors International conference

Makoto Fujii, Takashi Kanematsu and Masato Hirata

The 5th Korea-Japan Conference on Cellular Signaling for Young Scientists 2007.7

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Country：Korea, Republic of
新奇シグナリング分子として見いだしたタンパク質の機能の広がり Invited

平田　雅人、兼松　隆

第49回歯科基礎医学会 2007.8

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Venue：札幌市 Country：Japan
インスリン分泌における新規分子（PRIP）の関わり

兼松　隆、平田　雅人

第49回歯科基礎医学会 2007.8

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Venue：札幌市 Country：Japan
開口分泌現象への PRIP 分子の関わり

竹内　弘、兼松　隆、松田美穂、塩井誠次郎、平田雅人

第117回日本薬理学会関東部会 2007.10

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Venue：東京都 Country：Japan
Action of PRIP, an Ins(1,4,5)P3 binding protein, in insulin secretion

Takashi Kanematsu, Seijiro Shioi, Masato Hirata

2007.12

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Country：Japan
PRIP modulates the insulin-induced cell surface expression of GABAA receptors

Makoto Fujii, Takashi Kanematsu and Masato Hirata

2007.12

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Country：Japan
Differential membrane localization of pleckstrin homology domains from 2 isoforms of phospholipase C-related inactive protein.

Gao Jing, Hiroshi Takeuchi, Takashi Kanematsu and Masato Hirata

2007.12

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Country：Japan
Expression of GABAA Receptors on the Surface Membrane, with special reference to the Trafficking of the gamma2 subunit containing Receptors International conference

Takashi Kanematsu

KUSCR Japan/Korea Symposium on Cellular Signaling 2007.12

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Country：Japan
PRIPによるGABAA受容体の膜発現調節機構

兼松　隆

GABAとクロライドに関する最新トピックセミナー 2008.1

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Venue：福岡市 Country：Japan
生殖機能における PRIP 働き

松田美穂、堤康史郎、兼松隆、平田雅人

第81回　日本薬理学会 2008.3

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Venue：横浜市 Country：Japan
Action of PRIP, an Ins(1,4,5)P3 binding protein, in insulin secretion International conference

Takashi Kanematsu, Seijiro Shioi, Tamotsu Kiyoshima, Hidetaka Sakai, Masato Hirata

Keystone Symposia (Islet and Beta Cell Biology) 2008.4

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Country：United States
閉経後骨粗鬆症モデルマウスの味覚行動の変化(The behavioral taste responses of postmenopausal osteoporosis in mice)

川端由子, 尾池麻未, 高井信吾, 岩田周介, 實松敬介, 重村憲徳, 兼松隆, 自見英治郎

Journal of Oral Biosciences Supplement 2022.9 (一社)歯科基礎医学会

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閉経後骨粗鬆症モデルマウスの味覚変調とその分子機構の解析

川端由子, 高井信吾, 岩田周介, 實松敬介, 兼松隆, 自見英治郎, 重村憲徳

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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閉経後骨粗鬆症モデルマウスにおける金属味感受性の変化(Modification of metallic taste in postmenopausal osteoporosis model mice)

Kawabata Yuko, Takai Shingo, Iwata Shusuke, Sanematsu Keisuke, Kawabata Fuminori, Kanematsu Takashi, Jimi Eijiro, Shigemura Noriatsu

The Journal of Physiological Sciences 2024.5 (一社)日本生理学会

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腫瘍微小環境における腫瘍随伴マクロファージの制御機構(Regulatory mechanisms of tumor-associated macrophages in the tumor microenvironment)

佐野朋美, Du Haiyan, 溝上顕子, 兼松隆

Journal of Oral Biosciences Supplement 2022.9 (一社)歯科基礎医学会

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脂肪組織炎症を制御するmicroRNAの同定(Identification and characterization of a microRNA regulating adipocyte inflammation)

Elsheikh Malaz, 佐野朋美, 溝上顕子, 兼松隆

Journal of Oral Biosciences Supplement 2022.9 (一社)歯科基礎医学会

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糖類センサーとしてのGPRC5Cの機能分析(The functional analysis of GPRC5C as a saccharide sensor)

Takai Shingo, Kawabata Yuko, Sanematsu Keisuke, Iwata Syusuke, Kawabata Fuminori, Kanematsu Takashi, Jimi Eijiro, Shigemura Noriatsu

The Journal of Physiological Sciences 2024.5 (一社)日本生理学会

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性ホルモンのテストステロンがミクログリアにおけるNF-κB炎症経路を抑制する(Sex hormone testosterone inhibits NF-K B inflammatory pathway in microglia)

Zheng Haolin, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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加齢に伴う病態変化の生化学　リン脂質代謝変調による細胞の癌化機構

兼松隆, 浅野智志, 佐野朋美, 溝上顕子, 袁美群, Malaz Elsheikh

日本生化学会大会プログラム・講演要旨集 2023.10 (公社)日本生化学会

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三環系抗うつ薬イミプラミンは歯周病原細菌由来LPSが誘導するミクログリアによる神経障害を抑制する

山脇洋輔, 兼松隆

日本神経精神薬理学会年会プログラム・抄録集 2023.9 (一社)日本神経精神薬理学会

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ミクログリアのオートファジー誘導におけるGPRC6A-テストステロンシグナルの役割

杜海妍, 溝上顕子, 兼松隆, 佐野朋美, 山脇洋輔, 自見英治郎

日本生化学会大会プログラム・講演要旨集 2023.10 (公社)日本生化学会

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ミクログリアにおけるmiRNA発現の性差(Differences in microRNA expression patterns contribute to sexually differential characteristics of microglia)

溝上顕子, 佐野朋美, 山脇洋輔, 自見英治郎, 兼松隆

Journal of Oral Biosciences Supplement 2022.9 (一社)歯科基礎医学会

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テストステロンシグナルはミクログリアにおけるオートファジーを増強する(Testosterone signaling enhances autophagic activity in microglia)

杜海妍, 溝上顕子, 兼松隆, 佐野朋美, 山脇洋輔

Journal of Oral Biosciences Supplement 2022.9 (一社)歯科基礎医学会

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テストステロンはmiRNA3535を介した脂肪酸合成制御にようりミクログリアにおける炎症反応を抑制する

鄭昊林, 溝上顕子, 兼松隆, 佐野朋美, 山脇洋輔, 自見英治郎

日本生化学会大会プログラム・講演要旨集 2023.10 (公社)日本生化学会

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エピカテキンはCCL19の発現抑制を介して歯周病に抗炎症効果を示す

佐野朋美, 李栄智, 西村英紀, 兼松隆

日本生化学会大会プログラム・講演要旨集 2023.10 (公社)日本生化学会

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アルツハイマー病の性差の分子基盤におけるミクログリアの役割解明(Elucidating the role of microglia in the molecular basis of sex differences in Alzheimer's disease)

Du Haiyan, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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アポトーシスシグナル伝達に関与する新規microRNAの同定(Identification of a novel microRNA involving in apoptosis signaling)

Elsheikh Malaz, Sano Tomomi, Mizokami Akiko, Kanematsu Takashi

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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Prip欠損によるYAPシグナル経路の活性化は腎維線化を促進する

袁美群, 佐野朋美, 溝上顕子, 高靖, 兼松隆

日本生化学会大会プログラム・講演要旨集 2023.10 (公社)日本生化学会

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PRIPがM1/M2マクロファージの分極化に与える影響についての検討

佐野朋美, Elsheikh Malaz, 溝上顕子, 清島保, 兼松隆

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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P.gingivalis由来LPSが誘導する炎症に対するリコピンとキシリトールの抑制効果

桂淑格, 高間立, 上野功騎, 五十野貴大, 行圓元朗, 武洲, 兼松隆

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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GPRC5ファミリーによる糖受容機構の探索

高井信吾, 川端由子, 實松敬介, 岩田周介, 兼松隆, 自見英治郎, 重村憲徳

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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AKTシグナル伝達の制御分子PRIPは腎線維症の進行を負に制御する(PRIP, a regulatory molecule for AKT signaling, negatively modulates renal fibrosis progression)

Yuan Meiqun, Sano Tomomi, Mizokami Akiko, Gao Jing, Kanematsu Takashi

Journal of Oral Biosciences Supplement 2023.9 (一社)歯科基礎医学会

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口腔から考える健康戦略

兼松隆

學士會会報 2021.9

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九州大学の口腔からアプローチする全身の健康戦略のビジョンを紹介した

DOI： https://www.gakushikai.or.jp/magazine/bulletin/950.html
Regulation of GABA(A) receptor surface expression with special reference to the invilvement of GABARAP and PRIP.

Kanematsu T., Mizokami A., Watanabe K., Hirata M.

J. Pharmacol. Sci. 2007.8

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PRIP, a novel Ins(1,4,5)P3 binding protein, functional significance in Ca2+ signaling and extension to neuroscience and beond.

Kanematsu T., Takeuchi H., Terunuma M., Hirata M.

Mol. Cells 2005.1

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GABA(A) 受容体の一生とそれを調節する分子達

兼松　隆、照沼美穂、後藤英文、倉谷顕子、平田雅人．

日本薬理学雑誌 2004.1

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多機能性分子PRIPと抑制性シナプス構築の分子メカニズム

兼松　隆．

基礎歯科医学会雑誌 2003.1

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GABAA受容体構築に関わる分子達

兼松　隆、平田雅人．

生化学 2003.1

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新しい情報伝達蛋白質ファミリーの機能

兼松　隆、竹内　弘、吉村研治、平田雅人．

生体の科学 2000.1

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新規 Ins(1,4,5)P3 結合蛋白質と GABAA 受容体シグナリング

兼松　隆、平田雅人．

福岡医学雑誌 2000.1

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閉経後骨粗鬆症モデルマウスの味覚行動の変化(The behavioral taste responses of postmenopausal osteoporosis in mice)

川端由子, 尾池麻未, 高井信吾, 岩田周介, 實松敬介, 重村憲徳, 兼松隆, 自見英治郎

Journal of Oral Biosciences Supplement 2022 317 - 317 2022.9 （ ISSN:2187-2333 eISSN:2187-9109 ）

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Phospholipase C-related catalytically inactive protein: A novel signaling molecule for modulating fat metabolism and energy expenditure Reviewed

Kanematsu T, Oue K, Okumura T, Harada K, Yamawaki Y, Asano S, Mizokami A, Irifune M, Hirata M.

The Journal of Oral Biosciences 2019.5

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Phospholipase C-related catalytically inactive protein can regulate obesity, a state of peripheral inflammation Reviewed

Yamawaki Y, Oue K, Shirawachi S, Asano S, Harada K, Kanematsu T

Japanese Dental Science Review 2017.6

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オートファジーによる細菌排除システム Reviewed

原田佳枝，兼松隆

広島歯科医学雑誌 2016.6

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脱リン酸化制御による脂肪分解の新たな分子基盤 Reviewed

大植香奈、原田佳枝、兼松隆

日本薬理学会誌 2015.6

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Surface Expression of GABA(A) Receptors -Roles for the Binding Partners- Reviewed

Kanematsu T., Fujii M., Tanaka H., Umebayashi H., Hirata M.

The Journal of Oral Biosciences 2010.6

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Roles of PRIP in GABAA receptor signaling.

Mizokami A., Kanematsu T., Hirata M.

J. Oral Biosci. 2007.6

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けいれん/てんかんの病因遺伝子としてのPRIP

平田雅人、倉谷顕子、兼松　隆

てんかん治療研究振興財団研究年報 2006.10

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GABA(A) 受容体の構築と輸送

兼松　隆、平田雅人．

中外医学社 2004.1

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抑制性シナプス情報伝達の分子機構の解明に関する研究

兼松　隆

稲盛財団研究報告書 2003.1

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新規イノシトール1,4,5-三リン酸結合蛋白質はGABA受容体の機能を修飾するか？

兼松　隆、平田雅人．

興和生命科学振興財団研究報告書 2003.1

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タンパク質間相互作用解析のアプローチ

兼松　隆、平田雅人．

日本薬理学雑誌 2002.1

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Language：Japanese
ノックアウトマウス・培養細胞を用いた新規イノシトール1,4,5-三リン酸結合蛋白質（p130）の生理機能解明に関する研究

兼松　隆．

上原記念生命科学財団研究成果報告集 2000.1

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Language：Japanese Publishing type：Internal/External technical report, pre-print, etc.
Pleckstrin homology domain as an inositol compound binding module

Hirata M., Kanematsu T., Takeuchi H. & Yagisawa H.

Jpn. J. Pharmacol. 1998.1

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Language：English Publishing type：Article, review, commentary, editorial, etc. (scientific journal)
細胞内に広がる分子の世界　−細胞内情報伝達−

兼松　隆、平田雅人

九大広報 1998.1

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Professional Memberships

北米神経科学会
西日本骨関節関連疾患懇話会
福岡医学会
日本細胞生物学会
日本分子生物学会
Japan Research Society for Dementia and Oral Function (JRSDOF)
歯科基礎医学会
日本生化学会
日本薬理学会

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Committee Memberships

Executive Domestic

2023.7 - 2024.6
一般社団法人歯科基礎医学会常任理事 Domestic

2023.7 - 2024.6
認知症と口腔機能研究会世話人 Domestic

2023.4 - 2025.3
Executive Domestic

2020.7 - 2022.6
一般社団法人歯科基礎医学会常任理事・国際交流委員長 Domestic

2020.7 - 2022.6
一般社団法人歯科基礎医学会理事

2020.7 - 2022.6

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認知症と口腔機能研究会世話人 Domestic

2019.8 - 2023.4
認知症と口腔機能研究会世話人

2019.8 - 2023.4

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Executive Domestic

2018.5 - 2020.6
一般社団法人歯科基礎医学会常任理事・国際交流委員長 Domestic

2018.5 - 2020.6
公益社団法人日本薬理学会日本薬理学会編集委員 Domestic

2016.5 - 2018.6
Executive Domestic

2012.4 - 2016.3
一般社団法人歯科基礎医学会理事・評議員 Domestic

2012.4 - 2016.3
Councilor Domestic

2010.4 - 2014.3
公益社団法人日本薬理学会学術評議員 Domestic

2010.4 - 2014.3
Organizer Domestic

2001.4 - 2009.1
Councilor Domestic

2000.4 - 2018.3

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Academic Activities

シンポジウム座長

認知症と⼝腔機能研究会 JRSDOF 第４回学術集会（東京医科歯科大学） 2024.8

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Type：Competition, symposium, etc.

Number of participants：100
座長（Chairmanship） International contribution

KOB/OBT/DDR 国際シンポジウム（九州大学） 2024.2

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Type：Competition, symposium, etc.

Number of participants：80
組織委員（大会幹事）

第96回日本生化学会大会（福岡国際会議場・マリンメッセ福岡B館） 2023.10 - 2023.11

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Type：Competition, symposium, etc.
シンポジウムオーガナイザー

第96回日本生化学会大会（福岡国際会議場・マリンメッセ福岡B館） 2023.10 - 2023.11

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Type：Competition, symposium, etc.
第96回日本生化学会大会

（福岡国際会議場・マリンメッセ福岡B館 Japan ） 2023.10 - 2023.11

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Type：Competition, symposium, etc.

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Screening of academic papers

Role(s)： Peer review

2023

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Type：Peer review

Number of peer-reviewed articles in foreign language journals：3

Number of peer-reviewed articles in Japanese journals：0
日本薬理学会・歯科基礎医学会合同シンポジウム　オーガナイザー

第95回日本薬理学会年会（福岡国際会議場・福岡サンパレス） 2022.3

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Type：Competition, symposium, etc.

Number of participants：1,000
第95回日本薬理学会年会

（福岡国際会議場・福岡サンパレス Japan ） 2022.3

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Type：Competition, symposium, etc.

researchmap
Screening of academic papers

Role(s)： Peer review

2022

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Type：Peer review

Number of peer-reviewed articles in foreign language journals：2

Number of peer-reviewed articles in Japanese journals：4
現代歯科薬理学　第７版

2021.12 - 2025.3

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Type：Academic society, research group, etc.
現代歯科薬理学第７版

Role(s)： Review, evaluation

2021.12 - 2025.3

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Type：Peer review

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日韓シンポジウムオーガナイザー

第63回歯科基礎医学会学術大会（神奈川歯科大学） 2021.10

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Type：Competition, symposium, etc.

Number of participants：500
シンポジウム座長

認知症と⼝腔機能研究会 JRSDOF 第２回学術集会（オンライン） 2021.8

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Type：Competition, symposium, etc.

Number of participants：100
第３版　ポイントがよくわかる　シンプル歯科薬理学

2021.4 - 2023.3

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Type：Academic society, research group, etc.
第３版ポイントがよくわかるシンプル歯科薬理学

Role(s)： Review, evaluation

2021.4 - 2023.3

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Type：Peer review

researchmap
Screening of academic papers

Role(s)： Peer review

2021

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Type：Peer review

Number of peer-reviewed articles in foreign language journals：3
現代歯科薬理学　第６版

2020.4 - 2021.3

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Type：Academic society, research group, etc.
Screening of academic papers

Role(s)： Peer review

2020

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Type：Peer review

Number of peer-reviewed articles in foreign language journals：1
日韓シンポジウムオーガナイザー

第61回歯科基礎医学会学術大会（東京歯科大学） 2019.10

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Type：Competition, symposium, etc.

Number of participants：500
座長

第1回JRSDOF （東京医科歯科大学） 2019.9

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Type：Competition, symposium, etc.

Number of participants：80
第２版　ポイントがよくわかる　シンプル歯科薬理学

2019.6 - 2021.12

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Type：Academic society, research group, etc.
Screening of academic papers

Role(s)： Peer review

2019

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Type：Peer review

Number of peer-reviewed articles in foreign language journals：1
科学研究費委員会専門委員

Role(s)： Review, evaluation

日本学術振興会 2017.12 - 2018.11

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Type：Scientific advice/Review
現代歯科薬理学　第６版

2017.4 - 2021.12

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Type：Academic society, research group, etc.
科学研究費委員会専門委員

Role(s)： Review, evaluation

日本学術振興会 2016.12 - 2017.11

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Type：Scientific advice/Review
Journal of Pharmacological Sciences International contribution

2016.5 - 2020.5

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Type：Academic society, research group, etc.
科学研究費委員会専門委員（医歯薬学III小委員会）

Role(s)： Review, evaluation

日本学術振興会 2015.6 - 2015.11

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Type：Scientific advice/Review
科学研究費委員会専門委員（医歯薬学III小委員会）

Role(s)： Review, evaluation

日本学術振興会 2014.6 - 2014.11

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Type：Scientific advice/Review
科学研究費委員会専門委員

Role(s)： Review, evaluation

日本学術振興会 2011.12 - 2012.11

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Type：Scientific advice/Review
科学研究費委員会専門委員

Role(s)： Review, evaluation

日本学術振興会 2010.12 - 2011.11

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Type：Scientific advice/Review
特別研究員等審査会専門委員・国際事業委員会委員

Role(s)： Review, evaluation

日本学術振興会科学研究費委員会 2009.8 - 2010.7

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Type：Scientific advice/Review
特別研究員等審査会専門委員・国際事業委員会委員

Role(s)： Review, evaluation

日本学術振興会科学研究費委員会 2009.4 - 2009.7

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Type：Scientific advice/Review
座長（Chairmanship） International contribution

（九州大学） 2008.1

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Type：Competition, symposium, etc.
座長（Chairmanship）

第7回西日本骨・関節関連疾患懇話会（九州大学） 2007.7

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Type：Competition, symposium, etc.
会議実行委員 International contribution

日韓若手会議（慶州） 2007.7

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Type：Competition, symposium, etc.

Number of participants：150
座長（Chairmanship） International contribution

2007.7

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Type：Competition, symposium, etc.
座長（Chairmanship）

タンパク質解析講座（九州大学コラボステーション） 2005.10

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Type：Competition, symposium, etc.
司会（Moderator） International contribution

2005.7

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Type：Competition, symposium, etc.
会議実行委員 International contribution

日韓若手会議（福岡） 2005.7

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Type：Competition, symposium, etc.

Number of participants：100
座長（Chairmanship）

第５回西日本骨・関節関連疾患懇話会（福岡市） 2005.7

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Type：Competition, symposium, etc.
座長（Chairmanship） International contribution

2004.7

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Type：Competition, symposium, etc.
司会（Moderator） International contribution

2003.7

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Type：Competition, symposium, etc.
会議実行委員 International contribution

日韓若手会議（福岡） 2003.7

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Type：Competition, symposium, etc.

Number of participants：120
座長（Chairmanship）

第３回西日本骨・関節関連疾患懇話会（福岡市） 2003.7

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Type：Competition, symposium, etc.
司会（Moderator） International contribution

2003.7

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Type：Competition, symposium, etc.
座長（Chairmanship）

第２回西日本骨・関節関連疾患懇話会（福岡市） 2002.7

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Type：Competition, symposium, etc.

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Research Projects

組織慢性炎症を制御するM2マクロファージの機能解析研究

2024.4 - 2027.3

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Authorship：Principal investigator
Functional analysis of M2 macrophages regulating chronic inflammation in tissue

Grant number：24K12872 2024 - 2026

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

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Authorship：Principal investigator Grant type：Scientific research funding

CiNii Research
抗腫瘍免疫を賦活化する新しい制癌シグナル分子の機能解明研究

2021.4 - 2024.3

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Authorship：Principal investigator
Functional analysis of a new anti-cancer molecule that promotes anti-tumor immune responses

Grant number：21K09817 2021 - 2023

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

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Authorship：Principal investigator Grant type：Scientific research funding

CiNii Research
Development of novel cancer metastasis suppressing agent focusing on cell adhesion controling

Grant number：20K09905 2020 - 2022

Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Asano Satoshi

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Authorship：Coinvestigator(s) Grant type：Scientific research funding

We investigated whether vasoactive intestinal peptide (VIP) receptor 2 (VIPR2) is involved in exacerbation (cell migration and proliferation) of breast cancer. We demonstrated that stable expression of VIPR2 in breast cancer cells promoted VIP-induced cell migration and cell proliferation, and enhanced the proliferation in intraperitoneal in vivo. In contrast, treatment with the VIPR2-selective antagonist peptide KS-133 abolished the effects of VIPR2 overexpression and markedly inhibited VIP-induced cell migration and proliferation. These results indicate that VIPR2 signaling regulates breast cancer cell migration and proliferation, and suggest that disruption of this signaling by VIPR2 overexpression may lead to exacerbation of breast cancer.

CiNii Research
肥満による末梢炎症と２型糖尿病の解析研究

2019.4 - 2022.3

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Authorship：Principal investigator
３型糖尿病としてのアルツハイマー病に関する研究

2019.4 - 2022.3

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Authorship：Principal investigator
側坐核のドパミン神経刺激による下行性鎮痛系の増強を応用した新しい全身麻酔法の開発

Grant number：18K09812 2018 - 2021

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
PRIPの新奇癌細胞制御機構に着目した抗腫瘍薬開発研究

Grant number：17K11644 2017 - 2019

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
歯周病による中枢機能障害の基盤となるストレス応答性亢進機構の解明研究

Grant number：17K11670 2017 - 2019

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
膜リン脂質代謝変調がもたらす癌増悪メカニズムの解明研究

2016 - 2018

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Principal investigator Grant type：Scientific research funding
下行性鎮痛系の増強を応用した新しい全身麻酔法の開発：5-HT受容体リガンドの活用

2015 - 2017

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
オートファジーを介した黄色ブドウ球菌排除の分子基盤解明

2015 - 2017

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
脂肪細胞の分化と脱分化制御の分子基盤解明研究

2014 - 2015

日本学術振興会科学研究費助成事業挑戦的研究（萌芽）

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Authorship：Principal investigator Grant type：Scientific research funding
新規細胞内輸送調節分子を介した疼痛制御機構の解明

2012 - 2014

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
エネルギー代謝機構や摂食調節機構に関わる新規分子の機能解明研究

2010 - 2013

日本学術振興会最先端・次世代研究開発支援プログラム

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Authorship：Principal investigator Grant type：Joint research
難治性がん性疼痛緩和のための痛みの病態生理に立脚した新たな治療法の開発

2010 - 2012

日本学術振興会科学研究費助成事業基盤研究(B)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
GABAシグナリング調節分子による摂食調節メカニズムの解明研究

2009 - 2011

日本学術振興会科学研究費助成事業基盤研究(B)

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Authorship：Principal investigator Grant type：Scientific research funding
GABAA受容体輸送調節分子による神経因性疼痛制御の基礎的研究

2009 - 2010

日本学術振興会科学研究費助成事業挑戦的研究（萌芽）

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Authorship：Principal investigator Grant type：Scientific research funding
２光子顕微鏡をによる新奇分子を介した開口放出制御の解明研究

2008.4 - 2009.3

共同研究

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Authorship：Principal investigator Grant type：Other funds from industry-academia collaboration
GABA(A)受容体の膜発現調節の分子機構解明研究

2008.4 - 2009.3

共同研究

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Authorship：Coinvestigator(s) Grant type：Other funds from industry-academia collaboration
２光子顕微鏡による新奇分子を介した開口放出制御の解明研究

2008.4 - 2009.3

自然科学研究機構・生理学研究所

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Authorship：Principal investigator
GABA(A)受容体の膜発現量調節の分子機構解明研究

2008.4 - 2009.3

自然科学研究機構・生理学研究所

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Authorship：Coinvestigator(s)
インスリン開口放出を制御する新奇分子の役割解明研究

2008 - 2009

日本糖尿病財団

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Authorship：Principal investigator Grant type：Contract research
Action of PRIP, an Ins(1,4,5)P3 binding protein, in insulin secretion

2008

Japan Society for the Promotion of Science International Academic Society Dispatch Program

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Authorship：Principal investigator Grant type：Joint research
GABAシグナリングにおける新規分子PRIPの役割解明

2007.4 - 2008.3

共同研究

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Authorship：Coinvestigator(s) Grant type：Other funds from industry-academia collaboration
GABAシグナリングにおlける新規分子ＰＲＩＰの役割解明

2007.4 - 2007.12

自然科学研究機構・生理学研究所

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Authorship：Coinvestigator(s)
新奇分子PRIPを介するGABA(A)受容体情報伝達機構の解析

2007 - 2020

日本学術振興会二国間交流

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Authorship：Principal investigator Grant type：Joint research
新規分子とオートファジィーの関係を探る。−ＧＡＢＡ（Ａ）受容体の分子制御−

Grant number：19659488 2007 - 2008

科学研究費助成事業萌芽研究

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Authorship：Principal investigator Grant type：Scientific research funding
開口分泌を調節する新奇分子の機能解明

2007 - 2008

金原一郎記念医学医療振興財団

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Authorship：Principal investigator Grant type：Contract research
新規分子によるGABA(A)受容体の輸送調節

2007 - 2008

ブレインサイエンス振興財団

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Authorship：Principal investigator Grant type：Contract research
GABAシグナリングにおける新規分子PRIPの役割解明

2006.4 - 2007.3

共同研究

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Authorship：Coinvestigator(s) Grant type：Other funds from industry-academia collaboration
新規分子（ＰＲＩＰ）の機能解明研究

2006.4 - 2007.3

自然科学研究機構・生理学研究所

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Authorship：Coinvestigator(s)
ヒト認知機能を障害させる遺伝子異常を持つモデル動物の作出とその病態解析

Grant number：18390316 2006 - 2009

日本学術振興会科学研究費助成事業基盤研究(B)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
肥満やインスリン分泌異常を引き起こす新規分子の役割解明研究

Grant number：18390494 2006 - 2008

日本学術振興会科学研究費助成事業基盤研究(B)

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Authorship：Principal investigator Grant type：Scientific research funding
過食と肥満に関わる新規分子の基礎的研究

2006

武田科学振興財団一般研究奨励

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Authorship：Principal investigator Grant type：Contract research
GABAシグナリングにおける新規分子PRIPの役割解明

2005.4 - 2006.3

共同研究

　 More details

Authorship：Coinvestigator(s) Grant type：Other funds from industry-academia collaboration
新規分子（ＰＲＩＰ）の機能解明研究

2005.4 - 2006.3

自然科学研究機構・生理学研究所

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Authorship：Coinvestigator(s)
PRIP分子はBDNF刺激によっておこるGABA(A)受容体の膜発現量減少に関わる．

2005

日本学術振興会国際学会等派遣事業

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Authorship：Principal investigator Grant type：Joint research
新規分子（PRIP）によるGABA(A)受容体膜発現調節機構の分子メカニズム解明研究

2005

第３７回（2005年度）内藤記念科学奨励金（研究助成）

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Authorship：Principal investigator Grant type：Contract research
新しい情報伝達タンパク質研究から迫る咬合と脳機能の関連 −基礎歯科学から先駆的情報発信−

2004 - 2008

日本学術振興会科学研究費助成事業基盤研究(S)

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Authorship：Coinvestigator(s) Grant type：Scientific research funding
新規分子の機能解明研究

2004 - 2006

4-2-4アクションプラン（若手研究リーダー）

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Authorship：Principal investigator Grant type：On-campus funds, funds, etc.
新規情報伝達タンパク質（PRIP）の機能解析

2004

第１６回加藤記念研究助成

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Authorship：Principal investigator Grant type：Contract research
GABA(A)受容体構築の分子メカニズム解明

Grant number：15591969 2003 - 2004

日本学術振興会科学研究費助成事業基盤研究(C)

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Authorship：Principal investigator Grant type：Scientific research funding
GABAシグナリングに関わる新しい分子の役割

2003 - 2004

日本学術振興会二国間交流

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Authorship：Coinvestigator(s) Grant type：Joint research
新規Ins(1,4,5)P3結合性タンパク質PRIPの心臓・血管機能への関わり

2003

持田記念研究助成

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Authorship：Principal investigator Grant type：Contract research
新しい概念に基づいた抗不安薬／抗けいれん薬の研究開発動向の調査

2002 - 2003

日本学術振興会平成１４年度海外研究開発動向調査

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Authorship：Principal investigator Grant type：Joint research
PRIP-1分子はGABA(A)受容体の品質管理に関わるか

2002

武田科学振興財団医学系研究奨励

　 More details

Authorship：Principal investigator Grant type：Contract research
抑制性シナプス情報伝達の分子機構の解明に関する研究

2001

平成１３年度　稲盛財団研究助成金

　 More details

Authorship：Principal investigator Grant type：Contract research
GABA(A)受容体に対する新規Ins(1,4,5) P3結合蛋白質の役割解明

Grant number：12770062 2000 - 2001

科学研究費助成事業奨励研究(A)

　 More details

Authorship：Principal investigator Grant type：Scientific research funding
新規Ins(1,4,5)P3結合蛋白質はGABA(A)受容体の機能を修飾するか

Grant number：12050230 2000 - 2001

科学研究費助成事業特定領域研究(A)特定領域研究(B)

　 More details

Authorship：Principal investigator Grant type：Scientific research funding
GABA受容体構築における新しい分子の意外な関わり

2000

平成１２年度　興和生命科学振興財団研究助成金

　 More details

Authorship：Principal investigator Grant type：Contract research
ノックアウトマウス・培養細胞を用いた、新規イノシトール1,4,5-三リン酸結合蛋白質（p130）の生理機能解明に関する研究

1998

平成１０年度　上原記念生命科学財団研究奨励金

　 More details

Authorship：Principal investigator Grant type：Contract research
新規イノシトール1,4,5-三リン酸結合蛋白質の変異マウスの作製

Grant number：09770083 1997 - 1998

科学研究費助成事業奨励研究(A)

　 More details

Authorship：Principal investigator Grant type：Scientific research funding
新規イノシトール三リン酸結合タンパク質の精製

1992

加藤記念バイオサイエンス研究振興財団（海外派遣助成金）

　 More details

Authorship：Principal investigator Grant type：Contract research

▼display all

Class subject

薬理学３

2024.12 - 2025.2 Winter quarter
臨床歯科薬理学

2024.10 - 2024.12 Fall quarter
薬理学２

2024.6 - 2024.8 Summer quarter
歯科薬理学

2024.4 - 2025.3 Full year
歯学オリエンテーション

2024.4 - 2024.9 First semester
薬理学１

2024.4 - 2024.6 Spring quarter
Aging Science and Pharmacology(Core)　D

2023.12 - 2024.2 Winter quarter
薬理学３

2023.12 - 2024.2 Winter quarter
口腔機能分子科学（コア）　D

2023.12 - 2024.2 Winter quarter
Aging Science and Pharmacology (Upper-grade) D

2023.12 - 2024.2 Winter quarter
Aging Science and Pharmacology(Core)　C

2023.10 - 2023.12 Fall quarter
臨床歯科薬理学

2023.10 - 2023.12 Fall quarter
口腔機能分子科学（コア）　C

2023.10 - 2023.12 Fall quarter
Aging Science and Pharmacology (Upper-grade) C

2023.10 - 2023.12 Fall quarter
Aging Science and Pharmacology(Core)　B

2023.6 - 2023.8 Summer quarter
薬理学２

2023.6 - 2023.8 Summer quarter
口腔機能分子科学（コア）　B

2023.6 - 2023.8 Summer quarter
Aging Science and Pharmacology (Upper-grade) B

2023.6 - 2023.8 Summer quarter
歯科薬理学

2023.4 - 2024.3 Full year
Introduction to Oral Biological Research（口腔機能分子科学）

2023.4 - 2024.3 Full year
Basic Dental Practice（口腔機能分子科学）

2023.4 - 2024.3 Full year
Advanced Dental Practice I(口腔機能分子科学）

2023.4 - 2024.3 Full year
Advanced Dental ScienceResearch（口腔機能分子科学）

2023.4 - 2024.3 Full year
Advanced Dental Practice Ⅱ（口腔機能分子科学）

2023.4 - 2024.3 Full year
歯学オリエンテーション

2023.4 - 2023.9 First semester
Aging Science and Pharmacology(Core)　A

2023.4 - 2023.6 Spring quarter
薬理学１

2023.4 - 2023.6 Spring quarter
口腔機能分子科学（コア）　A

2023.4 - 2023.6 Spring quarter
Aging Science and Pharmacology (Upper-grade) A

2023.4 - 2023.6 Spring quarter
Aging Science and Pharmacology (Lower-grade) D

2022.12 - 2023.2 Winter quarter
Aging Science and Pharmacology (Upper-grade) D

2022.12 - 2023.2 Winter quarter
Aging Science and Pharmacology(Core)　D

2022.12 - 2023.2 Winter quarter
口腔機能分子科学（低年次）　D

2022.12 - 2023.2 Winter quarter
Aging Science and Pharmacology (Lower-grade) C

2022.10 - 2022.12 Fall quarter
Aging Science and Pharmacology (Upper-grade) C

2022.10 - 2022.12 Fall quarter
Aging Science and Pharmacology(Core)　C

2022.10 - 2022.12 Fall quarter
口腔機能分子科学（低年次）　C

2022.10 - 2022.12 Fall quarter
口腔機能分子科学（低年次）　B

2022.6 - 2022.8 Summer quarter
Aging Science and Pharmacology (Lower-grade) B

2022.6 - 2022.8 Summer quarter
Aging Science and Pharmacology (Upper-grade) B

2022.6 - 2022.8 Summer quarter
Aging Science and Pharmacology(Core)　B

2022.6 - 2022.8 Summer quarter
Basic Dental Practice（口腔機能分子科学）

2022.4 - 2023.3 Full year
Introduction to Oral Biological Research（口腔機能分子科学）

2022.4 - 2023.3 Full year
Oral Phamacology

2022.4 - 2023.3 Full year
歯科薬理学

2022.4 - 2023.3 Full year
歯学オリエンテーション

2022.4 - 2022.9 First semester
口腔機能分子科学（低年次）　A

2022.4 - 2022.6 Spring quarter
Aging Science and Pharmacology (Lower-grade) A

2022.4 - 2022.6 Spring quarter
Aging Science and Pharmacology (Upper-grade) A

2022.4 - 2022.6 Spring quarter
Aging Science and Pharmacology(Core)　A

2022.4 - 2022.6 Spring quarter
Aging Science and Pharmacology (Lower-grade) D

2021.12 - 2022.2 Winter quarter
Aging Science and Pharmacology (Lower-grade) C

2021.10 - 2021.12 Fall quarter
Aging Science and Pharmacology (Lower-grade) B

2021.6 - 2021.8 Summer quarter
Oral Pharmacology

2021.4 - 2022.3 Full year
口腔機能分子科学

2021.4 - 2022.3 Full year
歯科薬理学

2021.4 - 2022.3 Full year
Aging Science and Pharmacology (Lower-grade) A

2021.4 - 2021.6 Spring quarter
Advanced Dental PracticeⅠ（口腔機能分子科学）

2020.4 - 2021.3 Full year
口腔機能分子科学演習

2020.4 - 2021.3 Full year
歯科薬理学

2020.4 - 2021.3 Full year
歯科薬理学

2019.4 - 2020.3 Full year
Advanced Dental Science Research（口腔機能分子科学）

2019.4 - 2020.3 Full year
口腔常態制御学研究入門

2007.4 - 2008.3 Full year
歯学概論

2007.4 - 2008.3 Full year
口腔生化学　分子遺伝学

2007.4 - 2008.3 Full year
口腔生化学　分子遺伝学

2007.4 - 2008.3 Full year
口腔細胞工学演習

2007.4 - 2008.3 Full year
口腔細胞工学

2007.4 - 2008.3 Full year
口腔常態制御学研究入門

2006.4 - 2007.3 Full year
口腔生化学　分子遺伝学

2006.4 - 2007.3 Full year
口腔生化学　分子遺伝学

2006.4 - 2007.3 Full year
口腔細胞工学演習

2006.4 - 2007.3 Full year
細胞の仕組み

2006.4 - 2007.3 Full year
口腔細胞工学

2006.4 - 2007.3 Full year
口腔生化学　分子遺伝学

2005.4 - 2006.3 Full year
口腔生化学　分子遺伝学

2005.4 - 2006.3 Full year

▼display all

FD Participation

2024.4 Role：Planning Title：歯科医師国家試験に向けた教員研修

Organizer：[Undergraduate school/graduate school/graduate faculty]
2024.1 Role：Participation Title：2023年度九州大学情報セキュリティ教育及び自己点検

Organizer：University-wide
2023.12 Role：Participation Title：2023年度ハラスメント防止・対策e-learning

Organizer：University-wide
2023.12 Role：Participation Title：九州大学個人情報保護研修

Organizer：University-wide
2023.12 Role：Participation Title：敷地内全面禁煙について

Organizer：University-wide
2023.12 Role：Participation Title：R6年度大学入学共通テストオンライン監督者説明会

Organizer：University-wide
2023.9 Role：Participation Title：ハラスメント防止

Organizer：University-wide
2023.6 Role：Participation Title：科学研究費補助金採択率向上に向けた工夫

Organizer：[Undergraduate school/graduate school/graduate faculty]
2023.6 Role：Participation Title：科研費セミナー

Organizer：University-wide
2023.3 Role：Participation Title：TF（ティーチング・フェロー）経験を通じて大学院生の教育能力を高める

Organizer：University-wide
2022.9 Role：Participation Title：令和４年度動物実験に係る教育講習会

Organizer：University-wide
2022.7 Role：Participation Title：科研費申請書ー採択に近づく書き方のコツ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2022.7 Role：Panelist Title：廃棄物の分別等についてのFD

Organizer：[Undergraduate school/graduate school/graduate faculty]
2022.3 Role：Participation Title：新M2Bシステムの使い方　～新機能を中心に紹介します～

Organizer：University-wide
2022.3 Role：Participation Title：メンタルヘルス講演会

Organizer：University-wide
2022.2 Role：Participation Title：令和３年度馬出地区４部局合同男女共同参画FD

Organizer：University-wide
2021.5 Role：Participation Title：Workshop: Online Teaching Experiences

Organizer：University-wide
2021.4 Role：Participation Title：CBT問題作問講習会

Organizer：[Undergraduate school/graduate school/graduate faculty]
2021.3 Role：Participation Title：九州大学オンライン授業のグッドプラクティス〜オンデマンド型授業編〜

Organizer：University-wide
2021.3 Role：Participation Title：九州大学オンライン授業のグッドプラクティス〜リアルタイム型授業編〜

Organizer：University-wide
2021.2 Role：Participation Title：ルーブリックを活用した評価と授業改善

Organizer：University-wide
2020.6 Role：Moderator Title：ジャーナルをめぐる現状と論文の投稿・入手について

Organizer：[Undergraduate school/graduate school/graduate faculty]
2020.6 Role：Planning Title：ジャーナルをめぐる現状と論文の投稿・入手について

Organizer：[Undergraduate school/graduate school/graduate faculty]
2019.10 Role：Participation Title：令和元年度馬出地区４部局合同男女共同参画FD

Organizer：University-wide
2019.9 Role：Participation Title：科研費申請のススメ！〜科学研究費補助金制度と研究計画調書作成時の注意点〜

Organizer：[Undergraduate school/graduate school/graduate faculty]
2008.3 Role：Participation Title：第４回「歯学研究院の将来を考えるプロジェクト設置について」

Organizer：[Undergraduate school/graduate school/graduate faculty]
2008.3 Role：Other Title：QUEST-MAP 第6回ＷＧ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2008.3 Role：Other Title：QUEST-MAP 第5回ＷＧ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2008.1 Role：Participation Title：「歯科医療領域の政策・経営シンクタンク」

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.11 Role：Other Title：QUEST-MAP 第4回ＷＧ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.10 Role：Other Title：QUEST-MAP 第3回ＷＧ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.9 Role：Other Title：QUEST-MAP 第２回ＷＧ

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.7 Role：Participation Title：第３回「歯学研究院の将来を考えるプロジェクト設置について」

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.5 Role：Participation Title：第２回「歯学研究院の将来を考えるプロジェクト設置について」

Organizer：[Undergraduate school/graduate school/graduate faculty]
2007.1 Role：Participation Title：平成18年度第2回FD（九州大学の新しい教員組織）

Organizer：[Undergraduate school/graduate school/graduate faculty]
2006.9 Role：Participation Title：平成18年度第2回全学FD（コアセミナーの目標と課題）

Organizer：University-wide
2006.7 Role：Participation Title：平成18年度第1回FD（中間評価と教員業績評価について）

Organizer：[Undergraduate school/graduate school/graduate faculty]
2006.3 Role：Participation Title：平成１７年度第１回FD

Organizer：[Undergraduate school/graduate school/graduate faculty]
2005.5 Role：Participation Title：第３期科学技術基本計画に向けて

Organizer：University-wide
2005.2 Role：Participation Title：WebCTに関するFD

Organizer：[Undergraduate school/graduate school/graduate faculty]
2005.1 Role：Participation Title：総長と部局職員との意見交換会

Organizer：University-wide
2004.9 Role：Participation Title：GPA制度の導入に向けて

Organizer：University-wide
2003.12 Role：Participation Title：第３回全学FD　九州大学における言語文化科目の教育内容の改善に向けて

Organizer：University-wide
2002.11 Role：Participation Title：パネルディスカッション

Organizer：[Undergraduate school/graduate school/graduate faculty]
2002.7 Role：Participation Title：第１回全学FD　全学教育を考える（at 西新交流プラザ）

Organizer：University-wide
2002.5 Role：Participation Title：米国州立大学及び私立大学歯学部の教育・研究・臨床

Organizer：[Undergraduate school/graduate school/graduate faculty]
2002.4 Role：Participation Title：九大歯学府におけるeラーニング

Organizer：[Undergraduate school/graduate school/graduate faculty]

▼display all

Visiting, concurrent, or part-time lecturers at other universities, institutions, etc.

2024 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・歯科衛生士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2024.04〜2025.02
2024 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・柔道整復科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2024.04〜2024.10
2024 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2024.4.〜2024.9.30.
2024 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2024.9.30.〜2025.3.31.
2024 学校法人　博多学園・博多メディカル専門学校・臨床工学技士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2024.11〜2025.2
2023 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・歯科衛生士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2023.04〜2024.02
2023 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・柔道整復科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2023.08〜2023.12
2023 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2023.4.〜2023.9.30.
2023 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2023.9.30.〜2024.3.31.
2023 学校法人　博多学園・博多メディカル専門学校・臨床工学技士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2023.11〜2024.2
2022 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・歯科衛生士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2022.04〜2023.02
2022 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・柔道整復科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2022.08〜2022.12
2022 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2022.4.6.〜2022.9.30.
2022 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2022.9.30.〜2023.3.31.
2022 学校法人　博多学園・博多メディカル専門学校・臨床工学技士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2022.11〜2023.2
2021 学校法人　博多学園・博多メディカル専門学校・臨床工学技士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2021.11〜2022.2
2021 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・柔道整復科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2021.07〜2021.11
2021 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・歯科衛生士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2021.04〜2022.02
2021 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2021.9.30.〜2022.3.31.
2021 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2021.4.6.〜2021.9.30.
2020 学校法人　博多学園・博多メディカル専門学校・臨床工学技士科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2020.11〜2021.1
2020 学校法人　滋慶文化学園・福岡医健・スポーツ専門学校・柔道整復科 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2020.08〜2020.12
2020 新潟大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2020.4.1.〜2021.3.31.
2020 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2020.9.30.〜2021.3.31.
2020 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2020.4.6.〜2019.9.30.
2019 国立大学法人広島大学　広島大学特任教授学術院（クロスアポイントメント） Classification:Faculty conurrently holding another post Domestic/International Classification:Japan

Semester, Day Time or Duration：2019.7.1〜2020.3.31.
2019 長崎大学歯学部　講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2019.9.30.〜2020.3.31.
2019 東北大学歯学部　非常勤講師 Classification:Part-time lecturer Domestic/International Classification:Japan

Semester, Day Time or Duration：2019.4.4.〜2019.9.30.
2019 国立大学法人広島大学　客員教授 Classification:Affiliate faculty Domestic/International Classification:Japan

Semester, Day Time or Duration：2019.5.1〜2019.6.30.

▼display all

Participation in international educational events, etc.

2024.3

アイルランガ大学歯学部（参加大学：九州大学歯学部、広島大学歯学部、鹿児島大学歯学部、マレーシア大学歯学部、アイルランガ大学歯学部）

Stovit Community Outreach 2024 Program

　 More details

Venue：インドネシア・

Number of participants：40
2023.7

九州大学歯学部・九州大学歯学部同窓会・釜山大学歯学部

釜山大学歯学部学生訪問交流事業

　 More details

Venue：日本

Number of participants：40
2007.8

九州大学／JICA

JICA

　 More details

Venue：日本

Number of participants：11
2006.5

九州大学／JICA

JICA

　 More details

Venue：日本

Number of participants：11

Other educational activity and Special note

2019 Special Affairs

Outline of Social Contribution and International Cooperation activities

Prof. Ni JunJUnとの国際共同研究
Prof. Francisco García-Garcíaとの国際共同研究
Prof. Tom Martinとの国際共同研究

Social Activities

偶然か必然か：基礎医学研究の世界（九州大学大学院歯学研究院口腔機能分子科学分野教授）久留米大学附設中・高等学校の中学３年生と高校１年生に対して卒業生の立場からのキャリアパス/進路指導

久留米大学附設高等学校同窓会久留米大学附設高等学校 2020.10

　More details

Audience： General,　Scientific,　Company,　Civic organization,　Governmental agency

Type：Lecture

久留米大学附設高等学校同窓会主催の先輩によるキャリアパスに関する進路指導
同窓生による推薦で医療系の進路指導（基礎医学研究）に関しての進路指導
「肥満はコントロールできるのか？　新たな分子標的の解析」

地域歯科医療勉強会歯科医師会館 2019.8

　More details

Audience： General,　Scientific,　Company,　Civic organization,　Governmental agency

Type：Seminar, workshop

Media Coverage

「口腔から考える健康戦略」の確立と普及に向けて Newspaper, magazine

クイント　オーラル　インフォメーション（QUINT ORAL Information）2022 これからの新しい口腔ケアをはじめましょう 2022.6

　More details

「口腔から考える健康戦略」の確立と普及に向けて
「口腔から考える健康戦略」の確立と普及に向けて Newspaper, magazine

クイントオーラルインフォメーション（QUINT ORAL Information）2022 これからの新しい口腔ケアをはじめましょう 2022.6

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Activities contributing to policy formation, academic promotion, etc.

2017.2 - 2019.2

医道審議会専門委員（歯科医師分科会員）
2016.5 - 2018.4

厚生労働省歯科医師試験委員
2015.4 - 2017.3

医療系大学間共用試験実施評価機構
共用試験歯学系CBT事後評価解析小委員会委員
2015.2 - 2017.2

医道審議会専門委員（歯科医師分科会員）
2014.5 - 2016.4

厚生労働省歯科医師試験委員
2013.4 - 2015.3

医療系大学間共用試験実施評価機構
共用試験歯学系CBT事後評価解析小委員会委員
2012.6 - 2014.5

医道審議会専門委員（歯科医師分科会員）
2012.5 - 2014.4

厚生労働省歯科医師試験委員

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Educational Activities for Highly-Specialized Professionals in Other Countries

2024.2 - 2024.3 Stovit Community Outreach 2024 Program

Main countries of student/trainee affiliation：Indonesia

Other countries of student/trainee affiliation：日本/アジア
2007.5 - 2007.9 JICA

Main countries of student/trainee affiliation：Other

Other countries of student/trainee affiliation：アジア／アフリカ／南米／オセアニア
2006.5 - 2006.9 JICA

Main countries of student/trainee affiliation：Other

Other countries of student/trainee affiliation：アジア／アフリカ／南米／オセアニア

Acceptance of Foreign Researchers, etc.

The Computational Biomedicine Lab (CBL), Prince Felipe Research Center

Acceptance period： 2023.10 （Period）：Less than 2 weeks

Nationality：Spain
Pusan National University School of Medicine

Acceptance period： 2007.12 （Period）：Less than 2 weeks

Nationality：Korea, Republic of

Business entity：Japan Society for the Promotion of Science
Pusan National University School of Medicine

Acceptance period： 2007.12 （Period）：Less than 2 weeks

Nationality：Korea, Republic of

Business entity：Japan Society for the Promotion of Science
University college London

Acceptance period： 2007.3 （Period）：Less than 2 weeks

Nationality：United Kingdom

Business entity：Japan Society for the Promotion of Science

Travel Abroad

2024.11 - 2024.12

Staying countory name 1：Australia Staying institution name 1：ASCEPT-APFP-APSA JOINT CONGRESS (Melbourne Convention and Exhibition Centre)
2024.5

Staying countory name 1：China Staying institution name 1：北京理工大学
2024.2 - 2024.3

Staying countory name 1：Indonesia Staying institution name 1：Airlangga University
2008.4

Staying countory name 1：United States Staying institution name 1：Keystone Symposia (Islet and beta cell biology)
2007.7

Staying countory name 1：Korea, Republic of Staying institution name 1：The 5th Korea-Japan Conference on Cellular Signaling for Young Scientists
2006.10 - 2006.11

Staying countory name 1：China Staying institution name 1：第５回アジア・太平洋細胞生物学会
2006.2 - 2006.3

Staying countory name 1：United States Staying institution name 1：Keystone Symposia (Islet and beta cell biology)
2005.8

Staying countory name 1：Austria Staying institution name 1：第２０回国際神経科学会
2004.7

Staying countory name 1：Korea, Republic of Staying institution name 1：The 3rd Korea-Japan Conference on Cellular Signaling for Young Scientists
2003.4 - 2003.6

Staying countory name 1：United Kingdom Staying institution name 1：University College London
2002.11 - 2003.1

Staying countory name 1：United Kingdom Staying institution name 1：University College London
2002.7

Staying countory name 1：Korea, Republic of Staying institution name 1：Pohang University of Science and Technology

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