Researcher basic information

• 博士（生命科学）, 東京薬科大学

• https://researchmap.jp/SeiichiSato?lang=en

• https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201301082581245200

• 201301082581245200

• ウイルス感染
• HBV
• 自然免疫応答
• Breast Cancer
• Cell Signaling

• Life Science, Virology
• Life Science, Tumor biology
• Life Science, Immunology
• Life Science, Cell biology
• Life Science, Medical biochemistry

• Master's degree program, Graduate School of Chemical Sciences and Engineering
• Doctoral (PhD) degree program, Graduate School of Chemical Sciences and Engineering

Research activity information

• May 2015, 塩田洋賞
  B型肝炎ウイルスの感染に対するRIG-Iを介した自然免疫応答機構 (第25回抗ウイルス療法学会総会)
  佐藤 精一

• 17β-Estradiol (E2) Activates Matrix Mineralization through Genomic/Nongenomic Pathways in MC3T3-E1 Cells.
  Hiraku Suzuki; Yuki Fujiwara; Winda Ariyani; Izuki Amano; Sumiyasu Ishii; Ayane Kate Ninomiya; Seiichi Sato; Akinori Takaoka; Noriyuki Koibuchi
  International journal of molecular sciences, 25, 9, 26 Apr. 2024, [International Magazine]
  English, Scientific journal, Estrogen plays an important role in osteoporosis prevention. We herein report the possible novel signaling pathway of 17β-estradiol (E2) in the matrix mineralization of MC3T3-E1, an osteoblast-like cell line. In the culture media-containing stripped serum, in which small lipophilic molecules such as steroid hormones including E2 were depleted, matrix mineralization was significantly reduced. However, the E2 treatment induced this. The E2 effects were suppressed by ICI182,780, the estrogen receptor (ER)α, and the ERβ antagonist, as well as their mRNA knockdown, whereas Raloxifene, an inhibitor of estrogen-induced transcription, and G15, a G-protein-coupled estrogen receptor (GPER) 1 inhibitor, had little or no effect. Furthermore, the E2-activated matrix mineralization was disrupted by PMA, a PKC activator, and SB202190, a p38 MAPK inhibitor, but not by wortmannin, a PI3K inhibitor. Matrix mineralization was also induced by the culture media from the E2-stimulated cell culture. This effect was hindered by PMA or heat treatment, but not by SB202190. These results indicate that E2 activates the p38 MAPK pathway via ERs independently from actions in the nucleus. Such activation may cause the secretion of certain signaling molecule(s), which inhibit the PKC pathway. Our study provides a novel pathway of E2 action that could be a therapeutic target to activate matrix mineralization under various diseases, including osteoporosis.
• Essential role of Rnd1 in innate immunity during viral and bacterial infections.
  Akhilesh Kumar; Shalabh Mishra; Ashish Kumar; Ashwin Ashok Raut; Seiichi Sato; Akinori Takaoka; Himanshu Kumar
  Cell death & disease, 13, 6, 520, 520, 02 Jun. 2022, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Intracellular and cell surface pattern-recognition receptors (PRRs) are an essential part of innate immune recognition and host defense. Here, we have compared the innate immune responses between humans and bats to identify a novel membrane-associated protein, Rnd1, which defends against viral and bacterial infection in an interferon-independent manner. Rnd1 belongs to the Rho GTPase family, but unlike other small GTPase members, it is constitutively active. We show that Rnd1 is induced by pro-inflammatory cytokines during viral and bacterial infections and provides protection against these pathogens through two distinct mechanisms. Rnd1 counteracts intracellular calcium fluctuations by inhibiting RhoA activation, thereby inhibiting virus internalisation. On the other hand, Rnd1 also facilitates pro-inflammatory cytokines IL-6 and TNF-α through Plxnb1, which are highly effective against intracellular bacterial infections. These data provide a novel Rnd1-mediated innate defense against viral and bacterial infections.
• Mindfulness intervention improves cognitive function in older adults by enhancing the level of miRNA-29c in neuron-derived extracellular vesicles
  Shin Hashizume; Masako Nakano; Kenta Kubota; Seiichi Sato; Nobuaki Himuro; Eiji Kobayashi; Akinori Takaoka; Mineko Fujimiya
  Scientific Reports, 11, 1, 21848, 21848, Springer Science and Business Media LLC, Dec. 2021, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Although mindfulness-based stress reduction (MBSR) improves cognitive function, the mechanism is not clear. In this study, people aged 65 years and older were recruited from elderly communities in Chitose City, Japan, and assigned to a non-MBSR group or a MBSR group. Before and after the intervention, the Japanese version of the Montreal Cognitive Assessment (MoCA-J) was administered, and blood samples were collected. Then, neuron-derived extracellular vesicles (NDEVs) were isolated from blood samples, and microRNAs, as well as the target mRNAs, were evaluated in NDEVs. A linear mixed model analysis showed significant effects of the MBSR x time interaction on the MoCA-J scores, the expression of miRNA(miR)-29c, DNA methyltransferase 3 alpha (DNMT3A), and DNMT3B in NDEVs. These results indicate that MBSR can improve cognitive function by increasing the expression of miR-29c and decreasing the expression of DNMT3A, as well as DNMT3B, in neurons. It was also found that intracerebroventricular injection of miR-29c mimic into 5xFAD mice prevented cognitive decline, as well as neuronal loss in the subiculum area, by down-regulating Dnmt3a  and Dnmt3b  in the hippocampus. The present study suggests that MBSR can prevent neuronal loss and cognitive impairment by increasing the neuronal expression of miR-29c.
• Dual Effect of Organogermanium Compound THGP on RIG-I-Mediated Viral Sensing and Viral Replication during Influenza a Virus Infection
  Sunanda Baidya; Yoko Nishimoto; Seiichi Sato; Yasuhiro Shimada; Nozomi Sakurai; Hirotaka Nonaka; Koki Noguchi; Mizuki Kido; Satoshi Tadano; Kozo Ishikawa; Kai Li; Aoi Okubo; Taisho Yamada; Yasuko Orba; Michihito Sasaki; Hirofumi Sawa; Hiroko Miyamoto; Ayato Takada; Takashi Nakamura; Akinori Takaoka
  Viruses, 13, 9, 1674, 1674, MDPI AG, 24 Aug. 2021, [Peer-reviewed], [Lead author, Corresponding author], [International Magazine]
  English, Scientific journal, The interaction of viral nucleic acid with protein factors is a crucial process for initiating viral polymerase-mediated viral genome replication while activating pattern recognition receptor (PRR)-mediated innate immune responses. It has previously been reported that a hydrolysate of Ge-132, 3-(trihydroxygermyl) propanoic acid (THGP), shows a modulatory effect on microbial infections, inflammation, and immune responses. However, the detailed mechanism by which THGP can modify these processes during viral infections remained unknown. Here, we show that THGP can specifically downregulate type I interferon (IFN) production in response to stimulation with a cytosolic RNA sensor RIG-I ligand 5′-triphosphate RNA (3pRNA) but not double-stranded RNA, DNA, or lipopolysaccharide. Consistently, treatment with THGP resulted in the dose-dependent suppression of type I IFN induction upon infections with influenza virus (IAV) and vesicular stomatitis virus, which are known to be mainly sensed by RIG-I. Mechanistically, THGP directly binds to the 5′-triphosphate moiety of viral RNA and competes with RIG-I-mediated recognition. Furthermore, we found that THGP can directly counteract the replication of IAV but not EMCV (encephalitismyocarditis virus), by inhibiting the interaction of viral polymerase with RNA genome. Finally, IAV RNA levels were significantly reduced in the lung tissues of THGP-treated mice when compared with untreated mice. These results suggest a possible therapeutic implication of THGP and show direct antiviral action, together with the suppressive activity of innate inflammation.
• RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells.
  Taisho Yamada; Seiichi Sato; Yuki Sotoyama; Yasuko Orba; Hirofumi Sawa; Hajime Yamauchi; Michihito Sasaki; Akinori Takaoka
  Nature immunology, 22, 7, 820, 828, Jul. 2021, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Efficient immune responses against viral infection are determined by sufficient activation of nucleic acid sensor-mediated innate immunity1,2. Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains an ongoing global pandemic. It is an urgent challenge to clarify the innate recognition mechanism to control this virus. Here we show that retinoic acid-inducible gene-I (RIG-I) sufficiently restrains SARS-CoV-2 replication in human lung cells in a type I/III interferon (IFN)-independent manner. RIG-I recognizes the 3' untranslated region of the SARS-CoV-2 RNA genome via the helicase domains, but not the C-terminal domain. This new mode of RIG-I recognition does not stimulate its ATPase, thereby aborting the activation of the conventional mitochondrial antiviral-signaling protein-dependent pathways, which is in accordance with lack of cytokine induction. Nevertheless, the interaction of RIG-I with the viral genome directly abrogates viral RNA-dependent RNA polymerase mediation of the first step of replication. Consistently, genetic ablation of RIG-I allows lung cells to produce viral particles that expressed the viral spike protein. By contrast, the anti-SARS-CoV-2 activity was restored by all-trans retinoic acid treatment through upregulation of RIG-I protein expression in primary lung cells derived from patients with chronic obstructive pulmonary disease. Thus, our findings demonstrate the distinctive role of RIG-I as a restraining factor in the early phase of SARS-CoV-2 infection in human lung cells.
• Disinfectant potential in inactivation of epidemic keratoconjunctivitis-related adenoviruses by potassium peroxymonosulfate.
  Mei Hashizume; Koki Aoki; Shigeaki Ohno; Nobuyoshi Kitaichi; Nobuyo Yawata; Gabriel Gonzalez; Hirotaka Nonaka; Seiichi Sato; Akinori Takaoka
  European journal of ophthalmology, 31, 2, 379, 384, Mar. 2021, [Peer-reviewed], [International Magazine]
  English, Scientific journal, PURPOSE: The aim of this study was to test the antiviral effectivity of potassium peroxymonosulfate (RUBYSTA®, KYORIN) against five epidemic keratoconjunctivitis-related types of Human adenovirus D in vitro. METHODS: Five types of Human adenovirus D (8, 37, 53, 54 and 56) were incubated with 1% potassium peroxymonosulfate, 0.1% sodium hypochlorite (NaClO) or alcohol-based disinfectant for 30 s or 1 min. These solutions were subjected to measurements of viral titres by infection assays in A549 cells. At day 6 post-infection, both, supernatants and cells, were collected and the viral genome was assessed by real-time polymerase chain reaction analysis. RESULTS: Treatments with 1% potassium peroxymonosulfate led to significant reduction in all tested Human adenovirus D types comparable to disinfecting effects by 0.1% NaClO. Overall, potassium peroxymonosulfate demonstrated sufficient inactivation of the major epidemic keratoconjunctivitis-causing Human adenovirus D to be considered for disinfection and prevention purposes in ophthalmological clinics and hospitals. CONCLUSION: This study demonstrated that potassium peroxymonosulfate is a promising disinfectant for the prevention of epidemic keratoconjunctivitis nosocomial infections in ophthalmological clinics.
• Interleukins
  Seiichi Sato; Akinori Takaoka
  Handbook of Hormones, 437, 439, Elsevier, 2021
  In book
• Immunological modulators
  Akinori Takaoka; Seiichi Sato; Taisho Yamada
  Handbook of Hormones, 435, 435, Elsevier, 2021
  In book
• Regulation of an adaptor protein STING by Hsp90β to enhance innate immune responses against microbial infections.
  Seiichi Sato; Kai Li; Nozomi Sakurai; Mei Hashizume; Sunanda Baidya; Hirotaka Nonaka; Koki Noguchi; Kozo Ishikawa; Chikashi Obuse; Akinori Takaoka
  Cellular immunology, 356, 104188, 104188, Oct. 2020, [Peer-reviewed], [Lead author, Corresponding author], [International Magazine]
  English, Scientific journal, Stimulator of interferon genes (STING) plays important roles in the DNA-mediated innate immune responses. However, the regulatory mechanism of STING in terms of stabilization is not fully understood. Here, we identified the chaperone protein Hsp90s as novel STING interacting proteins. Treatment with an Hsp90 inhibitor 17-AAG and knockdown of Hsp90β but not Hsp90α reduced STING at protein level, resulted in the suppression of IFN induction in response to stimulation with cGAMP, and infections with HSV-1 and Listeria monocytogenes. Collectively, our results suggest that the control of STING protein by Hsp90β is a critical biological process in the DNA sensing pathways.
• MicroRNA-30e-5p has an Integrated Role in the Regulation of the Innate Immune Response during Virus Infection and Systemic Lupus Erythematosus.
  Richa Mishra; Sanjana Bhattacharya; Bhupendra Singh Rawat; Ashish Kumar; Akhilesh Kumar; Kavita Niraj; Ajit Chande; Puneet Gandhi; Dheeraj Khetan; Amita Aggarwal; Seiichi Sato; Prafullakumar Tailor; Akinori Takaoka; Himanshu Kumar
  iScience, 23, 7, 101322, 101322, 24 Jul. 2020, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Precise regulation of innate immunity is crucial for development of appropriate host immunity against microbial infections and maintenance of immune homeostasis. MicroRNAs are small non-coding RNAs, post-transcriptional regulator of multiple genes, and act as a rheostat for protein expression. Here, we identified microRNA-30e-5p induced by hepatitis B virus and other viruses that act as a master regulator for innate immunity. Moreover, pegylated interferons treatment of patients with HBV for viral reduction also reduces miRNA. Additionally, we have also shown the immuno-pathological effects of miR-30e in patients with systemic lupus erythematosus (SLE) and mouse model. Mechanistically, miR-30e targets multiple negative regulators of innate immune signaling and enhances immune responses. Furthermore, sequestering of miR-30e in patients with SLE and mouse model significantly reduces type-I interferon and pro-inflammatory cytokines. Collectively, our study demonstrates the novel role of miR-30e in innate immunity and its prognostic and therapeutic potential in infectious and autoimmune diseases.
• The role of autonomously secreted PGE2 and its autocrine/paracrine effect on bone matrix mineralization at the different stages of differentiating MC3T3-E1 cells.
  Hiraku Suzuki; Noriyasu Ohshima; Kazuaki Tatei; Tomoyo Taniguchi; Seiichi Sato; Takashi Izumi
  Biochemical and biophysical research communications, 524, 4, 929, 935, 16 Apr. 2020, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Bone is consisted of osteoblast-linage cells, bone-forming cells in various differentiation stages. However, it is not fully understood how communicate and interact these cells immigrated from bone marrow. In this study, we showed that prostaglandin E2 (PGE2) had a role in autonomous modification of matrix mineralization in osteoblastic cell line, MC3T3-E1, and interactions across the cells in different differentiation stages. Analysis using LC-MS/MS and inhibitors showed the autonomous secretion of PGE2 among the prostanoids in differentiation stages and that depend on COX-2, a key enzyme for production of PGE2. Treatment with inhibitors of PGE2 receptors and COX-2 indicated that secreted PGE2 regulates matrix mineralization in an autocrine/paracrine manner. In addition, we showed that the expression profile of PGE2 receptors (EP1-EP4) and PGE2 effects on matrix mineralization derived from it changed during cell differentiation. Treatment with inhibitors of PGE2 signaling in the early differentiation stage of MC3T3-E1 cells induced significant changes in matrix mineralization several days after. Stimulation with the extracts from culture medium of the matured cells including PGE2 and co-culture with the matured cells secreting PGE2 significantly promoted matrix mineralization of the early stage cells, in contrast, treatment with inhibitor of COX-2 and PGE2 receptors failed to do so. These results support that PGE2 plays important roles in the interaction system of osteoblast-linage cells in bone tissue to regulate matrix mineralization reflecting condition of bone-forming cells, that is, population and maturation.
• Regulation of MC3T3-E1 differentiation by actin cytoskeleton through lipid mediators reflecting the cell differentiation stage.
  Hiraku Suzuki; Kazuaki Tatei; Noriyasu Ohshima; Seiichi Sato; Takashi Izumi
  Biochemical and biophysical research communications, 514, 2, 393, 400, 25 Jun. 2019, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Actin cytoskeleton is reported to be related in various functions of osteoblast, bone-forming cell. However the function of actin cytoskeleton in osteoblasts is not fully understood, since bone formation is derived from extracellular interactions of functional proteins produced from osteoblasts, including osteocalcin (Ocn), and it is a result of closely and complex organized sequence of biochemical events. In this study, we showed that actin cytoskeleton of MC3T3-E1 cells functioned in recognition of cell condition and regulation of extracellular matrix mineralization, bone formation. Maturation of MC3T3-E1 cells by 14 days of culture reduced F-actin filaments, while induced expression of Ocn mRNA known as late stage differentiation marker and matrix mineralization, terminal stage of cell differentiation. The disruption of actin cytoskeleton with Cyto D in immature MC3T3-E1 cells significantly increased expression of Ocn mRNA in 24 h. Both PTX-induced inhibition of signal transduction through GPCRs and celecoxib-induced suppression of lipid mediators in immature MC3T3-E1 cells reduced actin filaments and suppressed matrix mineralization. Furthermore, addition of lipid mediators extracted from culture mediums of differentiated MC3T3-E1 cells by Bligh-Dyer method induced actin cytoskeleton reorganization and matrix mineralization change in MC3T3-E1 cells. Taken together, our data suggest that actin cytoskeleton of MC3T3-E1 cells regulates activation of developmental pathway reflecting cell differentiation stages through lipid mediators. The function we identified is important for bone formation tightly regulated by mechanical stress, since actin cytoskeleton is also known as a mechanosensor of osteoblasts.
• The antiviral effects of human microRNA miR-302c-3p against hepatitis B virus infection.
  Susumu Hamada-Tsutsumi; Yutaka Naito; Seiichi Sato; Akinori Takaoka; Keigo Kawashima; Masanori Isogawa; Takahiro Ochiya; Yasuhito Tanaka
  Alimentary pharmacology & therapeutics, 49, 8, 1060, 1070, Apr. 2019, [Peer-reviewed], [International Magazine]
  English, Scientific journal, BACKGROUND: Conventional treatments of chronic hepatitis B virus (HBV) infection rarely achieve a decline of serum hepatitis B surface antigen (HBsAg) levels and eradication of the virus. AIM: To elucidate the antiviral mechanisms of a human microRNA, miR-302c-3p, against HBV replication. METHODS: The antiviral effect of miR-302c-3p was evaluated in vitro and in vivo by transfecting the miR-302c-3p mimic into HBV-infected HepG2-hNTCP-C4 cells and HBV transgenic mice respectively. RESULTS: miR-302c-3p decreased not only HBV replication but also production of HBsAg. Pregenomic RNA and HBsAg mRNA concentrations decreased in the cells treated with miR-302c-3p. Interestingly, the amount of cccDNA was significantly reduced in the miR-302c-3p-treated cells, in association with disappearance of the HBV core protein. An RNA immunoprecipitation assay showed that miR-302c-3p decreased the binding of the HBV polymerase to the pregenomic RNA by hybridising with the ε-loop region. A number of host genes were downregulated in miR-302c-3p-treated cells, including BMPR2 and HNF4A. Knockdown of these two genes by corresponding siRNAs also suppressed HBV replication and HBsAg secretion. The antiviral effect of miR-302c-3p was also observed in HBV transgenic mice. CONCLUSION: miR-302c-3p had anti-HBV activity, in vitro and in vivo, via several mechanisms.
• Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells.
  Shoichiro Kameoka; Takeshi Kameyama; Takaya Hayashi; Seiichi Sato; Naomi Ohnishi; Takeru Hayashi; Naoko Murata-Kamiya; Hideaki Higashi; Masanori Hatakeyama; Akinori Takaoka
  Biomedical research (Tokyo, Japan), 37, 1, 21, 7, 2016, [Peer-reviewed], [Domestic magazines]
  English, Scientific journal
• The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex.
  Saki Sekino; Yuriko Kashiwagi; Hitoshi Kanazawa; Kazuki Takada; Takashi Baba; Seiichi Sato; Hiroki Inoue; Masaki Kojima; Katsuko Tani
  Cell communication and signaling : CCS, 13, 41, 41, 01 Oct. 2015, [Peer-reviewed], [International Magazine]
  English, Scientific journal
• The RNA sensor RIG-I dually functions as an innate sensor and direct antiviral factor for hepatitis B virus.
  Seiichi Sato; Kai Li; Takeshi Kameyama; Takaya Hayashi; Yuji Ishida; Shuko Murakami; Tsunamasa Watanabe; Sayuki Iijima; Yu Sakurai; Koichi Watashi; Susumu Tsutsumi; Yusuke Sato; Hidetaka Akita; Takaji Wakita; Charles M Rice; Hideyoshi Harashima; Michinori Kohara; Yasuhito Tanaka; Akinori Takaoka
  Immunity, 42, 1, 123, 32, 20 Jan. 2015, [Peer-reviewed], [Lead author], [International Magazine]
  English, Scientific journal
• Inhibition of CIN85-mediated invasion by a novel SH3 domain binding motif in the lysyl oxidase propeptide.
  Seiichi Sato; Yingshe Zhao; Misa Imai; Philip C Simister; Stephan M Feller; Philip C Trackman; Kathrin H Kirsch; Gail E Sonenshein
  PloS one, 8, 10, e77288, Oct. 2013, [Peer-reviewed], [Lead author], [International Magazine]
  English, Scientific journal
• Roles of SAM and DDHD domains in mammalian intracellular phospholipase A1 KIAA0725p.
  Inoue H; Baba T; Sato S; Ohtsuki R; Takemori A; Watanabe T; Tagaya M; Tani K
  Biochimica et biophysica acta, 1823, 930, 939, 4, Apr. 2012, [Peer-reviewed]
• Blimp1 Activation by AP-1 in Human Lung Cancer Cells Promotes a Migratory Phenotype and Is Inhibited by the Lysyl Oxidase Propeptide
  Ziyang Yu; Seiichi Sato; Philip C. Trackman; Kathrin H. Kirsch; Gail E. Sonenshein
  PLOS ONE, 7, 3, e33287, Mar. 2012, [Peer-reviewed]
  English, Scientific journal
• The Ras Signaling Inhibitor LOX-PP Interacts with Hsp70 and c-Raf To Reduce Erk Activation and Transformed Phenotype of Breast Cancer Cells
  Seiichi Sato; Philip C. Trackman; Joni M. Maki; Johanna Myllyharju; Kathrin H. Kirsch; Gail E. Sonenshein
  MOLECULAR AND CELLULAR BIOLOGY, 31, 13, 2683, 2695, Jul. 2011, [Peer-reviewed], [Lead author]
  English, Scientific journal
• Golgi-localized KIAA0725p regulates membrane trafficking from the Golgi apparatus to the plasma membrane in mammalian cells
  Sei-ichi Sato; Hiroki Inoue; Takeshi Kogure; Mitsuo Tagaya; Katsuko Tani
  FEBS LETTERS, 584, 21, 4389, 4395, Nov. 2010, [Peer-reviewed], [Lead author]
  English, Scientific journal
• NESH (Abi-3) is pre-sent in the Abi/WAVE complex but does not promote c-Abl-mediated phosphorylation
  Noriko Hirao; Seiichi Sato; Tetsuya Gotoh; Masahiro Maruoka; Jun Suzuki; Satoru Matsuda; Tornoyuki Shishido; Katsuko Tani
  FEBS LETTERS, 580, 27, 6464, 6470, Nov. 2006, [Peer-reviewed], [Lead author]
  English, Scientific journal
• Identification of B cell adaptor for PI3-kinase (BCAP) as an Abl interactor 1-regulated substrate of Abl kinases
  M Maruoka; J Suzuki; S Kawata; K Yoshida; N Hirao; S Sato; SP Goff; T Takeya; K Tani; T Shishido
  FEBS LETTERS, 579, 14, 2986, 2990, Jun. 2005, [Peer-reviewed]
  English, Scientific journal
• Abl interactor 1 promotes tyrosine 296 phosphorylation of mammalian enabled (Mena) by c-Abl kinase
  K Tani; S Sato; T Sukezane; H Kojima; H Hirose; H Hanafusa; T Shishido
  JOURNAL OF BIOLOGICAL CHEMISTRY, 278, 24, 21685, 21692, Jun. 2003, [Peer-reviewed]
  English, Scientific journal

• がん細胞におけるcGAMP分解酵素による自然免疫回避機構の解明
  Seiichi Sato; Akinori Takaoka, 第29回日本がん免疫学会学術総会, Jul. 2025
• Cytosolic IRF-3/HSD11B2 modulates glucocorticoid sensitivity during influenza infection
  齋秀二; 山田大翔; 佐藤精一; CHAPMAN Karen; 高岡晃教, 日本内分泌学会雑誌, 100, 1, 311, 311, 2024
  (一社)日本内分泌学会, English
• 細胞外脂質シグナルを介した骨芽細胞のメカノストレスの細胞外伝播機構
  鈴木 啓; 佐藤 精一; 鯉淵 典之, アレルギーの臨床, 43, 11, 891, 896, Oct. 2023
  (株)北隆館, Japanese
• がん免疫の基礎、1 自然免疫
  佐藤精一; 高岡晃教, 先進医療NAVIGATOR がん免疫療法最前線, 1, 5, Jul. 2023
  Introduction scientific journal
• ウイルス感染における自然免疫系バックアップディフェンス機構の構築
  佐藤 精一, 先進医薬研究振興財団研究成果報告集, 2022年度, 128, 130, Mar. 2023
  (公財)先進医薬研究振興財団, Japanese
• 骨組織のメカニカルストレス伝播機構
  鈴木啓; 佐藤精一; 鯉淵典之, BIO Clinica, 38, 67, 72, 2023
• マインドフルネスストレス低減法はニューロン由来細胞外小胞のmiRNA-29cを高め、高齢者の認知機能を向上させる
  橋爪 紳; 中野 正子; 久保田 健太; 佐藤 精一; 藤宮 峯子, 日本予防理学療法学会学術大会プログラム・抄録集, 9回, 28, 28, Dec. 2022
  (一社)日本予防理学療法学会, Japanese
• RIG-Iはヒト肺細胞においてシグナル伝達非依存的な抗SARS-CoV-2防御を誘導する
  山田大翔; 山田大翔; 佐藤精一; 佐藤精一; 外山雄貴; 外山雄貴; 大場靖子; 澤洋文; 山内肇; 佐々木道仁; 高岡晃教; 高岡晃教, 日本インターフェロン・サイトカイン学会学術集会抄録集, 85th (CD-ROM), 2021
• Assessment of rapid diagnostic kit for detecting human adenovirus causing epidemic keratoconjunctivitis
  橋爪芽衣; 青木功喜; 青木功喜; 青木功喜; 八幡信代; GONZALEZ Gabriel; 石田晋; 大野重昭; 大野重昭; 佐藤精一; 高岡晃教; 北市伸義; 北市伸義, 臨床眼科, 75, 4, 2021
• MC3T3-E1における,脂質オートクライン刺激とエストラジオール刺激のクロストーク機構の解析
  鈴木啓; 大嶋紀安; 小西昭充; 立井一明; 佐藤精一; 和泉孝志; 南嶋洋司, 日本分子生物学会年会プログラム・要旨集(Web), 43rd, 2020
• 骨芽細胞様細胞MC3T3-E1の細胞内外の脂質メディエーターがアクチン細胞骨格変化を介して骨形成を制御する
  鈴木啓; 大嶋紀安; 立井一明; 佐藤精一; 南嶋洋司; 和泉孝志; 小西昭充, 日本分子生物学会年会プログラム・要旨集(Web), 42nd, 2019
• Genotoxicなストレスに対する自然免疫応答に対する新規抑制因子の同定
  佐藤精一; 高岡晃教, 日本インターフェロン・サイトカイン学会学術集会抄録集, 84th, 2019
• 自然免疫系細胞内核酸センサーであるRIG-Iとそのリガンドとの認識を制御する有機化合物の同定
  佐藤精一; 西本遥子; 只野慧; 島田康弘; 中村宜司; 高岡晃教, 日本インターフェロン・サイトカイン学会学術集会抄録集, 83rd, 2018
• E3 ubiquitin-protein ligase RBX1 interacts with RIG-I receptor to inhibit its helicase activity
  Seiichi Sato; Naoya Katsuyama; Mei Hashizume; Nozomi Sakurai; Yohei Miyashita; Kai Li; Akinori Takaoka, CYTOKINE, 100, 102, 102, Dec. 2017
  English, Summary international conference
• 骨芽細胞様細胞MC3T3-E1における分化段階に応じた機械的刺激による骨形成制御応答の解析
  鈴木 啓; 大嶋 紀安; 小西 昭充; 立井 一明; 佐藤 精一; 和泉 孝志, 生命科学系学会合同年次大会, 2017年度, [2P, 0735], Dec. 2017
  生命科学系学会合同年次大会運営事務局, Japanese
• DNA損傷を感知する自然免疫応答制御因子の解析
  佐藤精一, 上原記念生命科学財団研究報告集(CD-ROM), 31, 2017
• B型肝炎ウイルス感染に対するRNAセンサーRIG‐Iのデュアル機能による生体防御機構
  佐藤精一; 亀山武志; 高岡晃教; 佐藤精一; 亀山武志; 高岡晃教, 感染・炎症・免疫, 45, 4, 270‐277, 15 Jan. 2016
  Japanese
• B型肝炎ウイルス感染におけるRIG‐Iのウイルスセンサーおよび抗ウイルス因子としてのデュアル機能
  亀山武志; 亀山武志; 佐藤精一; 佐藤精一; 高岡晃教; 高岡晃教, 月刊臨床免疫・アレルギー科, 64, 1, 78, 84, 25 Jul. 2015
  科学評論社, Japanese
• ピロリ菌の病原因子CagAはNLRP3inflammasomeを活性化し,IL-1βを産生する
  亀岡章一郎; 亀山武志; 佐藤精一; 林剛瑠; 大西なおみ; 紙谷尚子; 東秀明; 畠山昌則; 高岡晃教, 日本生化学会大会(Web), 88th, 2015
• B型肝炎ウイルスの持続感染を再現する効率的な培養細胞評価系の開発に関する研究 自然免疫認識機構の制御によるHBV複製への影響
  高岡晃教; 佐藤精一; LI Kai; 亀山武志; 林隆也; 原島秀吉; 秋田英万; 櫻井遊; 小原道法; 脇田隆字; 渡士幸一, B型肝炎ウイルスの持続感染を再現する効率的な培養細胞評価系の開発に関する研究 平成26年度 総括・分担研究報告書, 56‐61, 2015
  Japanese
• 核酸を用いた自然免疫経路活性化による抗腫瘍効果の検討
  亀山武志; 木口舞美; 佐藤精一; 石川浩三; 高岡晃教, 日本がん免疫学会総会プログラム・抄録集, 18th, 2014
• B型肝炎ウイルスの持続感染を再現する効率的な培養細胞評価系の開発に関する研究 自然免疫認識機構の制御によるHBV複製への影響
  高岡晃教; 佐藤精一; LI Kai; 亀山武志; 林隆也; 原島秀吉; 秋田英万; 櫻井遊, B型肝炎ウイルスの持続感染を再現する効率的な培養細胞評価系の開発に関する研究 平成25年度 総括・分担研究報告書, 55‐59, 2014
  Japanese

• 抗ウイルス療法学会
• 日本インターフェロン・サイトカイン学会

• lncRNAからエンコードされる新しい抗ウイルスサイトカインの同定と性状解析
  科学研究費助成事業
  28 Jun. 2024 - 31 Mar. 2027
  高岡 晃教; 久米田 博之; 佐藤 精一
  日本学術振興会, 挑戦的研究(萌芽), 北海道大学, 24K22043
• パターン認識受容体STINGによる抗原提示プロセスにおける内因性制御機構の解明
  科学研究費助成事業
  01 Apr. 2024 - 31 Mar. 2027
  佐藤 精一
  日本学術振興会, 基盤研究(C), 北海道大学, 24K10266
• RIG-I作動性核酸（3pRNA）の白血病治療応用に向けた基礎研究
  科学研究費助成事業
  01 Apr. 2022 - 31 Mar. 2025
  石川 浩三; 佐藤 精一
  日本学術振興会, 基盤研究(C), 北海道大学, 22K08445
• Research on the immune system in uninfected cells that defines the immune response during viral infection
  Grants-in-Aid for Scientific Research
  01 Apr. 2018 - 31 Mar. 2021
  Kameyama Takeshi
  Interferons (IFNs) are the main cytokines for the innate immune response against viral infection. It is known that IFNs are constitutively induced at very low levels in the absence of viral infection. These constitutively induced IFNs and their signals are essential for the rapid and robust induction of IFN induction after viral infection and for the suppression of carcinogenesis. However, the mechanism of this constitutive IFN induction and its regulation remains unclear. In this study, we found that the constitutive IFNs are induced through an intracellular RNA sensor-dependent recognition of endogenous RNAs and the downstream signaling pathway. Furthermore, we found several regulatory factors that regulate cytosolic nucleic acid-mediated innate immune responses. These results identified a novel regulatory mechanism that controls constitutively induced IFNs, which may provide a novel prophylactic target for viral control and suppression of carcinogenesis.
  Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (C), Kobe University, 18K07162
• Elucidation of the acquisition of anti-tumor immunity by novel STING interacting proteins in cancer
  Grants-in-Aid for Scientific Research
  01 Apr. 2018 - 31 Mar. 2021
  Sato Seiichi
  Based on the previous study elucidating the signaling pathways of properties of cancer and innate immune response, we hypothesize whether our previous effort can extend in tumor therapy. It is unknown how cancer cells acquire anti-tumor immunity. In this study, we identified some STING interacting proteins, we demonstrated that STING is a client protein of Hsp90beta, in particular stabilization of STING protein is crucial for efficient innate immune response, and ANT2 is a negative regulator of STING pathway.
  Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (C), Hokkaido University, 18K07191
• Investigation of new self-defense mechanism with innate immunity and glucocorticoid metabolizing enzyme
  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
  01 Apr. 2016 - 31 Mar. 2019
  SAI SHUJI; Yamada Taisho; Sato Seiichi; Takaoka Akinori
  Innate immune receptor RIG-I, which senses influenza virus (Flu), produces interferon (IFN) to play a critical role for self-defense. Glucocorticoid hormones (GC) suppress abnormal activation of RIG-I. In this study we found the mechanism that intracellular GC metabolizing enzyme 11b-HSD1 suppressed RIG-I signaling. 11b-HSD1, which induced by Flu infection, converts inert GC to active GC suppressing IFN production. GC and RIG-I synergistically induced 11b-HSD1 and independently suppressed RIG-I signaling. There is a cross network and self-defense mechanism between innate immunity and GC signaling.
  Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (C), Hokkaido University, 16K09792
• Establishment of local and switchable innate immune activation by novel nucleic acid adjuvant
  Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research
  01 Apr. 2013 - 31 Mar. 2015
  TAKAOKA Akinori; SATO Seiichi; KAMEYAMA Takeshi
  Adjuvant is an important component for effective vaccination and antitumor therapy. Establishment of local and switchable adjuvant is considered to be an efficient strategy to reduce side effects and efficiently activate innate immune responses. The purpose of this study is the establishment of a novel nucleic acid adjuvant that can trigger the activation of innate immune system in response to X-ray irradiation. In this study, type-C CpG ligands contained with cystamine-modified cytosine were used and showed its structural change by X-ray irradiation, albeit their low efficiency. These results showed these ligands could be a switchable activator and further investigation will be needed to improve their efficiency.
  Japan Society for the Promotion of Science, Grant-in-Aid for Challenging Exploratory Research, Hokkaido University, 25640084
• Elucidation of host innate sensing mechanism for nucleic acid of hepatitis B virus that possibly cause liver cancer
  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)
  01 Apr. 2013 - 31 Mar. 2015
  SATO Seiichi
  In this study, we have revealed that HBV infection is sensed by the RIG-I protein through its recognition of certain viral RNA (pregenomic RNA) within the cells, which triggers a predominant production of type III interferons, a well-known antiviral protein. We further determined that a key element for the RIG-I-mediated recognition is the 5′-ε region of HBV pregenomic RNA, which was previously reported to take a stem-loop structure and serve as a binding site of HBV polymerase, an essential enzyme for viral propagation. In relation to this, we also discovered a novel role of RIG-I as a direct antiviral factor that can competitively inhibit the interaction of HBV polymerase with the 5′-ε region of viral genome. These findings indicated that RIG-I dually functions not only as an HBV sensor but also as a counteractor against viral polymerase in human hepatocyte, and also suggest that the ε region-derived RNA would be a therapeutic tool for the treatment of HBV infection.
  Japan Society for the Promotion of Science, Grant-in-Aid for Young Scientists (B), Hokkaido University, Principal investigator, Competitive research funding, 25870015

• 有機ゲルマニウム化合物を有効成分として含有するＩ型インターフェロン産生抑制剤
  Patent right, 佐藤精一; 高岡晃教; 島田康弘; 中村宜司
  特願2019-014895
  特開2020-121946