TAKASAKI Teruaki

Department of Pharmaceutical SciencesLecturer

Last Updated :2024/10/10

■Researcher basic information

Research Field

  • Life sciences / Molecular biology

■Career

Educational Background

  •        - 2007/03  神戸大学 大学院自然科学研究科博士課程後期課程生命科学専攻修了

■Research activity information

Paper

  • Teruaki Takasaki; Asuka Bamba; Yuka Kukita; Aiko Nishida; Daiki Kanbayashi; Kanako Hagihara; Ryosuke Satoh; Keiichi Ishihara; Reiko Sugiura
    Genes to cells : devoted to molecular & cellular mechanisms 29 (7) 589 - 598 2024/07 
    Calcineurin (CN) is a conserved Ca2+/calmodulin-dependent phosphoprotein phosphatase that plays a key role in Ca2+ signaling. Regulator of calcineurin 1 (RCAN1), also known as Down syndrome critical region gene 1 (DSCR1), interacts with calcineurin and inhibits calcineurin-dependent signaling in various organisms. Ppb1, the fission yeast calcineurin regulates Cl--homeostasis, and Ppb1 deletion induces MgCl2 hypersensitivity. Here, we characterize the conserved and novel roles of the fission yeast RCAN1 homolog rcn1+. Consistent with its role as an endogenous calcineurin inhibitor, Rcn1 overproduction reproduced the calcineurin-null phenotypes, including MgCl2 hypersensitivity and inhibition of calcineurin signaling upon extracellular Ca2+ stimuli as evaluated by the nuclear translocation and transcriptional activation of the calcineurin substrate Prz1. Notably, overexpression of rcn1+ causes hypersensitivity to arsenite, whereas calcineurin deletion induces arsenite tolerance, showing a phenotypic discrepancy between Rcn1 overexpression and calcineurin deletion. Importantly, although Rcn1 deletion induces modest sensitivities to arsenite and MgCl2 in wild-type cells, the arsenite tolerance, but not MgCl2 sensitivity, associated with Ppb1 deletion was markedly suppressed by Rcn1 deletion. Collectively, our findings reveal a previously unrecognized functional collaboration between Rcn1 and calcineurin, wherein Rcn1 not only negatively regulates calcineurin in the Cl- homeostasis, but also Rcn1 mediates calcineurin signaling to modulate arsenite cytotoxicity.
  • Naofumi Tomimoto; Teruaki Takasaki; Reiko Sugiura
    Microbial cell (Graz, Austria) 11 242 - 253 2024 
    Various stress conditions, such as heat stress (HS) and oxidative stress, can cause biomolecular condensates represented by stress granules (SGs) via liquid-liquid phase separation. We have previously shown that Hsp90 forms aggregates in response to HS and that Hsp90 aggregates transiently co-localize with SGs as visualized by Pabp. Here, we showed that arsenite, one of the well-described SG-inducing stimuli, induces Hsp90 aggregates distinct from conventional SGs in fission yeast. Arsenite induced Hsp90 granules in a dose-dependent manner, and these granules were significantly diminished by the co-treatment with a ROS scavenger N-acetyl cysteine (NAC), indicating that ROS are required for the formation of Hsp90 granules upon arsenite stress. Notably, Hsp90 granules induced by arsenite do not overlap with conventional SGs as represented by eIF4G or Pabp, while HS-induced Hsp90 granules co-localize with SGs. Nrd1, an RNA-binding protein known as a HS-induced SG component, was recruited into Hsp90 aggregates but not to the conventional SGs upon arsenite stress. The non-phosphorylatable eIF2α mutants significantly delayed the Hsp90 granule formation upon arsenite treatment. Importantly, inhibition of Hsp90 by geldanamycin impaired the Hsp90 granule formation and reduced the arsenite tolerance. Collectively, arsenite stimulates two types of distinct aggregates, namely conventional SGs and a novel type of aggregates containing Hsp90 and Nrd1, wherein Hsp90 plays a role as a center for aggregation, and stress-specific compartmentalization of biomolecular condensates.
  • Teruaki Takasaki; Yasuyuki Hamabe; Kenta Touchi; Golam Iftakhar Khandakar; Takeshi Ueda; Hitoshi Okada; Kazuko Sakai; Kazuto Nishio; Genzoh Tanabe; Reiko Sugiura
    Oxidative medicine and cellular longevity 2024 7683793 - 7683793 2024 [Refereed]
     
    The extracellular signal-regulated kinase (ERK) MAPK pathway is dysregulated in various human cancers and is considered an attractive therapeutic target for cancer. Therefore, several inhibitors of this pathway are being developed, and some are already used in the clinic. We have previously identified an anticancer compound, ACA-28, with a unique property to preferentially induce ERK-dependent apoptosis in melanoma cells. To comprehensively understand the biological cellular impact induced by ACA-28, we performed a global gene expression analysis of human melanoma SK-MEL-28 cells exposed to ACA-28 using a DNA microarray. The transcriptome analysis identified nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcription factor that combats oxidative stress, as the most upregulated genetic pathway after ACA-28 treatment. Consistently, ACA-28 showed properties to increase the levels of reactive oxygen species (ROS) as well as Nrf2 protein, which is normally repressed by proteasomal degradation and activated in response to oxidative stresses. Furthermore, the ROS scavenger N-acetyl cysteine significantly attenuated the anticancer activity of ACA-28. Thus, ACA-28 activates Nrf2 signaling and exerts anticancer activity partly via its ROS-stimulating property. Interestingly, human A549 cancer cells with constitutively high levels of Nrf2 protein showed resistance to ACA-28, as compared with SK-MEL-28. Transient overexpression of Nrf2 also increased the resistance of cells to ACA-28, while knockdown of Nrf2 exerted the opposite effect. Thus, upregulation of Nrf2 signaling protects cancer cells from ACA-28-mediated cell death. Notably, the Nrf2 inhibitor ML385 substantially enhanced the cell death-inducing property of ACA-28 in pancreatic cancer cells, T3M4 and PANC-1. Our data suggest that Nrf2 plays a key role in determining cancer cell susceptibility to ACA-28 and provides a novel strategy for cancer therapy to combine the Nrf2 inhibitor and ACA-28.
  • Reiko Sugiura; Ryosuke Satoh; Naofumi Tomimoto; Teruaki Takasaki
    Phase Separation in Living Cells Springer Nature Singapore 209 - 252 2023/09
  • Teruaki Takasaki; Reo Obana; Daiki Fujiwara; Naofumi Tomimoto; Golam Iftakhar Khandakar; Ryosuke Satoh; Reiko Sugiura
    microPublication Biology 2023 2023/08 [Refereed]
     
    The nucleocytoplasmic transport of proteins is an important mechanism to control cell fate. Pap1 is a fission yeast nucleocytoplasmic shuttling transcription factor of which localization is redox regulated. The nuclear export factor Crm1/exportin negatively regulates Pap1 by exporting it from the nucleus to the cytoplasm. Here, we describe the effect of an anti-cancer compound ACA-28, an improved derivative of 1'-acetoxychavicol acetate (ACA), on the subcellular distribution of Pap1. ACA-28 induced nuclear accumulation of Pap1 more strongly than did ACA. ROS inhibitor N-acetyl-L-cysteine (NAC) partly antagonized the Pap1 nuclear accumulation induced by ACA-28. NAC almost abolished Pap1 nuclear localization upon H 2 O 2 , whereas leptomycin B (LMB)-mediated inhibition of Pap1 nuclear export was resistant to NAC. Collectively, ACA-28-mediated apoptosis in cancer cells may involve ROS-dependent and -independent mechanisms.
  • Teruaki Takasaki; Ryosuke Utsumi; Erika Shimada; Asuka Bamba; Kanako Hagihara; Ryosuke Satoh; Reiko Sugiura
    Microbial cell (Graz, Austria) 10 (6) 133 - 140 2023/06 [Refereed]
     
    Autophagy promotes or inhibits cell death depending on the environment and cell type. Our previous findings suggested that Atg1 is genetically involved in the regulation of Pmk1 MAPK in fission yeast. Here, we showed that Δatg1 displays lower levels of Pmk1 MAPK phosphorylation than did the wild-type (WT) cells upon treatment with a 1,3-β-D-glucan synthase inhibitor micafungin or CaCl2, both of which activate Pmk1. Moreover, the overproduction of Atg1, but not that of the kinase inactivating Atg1D193A activates Pmk1 without any extracellular stimuli, suggesting that Atg1 may promote Pmk1 MAPK signaling activation. Notably, the overproduction of Atg1 induces a toxic effect on the growth of WT cells and the deletion of Pmk1 failed to suppress the cell death induced by Atg1, indicating that the Atg1-mediated cell death requires additional mechanism(s) other than Pmk1 activation. Moreover, atg1 gene deletion induces tolerance to micafungin and CaCl2, whereas pmk1 deletion induces severe sensitivities to these compounds. The Δatg1Δpmk1 double mutants display intermediate sensitivities to these compounds, showing that atg1 deletion partly suppressed growth inhibition induced by Δpmk1. Thus, Atg1 may act to promote cell death upon micafungin and CaCl2 stimuli regardless of Pmk1 MAPK activity. Since micafungin and CaCl2 are intracellular calcium inducers, our data reveal a novel role of the autophagy regulator Atg1 to induce cell death upon calcium overload independent of its role in Pmk1 MAPK activation.
  • Golam Iftakhar Khandakar; Yoichi Miyamoto; Ryosuke Satoh; Kenta Kishimoto; Mingzuo Xie; Mengyu Shih; Teruaki Takasaki; Genzoh Tanabe; Masahiro Oka; Reiko Sugiura
    Genes to cells : devoted to molecular & cellular mechanisms 2023/03 [Refereed]
     
    The extracellular-signal-regulated-kinase (ERK) signaling pathway is essential for cell proliferation and is frequently deregulated in human tumors such as pancreatic cancers. ACAGT-007a (GT-7), an anti-cancer compound, stimulates ERK phosphorylation, thereby inducing growth inhibition and apoptosis in T3M4 pancreatic cancer cells. However, how GT-7 stimulates ERK phosphorylation and induces apoptosis in ERK-active T3M4 cells remains unclear. To look into the mechanism, we performed a spatiotemporal analysis of ERK phosphorylation mediated by GT-7 in T3M4 cells. The immunoblotting showed that GT-7 stimulates ERK phosphorylation within 1 hr, which was more remarkable after 2 hr. Importantly, apoptosis induction as evaluated by the cleaved Caspase-3 was observed only after 2 hr incubation with GT-7. The immunofluorescence staining revealed the enrichment of phosphorylated ERK (phospho-ERK) in the nucleus upon 1 hr incubation with GT-7. Fractionation experiments showed that GT-7 increases phospho-ERK levels in the cytoplasm within 1 hr, whereas nuclear phospho-ERK accumulation is observed after 2 hr incubation with GT-7. MEK inhibition by U0126 significantly diminishes nuclear phospho-ERK distribution and apoptosis induction stimulated by GT-7. Thus, GT-7 may initiate the induction of ERK phosphorylation in the cytoplasm, which leads to phospho-ERK enrichment in the nucleus. This nuclear phospho-ERK accumulation by GT-7 precedes and may underlie apoptosis induction in T3M4.
  • Ryosuke Satoh; Taemi Tanaka; Nobuyasu Yoshida; Chiaki Tanaka; Teruaki Takasaki; Reiko Sugiura
    Biological and Pharmaceutical Bulletin 46 (2) 163 - 169 2023/02 [Refereed][Invited]
     
    Phosphatidylinositol-4-phosphate 5-kinase (PI4P5K) is a highly conserved enzyme that generates phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) by phosphorylating phosphatidylinositol 4-phosphate (PI(4)P). Schizosaccharomyces pombe (S. pombe) its3-1 is a loss-of-function mutation in the essential its3+ gene that encodes a PI4P5K. Its3 regulates cell proliferation, cytokinesis, cell integrity, and membrane trafficking, but little is known about the regulatory mechanisms of Its3. To identify regulators of Its3, we performed a genetic screening utilizing the high-temperature sensitivity (TS) of its3-1 and identified puf3+ and puf4+, encoding Pumilio/PUF family RNA-binding proteins as multicopy suppressors of its3-1 cells. The deletions of the PUF domains in the puf3+ and puf4+ genes resulted in the reduced ability to suppress its3-1, suggesting that the suppression by Puf3 and Puf4 may involve their RNA-binding activities. The gene knockout of Puf4, but not that of Puf3, exacerbated the TS of its3-1. Interestingly, mutant Its3 expression levels both at mRNA and protein levels were lower than those of the wild-type (WT) Its3. Consistently, the overexpression of the mutant its3-1 gene suppressed the its3-1 phenotypes. Notably, Puf3 and Puf4 overexpression increased the mRNA and protein expression levels of both Its3 and Its3-1. Collectively, our genetic screening revealed a functional relationship between the Pumilio/PUF family RNA-binding proteins and PI4P5K.
  • Golam Iftakhar Khandakar; Ryosuke Satoh; Teruaki Takasaki; Kana Fujitani; Genzoh Tanabe; Kazuko Sakai; Kazuto Nishio; Reiko Sugiura
    Cells 11 (4) 2022/02 [Refereed]
     
    The mitogen-activated protein kinase (MAPK)/ERK and phosphatidylinositol-3 kinase (PI3K)/AKT pathways are dysregulated in various human cancers, including pancreatic ductal adenocarcinoma (PDAC), which has a very poor prognosis due to its lack of efficient therapies. We have previously identified ACAGT-007a (GT-7), an anti-cancer compound that kills ERK-active melanoma cells by inducing ERK-dependent apoptosis. Here, we investigated the apoptosis-inducing effect of GT-7 on three PDAC cell lines and its relevance with the MAPK/ERK and PI3K/AKT signaling pathways. GT-7 induced apoptosis in PDAC cells with different KRAS mutations (MIA-Pa-Ca-2 (KRAS G12C), T3M4 (KRAS Q61H), and PANC-1 (KRAS G12D)), being T3M4 most susceptible, followed by MIA-Pa-Ca-2, and PANC-1 was most resistant to apoptosis induction by GT-7. GT-7 stimulated ERK phosphorylation in the three PDAC cells, but only T3M4 displayed ERK-activation-dependent apoptosis. Furthermore, GT-7 induced a marked down-regulation of AKT phosphorylation after a transient peak in T3M4, whereas PANC-1 displayed the strongest and most sustained AKT activation, followed by MIA-Pa-Ca-2, suggesting that sustained AKT phosphorylation as a determinant for the resistance to GT-7-mediated apoptosis. Consistently, a PI3K inhibitor, Wortmannin, abolished AKT phosphorylation and enhanced GT-7-mediated apoptosis in T3M4 and MIA-Pa-Ca-2, but not in PANC-1, which showed residual AKT phosphorylation. This is the first report that ERK stimulation alone or in combination with AKT signaling inhibition can effectively induce apoptosis in PDAC and provides a rationale for a novel concurrent targeting of the PI3K/AKT and ERK pathways.
  • Teruaki Takasaki; Ryosuke Utsumi; Erika Shimada; Naofumi Tomimoto; Ryosuke Satoh; Reiko Sugiura
    microPublication biology 2022 2022 [Refereed]
     
    Apart from the highly conserved role in the cellular degradation process, autophagy also appears to play a key role in cellular proliferation. Here, we describe the genetic interaction of autophagy-related genes and Pmk1 MAPK signaling in fission yeast. atg1 deletion cells (Δ atg1 ) exhibit the vic (viable in the presence of immunosuppressant and Cl - ) phenotype, indicative of Pmk1 signaling inhibition. Moreover, the Δ atg1 Δ pmk1 double mutant resembles the single Δ pmk1 mutant, suggesting that Atg1 functions in the Pmk1 pathway. In addition, the growth defect induced by overexpression of Pck2, an upstream activator of Pmk1 MAPK was alleviated by the deletion of atg1 + . Finally, the deletion of autophagy-related genes recapitulates Pmk1 MAPK signaling inhibition. Our data suggest a novel role for autophagy in MAPK signaling regulation.
  • Kanako Hagihara; Kousuke Hosonaka; Shuhei Hoshino; Kazuki Iwata; Naoki Ogawa; Ryosuke Satoh; Teruaki Takasaki; Takuya Maeda; Reiko Sugiura
    Biocontrol science 27 (1) 31 - 39 2022 [Refereed]
     
    Calcineurin (CN) is a conserved Ca2+-calmodulin activated protein phosphatase, which plays important roles in immune regulation, cardiac hypertrophy, and apoptosis in humans. In pathogenic fungi, CN is essential for stress survival, sexual development, and virulence. The immunosuppressant tacrolimus (FK506) is a specific inhibitor of CN in humans and fungi including nonpathogenic fission yeast. Although calcineurin inhibition by FK506 or CN deletion in fission yeast does not induce growth defects, treatment with some anti-fungal drugs such as micafungin and valproic acid, induced synthetic lethality with calcineurin inhibition. Here, we searched for the compounds that induce synthetic growth defects with CN inhibition in fission yeast. We found that ellagic acid (EA) preferentially induced growth inhibition in CN deletion cells. Consistently, co-treatment with EA and FK506 induced severe growth inhibition in the wild-type cells, whereas neither of the single treatment with each compound did so. Moreover, deletion of the calcineurin-regulated transcription factor Prz1 also induced a marked EA sensitivity. Intriguingly, EA also enhanced the growth inhibitory effect of other anti-fungal drugs, including micafungin and miconazole. Thus, our data suggesting the synergistic growth inhibitory effect of the calcineurin inhibitor FK506 and EA may be useful to understand the mechanism to overcome the antifungal resistance.
  • Reiko Sugiura; Ryosuke Satoh; Teruaki Takasaki
    Cells 10 (10) 2021/09 [Refereed]
     
    The RAF/MEK/ERK signaling pathway regulates diverse cellular processes as exemplified by cell proliferation, differentiation, motility, and survival. Activation of ERK1/2 generally promotes cell proliferation, and its deregulated activity is a hallmark of many cancers. Therefore, components and regulators of the ERK pathway are considered potential therapeutic targets for cancer, and inhibitors of this pathway, including some MEK and BRAF inhibitors, are already being used in the clinic. Notably, ERK1/2 kinases also have pro-apoptotic functions under certain conditions and enhanced ERK1/2 signaling can cause tumor cell death. Although the repertoire of the compounds which mediate ERK activation and apoptosis is expanding, and various anti-cancer compounds induce ERK activation while exerting their anti-proliferative effects, the mechanisms underlying ERK1/2-mediated cell death are still vague. Recent studies highlight the importance of dual-specificity phosphatases (DUSPs) in determining the pro- versus anti-apoptotic function of ERK in cancer. In this review, we will summarize the recent major findings in understanding the role of ERK in apoptosis, focusing on the major compounds mediating ERK-dependent apoptosis. Studies that further define the molecular targets of these compounds relevant to cell death will be essential to harnessing these compounds for developing effective cancer treatments.
  • Teruaki Takasaki; Naofumi Tomimoto; Takumi Ikehata; Ryosuke Satoh; Reiko Sugiura
    microPublication biology 2021 2021/05 [Refereed]
     
    The molecular chaperone Hsp90 is highly conserved from bacteria to mammals. In fission yeast, Hsp90 is essential in many cellular processes and its expression is known to be increased by heat stress (HS). Here, we describe the distinct spatiotemporal distribution of Hsp90 under high-heat stress (HHS: 45˚C) and mild-heat stress (MHS: 37˚C). Hsp90 is largely distributed in the cytoplasm under non-stressed conditions (27˚C). Under HHS, Hsp90 forms several cytoplasmic granules within 5 minutes, then the granules disappear within 60 minutes. Under MHS, Hsp90 forms fewer granules than under HHS within 5 minutes and strikingly the granules persist and grow in size. In addition, nuclear enrichment of Hsp90 was observed after 60 minutes under both HS conditions. Our data suggest that assembly/disassembly of Hsp90 granules is differentially regulated by temperatures.
  • Yuki Kanda; Ryosuke Satoh; Teruaki Takasaki; Naofumi Tomimoto; Kiko Tsuchiya; Chun An Tsai; Taemi Tanaka; Shu Kyomoto; Kozo Hamada; Toshinobu Fujiwara; Reiko Sugiura
    Journal of Cell Science The Company of Biologists 134 (2) 0021-9533 2021/01 [Refereed]
     
    ABSTRACT Protein kinase C (PKC) signaling is a highly conserved signaling module that plays a central role in a myriad of physiological processes, ranging from cell proliferation to cell death, via various signaling pathways, including MAPK signaling. Stress granules (SGs) are non-membranous cytoplasmic foci that aggregate in cells exposed to environmental stresses. Here, we explored the role of SGs in PKC/MAPK signaling activation in fission yeast. High-heat stress (HHS) induced Pmk1 MAPK activation and Pck2 translocation from the cell tips into poly(A)-binding protein (Pabp)-positive SGs. Pck2 dispersal from the cell tips required Pck2 kinase activity, and constitutively active Pck2 exhibited increased translocation to SGs. Importantly, Pmk1 deletion impaired Pck2 recruitment to SGs, indicating that MAPK activation stimulates Pck2 SG translocation. Consistently, HHS-induced SGs delayed Pck2 relocalization at the cell tips, thereby blocking subsequent Pmk1 reactivation after recovery from HHS. HHS partitioned Pck2 into the Pabp-positive SG-containing fraction, which resulted in reduced Pck2 abundance and kinase activity in the soluble fraction. Taken together, these results indicate that MAPK-dependent Pck2 SG recruitment serves as a feedback mechanism to intercept PKC/MAPK activation induced by HHS, which might underlie PKC-related diseases.
  • Yuki Kanda; Ayami Mizuno; Teruaki Takasaki; Ryosuke Satoh; Kanako Hagihara; Takashi Masuko; Yuichi Endo; Genzoh Tanabe; Reiko Sugiura
    Genes to Cells Wiley 26 (2) 109 - 116 1356-9597 2020/11 [Refereed]
     
    Dual-specificity phosphatase 6 (DUSP6) is a key negative feedback regulator of the member of the RAS-ERK MAPK signaling pathway that is associated with cellular proliferation and differentiation. Deterioration of DUSP6 expression could therefore result in deregulated growth activity. We have previously discovered ACA-28, a novel anticancer compound with a unique property to stimulate ERK phosphorylation and induce apoptosis in ERK-active melanoma cells. However, the mechanism of cancer cell-specific-apoptosis by ACA-28 remains obscure. Here, we investigated the involvement of DUSP6 in the mechanisms of the ACA-28-mediated apoptosis by using the NIH/3T3 cells overexpressing HER2/ErbB2 (A4-15 cells), as A4-15 exhibited higher ERK phosphorylation and are more susceptible to ACA-28 than NIH/3T3. We showed that A4-15 exhibited high DUSP6 protein levels, which require ERK activation. Notably, the silencing of the DUDSP6 gene by siRNA inhibited proliferation and induced apoptosis in A4-15, but not in NIH/3T3, indicating that A4-15 requires high DUSP6 expression for growth. Importantly, ACA-28 preferentially down-regulated the DUSP6 protein and proliferation in A4-15 via the proteasome, while it stimulated ERK phosphorylation. Collectively, the up-regulation of DUSP6 may exert a growth-promoting role in cancer cells overexpressing HER2. DUSP6 down-regulation in ERK-active cancer cells might have the potential as a novel cancer measure.
  • Ryosuke Satoh; Naoya Hamada; Ami Yamada; Yuki Kanda; Fumihiro Ishikawa; Teruaki Takasaki; Genzoh Tanabe; Reiko Sugiura
    Bioorganic chemistry 103 104137 - 104137 2020/07 [Refereed]
     
    The recent discovery that an ERK signaling modulator [ACA-28 (2a)] preferentially kills human melanoma cell lines by inducing ERK-dependent apoptosis has generated significant interest in the field of anti-cancer therapy. In the first SAR study on 2a, here, we successfully developed candidates (2b, 2c) both of which induce more potent and selective apoptosis towards ERK-active melanoma cells than 2a, thus revealing the structural basis for inducing the ERK-dependent apoptosis and proposing the therapeutic prospect of these candidates against ERK-dependent cancers represented by melanoma.
  • Kanako Hagihara; Yuki Kanda; Kouki Ishida; Ryosuke Satoh; Teruaki Takasaki; Takuya Maeda; Reiko Sugiura
    Genes to cells : devoted to molecular & cellular mechanisms 25 (9) 637 - 645 2020/07 [Refereed]
     
    FTY720, a sphingosine-1-phosphate (S1P) analog, is used as an immune modulator to treat multiple sclerosis. Accumulating evidence has suggested the mode of action of FTY720 independent of an S1P modulator. In fission yeast, FTY720 induces an increase in intracellular Ca2+ and ROS levels. We have previously identified 49 genes of which deletion causes FTY720 sensitivity. Here, we characterized the FTY720-sensitive mutants in terms of their relevance to the Ca2+ homeostasis and identified the 16 FTY720- and Ca2+ - sensitive mutants (fcs mutants). Most of the FTY720-sensitive mutants showed elevated Ca2+ levels and exhibited Ca2+ dysregulation by FTY720 treatment. One of the functional categories among the genes whose deletion renders cells susceptible to FTY720 and Ca2+ include the Golgi/endosomal membrane trafficking. Notably, FTY720, but not phosphorylated FTY720 incapable of inducing Ca2+ increase, inhibited the secretion of acid phosphatase in the wild-type cells. Importantly, secretory defects of the Golgi/endosomal trafficking mutants, Vps45, or Ryh1 deletion, were further exacerbated by FTY720. Our fcs mutant screen also identified the adenylyl cyclase-associated protein Cap1 and a Rictor homolog Ste20, whose deletion markedly exacerbated FTY720-sensitive secretory impairment. Collectively, our data may suggest a synergistic impact of FTY720 combined with secretion perturbation on proliferation and Ca2+ homeostasis.
  • Kreher J; Takasaki T; Cockrum C; Sidoli S; Garcia BA; Jensen ON; Strome S
    Genetics 0016-6731 2018/09 [Refereed]
  • Satoh R; Hara N; Kawasaki A; Takasaki T; Sugiura R
    Genes to cells : devoted to molecular & cellular mechanisms 1356-9597 2018/07 [Refereed]
  • Takasaki Teruaki; Hagihara Kanako; Satoh Ryosuke; Sugiura Reiko
    Oxidative medicine and cellular longevity HINDAWI LTD 2018 4397159  1942-0994 2018/03 [Refereed][Invited]
     
    Fingolimod hydrochloride (FTY720) is a first-in-class of sphingosine-1-phosphate (S1P) receptor modulator approved to treat multiple sclerosis by its phosphorylated form (FTY720-P). In this review, we introduce our recent discoveries using a chemical genomics approach to uncover a signaling network relevant to FTY720-mediated ROS signaling and apoptosis, thereby proposing new potential targets for combination therapy as a means to enhance the antitumor efficacy of FTY720 as a ROS generator. We extend our knowledge by summarizing various measures targeting the vulnerability of cancer cells' defense mechanisms against oxidative stress. Future directions that may lead to the best use of FTY720 and ROS-targeted strategies as a promising cancer treatment are also discussed.
  • Hagihara K; Kinoshita K; Ishida K; Hojo S; Kameoka Y; Satoh R; Takasaki T; Sugiura R
    Microbial cell (Graz, Austria) 4 (12) 390 - 401 2017/11 [Refereed]
  • Takashi Miwa; Teruaki Takasaki; Kunio Inoue; Hiroshi Sakamoto
    GENES TO CELLS WILEY-BLACKWELL 20 (11) 932 - 942 1356-9597 2015/11 [Refereed]
     
    The chromodomain protein MRG-1 is an essential maternal factor for proper germline development that protects germ cells from cell death in C.elegans. Unlike germ granules, which are exclusively segregated to the germline blastomeres at each cell division from the first cleavage of the embryo, MRG-1 is abundant in all cells in early embryos and is then gradually restricted to the primordial germ cells (PGCs) by the morphogenesis stage. Here, we show that this characteristic spatiotemporal expression pattern is dictated by the mrg-1 3'UTR and is differentially regulated at the RNA level between germline and somatic cells. Asymmetric segregation of germ granules is not necessary to localize MRG-1 to the PGCs. We found that MES-4, an essential chromatin regulator in germ cells, also accumulates in the PGCs in a germ granule-independent manner. We propose that C.elegans PGCs have a novel mechanism to accumulate at least some chromatin-associated proteins that are essential for germline immortality.
  • Tao Liu; Andreas Rechtsteiner; Thea A. Egelhofer; Anne Vielle; Isabel Latorre; Ming-Sin Cheung; Sevinc Ercan; Kohta Ikegami; Morten Jensen; Paulina Kolasinska-Zwierz; Heidi Rosenbaum; Hyunjin Shin; Scott Taing; Teruaki Takasaki; A. Leonardo Iniguez; Arshad Desai; Abby F. Dernburg; Hiroshi Kimura; Jason D. Lieb; Julie Ahringer; Susan Strome; X. Shirley Liu
    GENOME RESEARCH COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT 21 (2) 227 - 236 1088-9051 2011/02 [Refereed]
     
    Chromatin immunoprecipitation identifies specific interactions between genomic DNA and proteins, advancing our understanding of gene-level and chromosome-level regulation. Based on chromatin immunoprecipitation experiments using validated antibodies, we define the genome-wide distributions of 19 histone modifications, one histone variant, and eight chromatin-associated proteins in Caenorhabditis elegans embryos and L3 larvae. Cluster analysis identified five groups of chromatin marks with shared features: Two groups correlate with gene repression, two with gene activation, and one with the X chromosome. The X chromosome displays numerous unique properties, including enrichment of monomethylated H4K20 and H3K27, which correlate with the different repressive mechanisms that operate in somatic tissues and germ cells, respectively. The data also revealed striking differences in chromatin composition between the autosomes and between chromosome arms and centers. Chromosomes I and III are globally enriched for marks of active genes, consistent with containing more highly expressed genes, compared to chromosomes II, IV, and especially V. Consistent with the absence of cytological heterochromatin and the holocentric nature of C. elegans chromosomes, markers of heterochromatin such as H3K9 methylation are not concentrated at a single region on each chromosome. Instead, H3K9 methylation is enriched on chromosome arms, coincident with zones of elevated meiotic recombination. Active genes in chromosome arms and centers have very similar histone mark distributions, suggesting that active domains in the arms are interspersed with heterochromatin-like structure. These data, which confirm and extend previous studies, allow for in-depth analysis of the organization and deployment of the C. elegans genome during development.
  • Mark B. Gerstein; Zhi John Lu; Eric L. Van Nostrand; Chao Cheng; Bradley I. Arshinoff; Tao Liu; Kevin Y. Yip; Rebecca Robilotto; Andreas Rechtsteiner; Kohta Ikegami; Pedro Alves; Aurelien Chateigner; Marc Perry; Mitzi Morris; Raymond K. Auerbach; Xin Feng; Jing Leng; Anne Vielle; Wei Niu; Kahn Rhrissorrakrai; Ashish Agarwal; Roger P. Alexander; Galt Barber; Cathleen M. Brdlik; Jennifer Brennan; Jeremy Jean Brouillet; Adrian Carr; Ming-Sin Cheung; Hiram Clawson; Sergio Contrino; Luke O. Dannenberg; Abby F. Dernburg; Arshad Desai; Lindsay Dick; Andrea C. Dose; Jiang Du; Thea Egelhofer; Sevinc Ercan; Ghia Euskirchen; Brent Ewing; Elise A. Feingold; Reto Gassmann; Peter J. Good; Phil Green; Francois Gullier; Michelle Gutwein; Mark S. Guyer; Lukas Habegger; Ting Han; Jorja G. Henikoff; Stefan R. Henz; Angie Hinrichs; Heather Holster; Tony Hyman; A. Leo Iniguez; Judith Janette; Morten Jensen; Masaomi Kato; W. James Kent; Ellen Kephart; Vishal Khivansara; Ekta Khurana; John K. Kim; Paulina Kolasinska-Zwierz; Eric C. Lai; Isabel Latorre; Amber Leahey; Suzanna Lewis; Paul Lloyd; Lucas Lochovsky; Rebecca F. Lowdon; Yaniv Lubling; Rachel Lyne; Michael MacCoss; Sebastian D. Mackowiak; Marco Mangone; Sheldon Mckay; Desirea Mecenas; Gennifer Merrihew; David M. Miller; Andrew Muroyama; John I. Murray; Siew-Loon Ooi; Hoang Pham; Taryn Phippen; Elicia A. Preston; Nikolaus Rajewsky; Gunnar Raetsch; Heidi Rosenbaum; Joel Rozowsky; Kim Rutherford; Peter Ruzanov; Mihail Sarov; Rajkumar Sasidharan; Andrea Sboner; Paul Scheid; Eran Segal; Hyunjin Shin; Chong Shou; Frank J. Slack; Cindie Slightam; Richard Smith; William C. Spencer; E. O. Stinson; Scott Taing; Teruaki Takasaki; Dionne Vafeados; Ksenia Voronina; Guilin Wang; Nicole L. Washington; Christina M. Whittle; Beijing Wu; Koon-Kiu Yan; Georg Zeller; Zheng Zha; Mei Zhong; Xingliang Zhou; Julie Ahringer; Susan Strome; Kristin C. Gunsalus; Gos Micklem; X. Shirley Liu; Valerie Reinke; Stuart K. Kim; LaDeana W. Hillier; Steven Henikoff; Fabio Piano; Michael Snyder; Lincoln Stein; Jason D. Lieb; Robert H. Waterston
    SCIENCE AMER ASSOC ADVANCEMENT SCIENCE 330 (6012) 1775 - 1787 0036-8075 2010/12 [Refereed]
     
    We systematically generated large-scale data sets to improve genome annotation for the nematode Caenorhabditis elegans, a key model organism. These data sets include transcriptome profiling across a developmental time course, genome-wide identification of transcription factor-binding sites, and maps of chromatin organization. From this, we created more complete and accurate gene models, including alternative splice forms and candidate noncoding RNAs. We constructed hierarchical networks of transcription factor-binding and microRNA interactions and discovered chromosomal locations bound by an unusually large number of transcription factors. Different patterns of chromatin composition and histone modification were revealed between chromosome arms and centers, with similarly prominent differences between autosomes and the X chromosome. Integrating data types, we built statistical models relating chromatin, transcription factor binding, and gene expression. Overall, our analyses ascribed putative functions to most of the conserved genome.
  • Andreas Rechtsteiner; Sevinc Ercan; Teruaki Takasaki; Taryn M. Phippen; Thea A. Egelhofer; Wenchao Wang; Hiroshi Kimura; Jason D. Lieb; Susan Strome
    PLOS GENETICS PUBLIC LIBRARY SCIENCE 6 (9) 1553-7390 2010/09 [Refereed]
     
    Methylation of histone H3K36 in higher eukaryotes is mediated by multiple methyltransferases. Set2-related H3K36 methyltransferases are targeted to genes by association with RNA Polymerase II and are involved in preventing aberrant transcription initiation within the body of genes. The targeting and roles of the NSD family of mammalian H3K36 methyltransferases, known to be involved in human developmental disorders and oncogenesis, are not known. We used genome-wide chromatin immunoprecipitation (ChIP) to investigate the targeting and roles of the Caenorhabditis elegans NSD homolog MES-4, which is maternally provided to progeny and is required for the survival of nascent germ cells. ChIP analysis in early C. elegans embryos revealed that, consistent with immunostaining results, MES-4 binding sites are concentrated on the autosomes and the leftmost similar to 2% (300 kb) of the X chromosome. MES-4 overlies the coding regions of approximately 5,000 genes, with a modest elevation in the 59 regions of gene bodies. Although MES-4 is generally found over Pol II-bound genes, analysis of gene sets with different temporal-spatial patterns of expression revealed that Pol II association with genes is neither necessary nor sufficient to recruit MES-4. In early embryos, MES-4 associates with genes that were previously expressed in the maternal germ line, an interaction that does not require continued association of Pol II with those loci. Conversely, Pol II association with genes newly expressed in embryos does not lead to recruitment of MES-4 to those genes. These and other findings suggest that MES-4, and perhaps the related mammalian NSD proteins, provide an epigenetic function for H3K36 methylation that is novel and likely to be unrelated to ongoing transcription. We propose that MES-4 transmits the memory of gene expression in the parental germ line to offspring and that this memory role is critical for the PGCs to execute a proper germline program.
  • Hirofumi Furuhashi; Teruaki Takasaki; Andreas Rechtsteiner; Tengguo Li; Hiroshi Kimura; Paula M. Checchi; Susan Strome; William G. Kelly
    EPIGENETICS & CHROMATIN BIOMED CENTRAL LTD 3 (1) 15  1756-8935 2010/08 [Refereed]
     
    Background: The processes through which the germline maintains its continuity across generations has long been the focus of biological research. Recent studies have suggested that germline continuity can involve epigenetic regulation, including regulation of histone modifications. However, it is not clear how histone modifications generated in one generation can influence the transcription program and development of germ cells of the next. Results: We show that the histone H3K36 methyltransferase maternal effect sterile (MES)-4 is an epigenetic modifier that prevents aberrant transcription activity in Caenorhabditis elegans primordial germ cells (PGCs). In mes-4 mutant PGCs, RNA Pol II activation is abnormally regulated and the PGCs degenerate. Genetic and genomewide analyses of MES-4-mediated H3K36 methylation suggest that MES-4 activity can operate independently of ongoing transcription, and may be predominantly responsible for maintenance methylation of H3K36 in germline-expressed loci. Conclusions: Our data suggest a model in which MES-4 helps to maintain an 'epigenetic memory' of transcription that occurred in germ cells of previous generations, and that MES-4 and its epigenetic product are essential for normal germ cell development.
  • A simple yet effective method to harvest worms from a liquid culture
    Takasaki, T; Fujiwara, T; Strome, S
    Worm Breeder’s Gazette 18 (2) 6 - 6 2010/06
  • Teruaki Takasaki; Zheng Liu; Yasuaki Habara; Kiyoji Nishiwaki; Jun-ichi Nakayama; Kunio Inoue; Hiroshi Sakamoto; Susan Strome
    DEVELOPMENT COMPANY OF BIOLOGISTS LTD 134 (4) 757 - 767 0950-1991 2007/02 [Refereed]
     
    MRG15, a mammalian protein related to the mortality factor MORF4, is required for cell proliferation and embryo survival. Our genetic analysis has revealed that the Caenorhabditis elegans ortholog MRG-1 serves similar roles. Maternal MRG-1 promotes embryo survival and is required for proliferation and immortality of the primordial germ cells (PGCs). As expected of a chromodomain protein, MRG-1 associates with chromatin. Unexpectedly, it is concentrated on the autosomes and not detectable on the X chromosomes. This association is not dependent on the autosome-enriched protein MES-4. Focusing on possible roles of MRG-1 in regulating gene expression, we determined that MRG-1 is required to maintain repression in the maternal germ line of transgenes on extrachromosomal arrays, and of several X-linked genes previously shown to depend on MES-4 for repression. MRG-1 is not required for PGCs to acquire transcriptional competence or for the turn-on of expression of several PGC-expressed genes (pgl-1, glh-1, glh-4 and nos-1). By contrast to this result in PGCs, MRG-1 is required for ectopic expression of those germline genes in somatic cells lacking the NuRD complex component MEP-1. We discuss how an autosome-enriched protein might repress genes on the X chromosome, promote PGC proliferation and survival, and influence the germ versus soma distinction.
  • Masaki Fujita; Teruaki Takasaki; Noboru Nakajima; Taizo Kawano; Yoshiro Shimura; Hiroshi Sakamoto
    Mechanisms of Development Elsevier Ireland Ltd 120 (3) 397  0925-4773 2003 [Refereed]
  • M Fujita; T Takasaki; N Nakajima; T Kawano; Y Shimura; H Sakamoto
    MECHANISMS OF DEVELOPMENT ELSEVIER SCIENCE BV 114 (1-2) 61 - 69 0925-4773 2002/06 [Refereed]
     
    We identified MRG-1, a Caenorhabditis elegans chromodomain-containing protein that is similar to the human mortality factor-related gene 15 product (MRG15). RNA-mediated interference (RNAi) of mrg-1 resulted in complete absence of the germline in both hermaphrodite and male adults. Examination of the expression of PGL-1, a component of P granules, revealed that two primordial germ cells (PGCs) are produced during embryogenesis in mrg-1(RNAi) animals, but these PGCs cannot undergo mitotic proliferation, and they ultimately degenerate during post-embryonic development. Zygotic RNAi experiments using RNAi-deficient hermaphrodites and wild-type males demonstrated that MRG-1 functions maternally. Moreover, immunoblot analysis using mutant animals with germline deficiencies indicated that MRG-1 is synthesized predominantly in oocytes. These results suggest that MRG-1 is required maternally to form normal PGCs with the potential to start mitotic proliferation during post-embryonic development. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

MISC

Books and other publications

Lectures, oral presentations, etc.

  • Role of DNA damage response protein BRAT1 in the mechanisms of cell death induced by a novel anticancer compound ACAGT-007a
    田中達也; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    第97回 日本薬理学会年会  2023/12
  • 新規抗がん剤候補化合物ACAGT-007aによるROSを介した細胞死誘導におけるDNA損傷応答タンパク質BRAT1の役割  [Not invited]
    田中達也; 佐藤亮介; 高崎輝恒; 杉浦麗子; 杉浦麗子
    第46回日本分子生物学会年会  2023/12
  • RNA結合タンパクRnc1のストレス顆粒移行とリン酸化の関係  [Not invited]
    吉田展康; 川崎有紀; 原信樹; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第46回日本分子生物学会年会  2023/12
  • バルプロ酸によるα-シヌクレインの毒性と凝集体形成への影響~α-シヌクレインと細胞内輸送機構・糖鎖修飾の関わり~  [Not invited]
    山田南; 杉本恵崇; 黒崎亮; 高崎輝恒; 佐藤亮介; 杉浦麗子
    第46回日本分子生物学会年会  2023/12
  • 熱ストレス応答タンパク質 Hsp90 は酸化ストレス条件下で凝集体を形成する ―Hsp90 と MAPK シグナル伝達経路の機能的関わりの解明に向けて―
    壽 美月; 冨本尚史; 高崎輝恒; 佐藤亮介; 杉浦麗子
    2023/10
  • 新規抗がん剤候補化合物 ACAGT-007a による細胞死誘導への BRAT1 の関与
    田中達也; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第73回薬学会関西支部総会・大会  2023/10
  • 新規抗がん剤シーズ ACA-28 の ERK 依存的細胞死誘導機構の解析 ―CRM1 依存的核外輸送レポーターPap1 を用いた核外輸送阻害活性の評価―
    尾花玲緒; 高崎輝恒; 冨本尚史; 佐藤亮介; 杉浦麗子
    第73回薬学会関西支部総会・大会  2023/10
  • 抗がん剤候補化合物 ACA-28 による細胞死誘導機構と小胞体ストレス応答経路の関わり ―骨肉腫由来細胞株を用いて―
    河合瑛美; 高崎輝恒; 上山紗依; 上野七海; 佐藤亮介; 杉浦麗子
    第73回薬学会関西支部総会・大会  2023/10
  • ERK: A DOUBLE-EDGED SWORD IN CANCER. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer  [Invited]
    Teruaki Takasaki; Golam Iftakhar Khandakar; Sae Kamiyama; Ryosuke Satoh; Reiko Sugiura
    The Protein Phosphatases Conference Jointly hosted by FASEB and the Japanese Association for Protein Phosphatase Research (JAPPR)  2022/12
  • FISSION YEAST PUF PROTEINS PUF3 AND PUF4 ARE NOVEL REGULATORS OF PI4P5K SIGNALING
    Ryosuke Satoh; Taemi Tanaka; Nobuyasu Yoshida; Teruaki Takasaki; Reiko Sugiura
    The Protein Phosphatases Conference Jointly hosted by FASEB and the Japanese Association for Protein Phosphatase Research (JAPPR)  2022/12
  • ACAGT-007a, A NEW ERK MAPK SIGNALING MODULATOR, WHEN COMBINED WITH AKT SIGNALING INHIBITOR, INHIBITS CELL GROWTH AND TRIGGERS APOPTOSIS IN PANCREATIC CANCER CELLS
    Golam Iftakhar Khandakar; Ryosuke Satoh; Teruaki Takasaki; Kana Fujitani; Shih Mengyu; Genzoh Tanabe; Kazuko Sakai; Kazuto Nishio; Yoichi Miyamoto; Masahiro Oka; Reiko Sugiura
    The Protein Phosphatases Conference Jointly hosted by FASEB and the Japanese Association for Protein Phosphatase Research (JAPPR)  2022/12
  • ACA-28, A NOVEL ANTI-CANCER COMPOUND, INDUCES ERK- OR AUTOPHAGY-DEPENDENT APOPTOSIS DEPENDING ON THE CELL TYPES ON OSTEOSARCOMA
    Sae Kamiyama; Teruaki Takasaki; Golam Iftakhar Khandakar; Nanami Ueno; Eimi Kawai; Ryosuke Satoh; Toshihiro Akisue; Reiko Sugiura
    The Protein Phosphatases Conference Jointly hosted by FASEB and the Japanese Association for Protein Phosphatase Research (JAPPR)  2022/12
  • REGULATION OF PKC/MAPK SIGNALING BY PHASE SEPARATION MEDIATED BY AN RNA HELICASE Ded1
    Naofumi Tomimoto; Teruaki Takasaki; Ryosuke Satoh; Reiko Sugiura
    The Protein Phosphatases Conference Jointly hosted by FASEB and the Japanese Association for Protein Phosphatase Research (JAPPR)  2022/12
  • ACA-28とその誘導体ACAGT-007aはがん細胞におけるERK MAPKシグナルのさらなる活性化を介してアポトーシスを誘導する
    佐藤 亮介; カンダカール イフタカール; 石川 文洋; 高崎 輝恒; 田邉 元三; 杉浦 麗子
    第45回日本分子生物学会年会  2022/12
  • Lewy小体病の発症機序の解明に向けたα-シヌクレイン(α-Syn)の凝集能低下型変異タンパク質を発現する分裂酵母株の作成
    杉本 恵崇; 高崎 輝恒; 黒崎 亮; 巽 祐司; 山田 南; 佐藤 亮介; 杉浦 麗子
    第45回日本分子生物学会年会  2022/11
  • MAPK活性依存的抗がん剤シーズACA-28がMAPKシグナル上流因子の輸送に与える影響
    藤原 大輝; 高崎 輝恒; 冨本 尚史; Golam Iftakhar Khandakar; 佐藤 亮介; 岡 正啓; 杉浦 麗子
    第45回日本分子生物学会年会  2022/11
  • ERK MAPKシグナル調節薬ACA-28による活性化ERKの細胞内動態の可視化とExportinの関わり
    謝 明作; カンダカール ゴラム; イフタカール; 岸本 健太; 佐藤 亮介; 高崎 輝恒; 田邉 元三; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • RNA結合タンパクPuf3とPuf4はホスファチジルイノシトール4リン酸キナーゼ(PI4P5K)の発現量を調節する
    吉田 展康; 佐藤 亮介; 田中 妙美; 高崎 輝恒; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • 細胞内輸送と糖鎖修飾に着目したα-シヌクレインによる細胞傷害メカニズムの解析
    山田 南; 高崎 輝恒; 杉本 恵祟; 黒崎 亮; 巽 祐司; 壽 美月; 佐藤 亮介; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • α-synが引き起こす細胞死を増強する細胞内輸送経路のステップの特定
    巽 祐司; 高崎 輝恒; 杉本 恵崇; 黒崎 亮; 山田 南; 壽 美月; 佐藤 亮介; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • 新規抗がん剤候補化合物ACAGT-007aによる膵がん細胞T3M4のアポトーシス誘導機構に関する解析
    石 孟玉; Khandakar Golam; Iftakhar; 謝 明作; 岸本 健太; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • ERK MAPKシグナル調節化合物ACA-28によるVimentinのリン酸化誘導
    芝本 雄威; 田中 達也; 佐藤 亮介; 高崎 輝恒; 足立 淳; 朝長 毅; 杉浦 麗子
    第142回日本薬理学会近畿部会  2022/11
  • ERK MAPKシグナル調節化合物ACA-28によるVimentinのリン酸化誘導
    芝本 雄威; 田中 達也; 佐藤 亮介; 高崎 輝恒; 足立 淳; 朝長 毅; 杉浦 麗子
    第72回日本薬学会関西支部総会・大会  2022/10
  • ERK MAPK活性依存的抗がん剤シーズACA-28のCRM1依存的核外輸送阻害活性の評価
    藤原 大輝; 高崎 輝恒; 冨本 尚史; Golam Iftakhar Khandaka; 佐藤 亮介; 岡 正啓; 杉浦 麗子
    第72回日本薬学会関西支部総会・大会  2022/10
  • its3-1の解析から浮かび上がったPI4P代謝経路とPI3P代謝経路のクロストーク
    田中妙美; 佐藤亮介; 吉田展康; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第55回研究報告会  2022/09
  • 濃度依存的なPck2の相分離が引き起こす細胞毒性とRNA helicase Ded1の関係
    冨本尚史; 高崎輝恒; 佐藤亮介; 杉浦麗子
    酵母遺伝学フォーラム第55回研究報告会  2022/09
  • RNA結合タンパク質Puf3とPuf4はPI4P5KのmRNA発現量を調節する
    佐藤亮介; 田中妙美; 吉田展康; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第55回研究報告会  2022/09
  • PKC/Pck2がストレス顆粒へ移行するメカニズムとPKC/MAPKシグナルの負のフィードバック機構の解析
    冨本 尚史; 神田 勇輝; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    日本薬学会年会要旨集  2022/03  (公社)日本薬学会
  • 核外輸送システムに注目した新規抗がん剤シーズACA-28のERK MAPK経路調節機構の解析
    藤原大輝; 髙崎輝恒; 冨本尚史; 豊田教幹; Golam Khandakar; 佐藤亮介; 岡正啓; 米田悦啓; 杉浦麗子
    第44回日本分子生物学会年会  2021/12
  • パーキンソン病の分裂酵母モデル系を用いたα-シヌクレインの凝集抑制や細胞障害の軽減を目的とした医薬品の探索
    杉本恵崇; 髙崎輝恒; 黒崎亮; 垂井祐大; 巽祐司; 佐藤亮介; 杉浦麗子
    第44回日本分子生物学会年会  2021/12
  • 新規がん治療薬候補化合物ACA-28が骨肉腫細胞において誘導するアポトーシスとオートファジーの関わり
    上山紗依; 髙崎輝恒; 上野七海; 佐藤亮介; 秋末敏宏; 杉浦麗子
    第44回日本分子生物学会年会  2021/12
  • Pck2/PKC過剰発現依存的な細胞増殖抑制はDEAD-box型RNA helicase DDX3/Ded1を介して回復する
    冨本尚史; 神田勇輝; 佐藤亮介; 髙崎輝恒; Chun Tsai; 梅田茉実; 杉浦麗子
    第44回日本分子生物学会年会  2021/12
  • ACAGT-007a, an ERK MAPK Signaling Modulator, when combined with AKT Signaling Inhibitor, Promotes Antitumor Activity in Pancreatic Cancer Cells
    Golam Khandakar; Ryosuke Satoh; Teruaki Takasaki; Kana Fujitani; Genzo Tanabe; Reiko Sugiura
    第44回日本分子生物学会年会  2021/12
  • 分裂酵母モデル系を用いたα-シヌクレインの凝集や細胞障害を抑制する医薬品の探索とその作用メカニズムの解明
    杉本恵崇; 髙崎輝恒; 黒崎亮; 垂井祐大; 巽祐司; 佐藤亮介; 杉浦麗子
    第140回日本薬理学会近畿部会  2021/11
  • MAPKシグナル活性化因子Protien Kinase Cの時空間的制御機構におけるストレス顆粒の役割
    神田勇輝; 冨本尚史; 佐藤亮介; 髙崎輝恒; 杉浦麗子
    第140回日本薬理学会近畿部会  2021/11
  • Combination of ACAGT-007a, a novel ERK signaling modulator, with AKT signaling inhibitor effectively induces apoptosis in pancreatic cancer cells
    Khandakar Golam Iftakhar; 藤谷佳奈; 佐藤亮介; 髙崎輝恒; 田邊元三; 杉浦麗子
    第140回日本薬理学会近畿部会  2021/11
  • ストレス顆粒を介したPKC/MAPKシグナル制御機構メカニズムの解析 ーRNA helicase Ded1がPck2の過剰発現依存的な細胞増殖抑制から回復させるー
    冨本尚史; 神田勇輝; 佐藤亮介; 髙崎輝恒; Chun An Tsai; 梅田茉実; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • 核外輸送システムに注目した新規抗がん剤シーズACA-28のERK依存的細胞死誘導作用の解析
    藤原大輝; 髙崎輝恒; Golam Iftakar Khandakar; 神田勇輝; 佐藤亮介; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • 新規抗がん剤候補化合物ACA-28がERK活性化依存的細胞死を誘導するメカニズムの探索
    安藤成美; 佐藤亮介; 髙崎輝恒; 芝本雄威; 足立淳; 朝長毅; 田邊元三; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • Acremomannolipin Aによる細胞死誘導機構におけるCaMKの関わり
    中塚華蓮; 髙崎輝恒; 濱田構造; 佐藤亮介; 高島克輝; 田邊元三; 鎌田春彦; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • 分裂酵母モデル系を用いたαシヌクレイン凝集体の細胞毒性を増強する因子の探索 ーパーキンソン病治療薬を目指したαシヌクレイン凝集抑制因子の探索に向けてー
    垂井祐大; 髙崎輝恒; 杉本恵崇; 黒崎亮; 佐藤亮介; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • ERK経路の活性化を介した新規アポトーシス誘導剤ACA-28の構造活性相関
    大西里奈; 佐藤亮介; 髙崎輝恒; 芝本雄威; 田邊元三; 杉浦麗子
    第71回日本薬学会関西支部総会・大会  2021/10
  • 新規抗がん剤シーズACAGT-007aの膵臓癌細胞に対する効果とアポトーシス誘導機構:ERK MAPKシグナルおよびPI3K/AKTシグナルの関わり
    藤谷佳奈; Khandakar Golam; Iftakhar; 佐藤亮介; 髙崎輝恒; 田邊元三; 杉浦麗子
    第139回日本薬理学会近畿部会  2021/06
  • 新規抗がん剤シーズACA-28のERK依存的抗がん活性と核外移行システムの関わり
    藤原 大輝; 高崎 輝恒; Golam Iftakhar Khandakar; 神田 勇輝; 佐藤 亮介; 杉浦 麗子
    第139回日本薬理学会近畿部会  2021/06
  • 新規ERK活性調節剤ACA-28は骨肉腫由来細胞株においてアポトーシスとオートファジーを誘導する
    上山紗依; 上野七海; 當内健太; 高崎輝恒; 佐藤亮介; 秋末敏宏; 杉浦麗子
    第139回日本薬理学会近畿部会  2021/06
  • ストレス顆粒構成因子RNA helicase Ded1とPKC/MAPKシグナル制御機構の関係
    冨本尚史; 神田勇輝; 佐藤亮介; 高崎輝恒; Chun An Tsai; 梅田茉美; 杉浦麗子
    第139回日本薬理学会近畿部会  2021/06
  • RNA結合タンパク質Puf4による酸化ストレス応答に関わるシグナル制御機構の探索
    土屋葵子; 高崎輝恒; 佐藤亮介; 神田勇輝; Deiter A. Wolf; 杉浦 麗子
    第139回日本薬理学会近畿部会  2021/06
  • 新規抗がん剤シーズACA-28の骨肉腫細胞における細胞死誘導機構の解析
    上山紗依; 當内健太; 上野七海; 高崎輝恒; 佐藤亮介; 秋末敏宏; 杉浦麗子
    第67回日本生化学会近畿支部例会  2021/05
  • RNA結合タンパク質Puf4による酸化ストレス応答に関わるシグナル制御機の探索
    土屋葵子; 高崎輝恒; 佐藤亮介; 神田勇輝; Deiter A. Wolf; 杉浦 麗子
    第67回日本生化学会近畿支部例会  2021/05
  • PKC/MAPKシグナル制御におけるRNA helicase Ded1とストレス顆粒の役割
    冨本尚史; 神田勇輝; 佐藤亮介; 高崎輝恒; Chun An Tsai; 梅田茉美; 杉浦麗子
    第67回日本生化学会近畿支部例会  2021/05
  • Chemical genetic analysis of FTY720- and Ca2+-sensitive mutants reveals a functional connection between FTY720 and membrane trafficking
    Kanako Hagihara; Yuki Kanda; Kouki Ishida; Ryosuke Satoh; Teruaki Takasaki; Takuya Maeda; Reiko Sugiura
    The 14th International Conference on Protein Phosphatase (ICPP14)  2020/12
  • Impacts of ACA-28 derivatives on the ERK MAPK & PI3K/AKT signaling pathways in pancreatic cancer cells
    Golam Iftakhar Khandakar; Ayami Mizuno; Ryosuke Satoh; Teruaki Takasaki; Genzo Tanabe; Reiko Sugiura
    The 14th International Conference on Protein Phosphatase (ICPP14)  2020/12
  • The MAPK Phosphatase DUSP6 plays an important role in the mechanisms of apoptosis induced by a novel anti-cancer compound ACA-28
    Ayami Mizuno; Yuki Kanda; Riho Miyamoto; Daiki Hujiwara; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    The 14th International Conference on Protein Phosphatase (ICPP14)  2020/12
  • PKC / MAPK signal suppression mechanism via the DEAD-box RNA helicase DDX3/Ded1
    Naofumi Tomimoto; Yuki Kanda; Chun An Tsai; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    The 14th International Conference on Protein Phosphatase (ICPP14)  2020/12
  • Importance of the activation-loop phosphorylation of Pck2/PKC for the stress granule translocation
    Shu Kyomoto; Yuki Kanda; Naofumi Tomimoto; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    The 14th International Conference on Protein Phosphatase (ICPP14)  2020/12
  • 新規ERKシグナル調節薬ACA-28のERK活性化がん細胞に対するアポトーシス誘導活性とその作用機構の解析
    濱田 直弥; 佐藤 亮介; 高崎 輝恒; 田邉 元三; 足立 淳; 朝長 毅; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • ERK経路の活性化によりヒトメラノーマのアポトーシスを強力かつ選択的に誘導する新規ベンズヒドロール誘導体の発見
    佐藤 亮介; 濱田 直弥; 石川 文洋; 高崎 輝恒; 田邉 元三; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • 新規抗がん剤候補化合物ACA-28依存的なアポトーシス誘導機構におけるMAPK Phosphatase DUSP6の役割
    水野 綾美; 神田 勇輝; 高崎 輝恒; 宮本 理穂; 藤原 大輝; 佐藤 亮介; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • DEAD-box型タンパク質DDX3/Ded1によるPKC/MAPKシグナル制御メカニズムの解析
    冨本 尚史; 神田 勇輝; AN TSAI Chun; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • ERKシグナル調節薬ACA-28を介するERK依存的細胞死とNRF-2経路の関わり
    當内 健太; 森 梓; 上山 紗依; 萩原 加奈子; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • 酵母遺伝学から明らかとなったカルシニューリン抑制因子RCAN1ホモログの新たな機能  [Invited]
    高崎 輝恒; 久木田 優香; 野田 章博; 眞鍋 涼; 佐藤 亮介; 杉浦 麗子
    第43回日本分子生物学会年会  2020/12
  • ダウン症候群関連遺伝子Rcn1のカルシニューリン依存的、非依存的な酸化ストレス応答機構の解析
    久木田 優香; 高崎 輝恒; 野田 章博; 佐藤 亮介; 杉浦 麗子
    第138回日本薬理学会近畿部会  2020/11
  • PKC/MAPKシグナル活性調節におけるストレス顆粒の役割
    Tsai Chun A; 神田 勇輝; 冨本 尚史; 田中 妙美; 土屋 葵子; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    第138回日本薬理学会近畿部会  2020/11
  • MAPKシグナルを標的としたがん細胞増殖抑制効果を有する天然物抽出成分の探索
    山本 真鈴; 高崎 輝恒; 藪野 真也; 佐藤 亮介; 遠藤 雄一; 杉浦 麗子
    第138回日本薬理学会近畿部会  2020/11
  • RRNA結合タンパク質Puf4による酸化ストレス応答シグナル制御機構の探索
    土屋 葵子; 神田 勇輝; 佐藤 亮介; 高崎 輝恒; Dieter A. Wol; 杉浦 麗子
    第138回日本薬理学会近畿部会  2020/11
  • 骨肉腫細胞に対するACA-28の細胞増殖抑制効果と作用機序の解析
    上山 紗依; 當内 健太; 高崎 輝恒; 佐藤 亮介; 秋末 敏宏; 杉浦 麗子
    第138回日本薬理学会近畿部会  2020/11
  • Puf4による酸化ストレス応答シグナル制御機構の探索
    土屋葵子; 神田勇輝; 佐藤亮介; 髙崎輝恒; Dieter A Wolf; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • 骨肉腫細胞に対するACA-28の細胞増殖抑制効果と作用機序の解明
    上山紗依; 當内健太; 髙崎輝恒; 佐藤亮介; 秋末敏宏; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • 新規ERKシグナル調節薬ACA-28の適応拡大と細胞死誘導機構の解析
    濵田直弥; 佐藤亮介; 髙崎輝恒; 田邉元三; 足立淳; 朝長毅; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • ERKシグナル調節薬ACA-28はERK依存的細胞死と抗酸化転写因子NRF-2依存的遺伝子発現を誘導する
    當内健太; 森梓; 上山紗依; 佐藤亮介; 髙崎輝恒; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • 新規抗がん剤候補化合物ACA-28依存的なアポトーシス誘導機構におけるMAPK Phosphatase DUSP6の役割
    水野綾美; 宮本理穂; 藤原大樹; 神田勇輝; 髙崎輝恒; 佐藤亮介; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • RNA helicase活性低下型Ded1DAAD変異はPmk1 MAPKシグナルを正に制御する
    冨本尚史; 神田勇輝; Tsai Chun An; 佐藤亮介; 髙崎輝恒; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • 新規抗がん剤シーズACA-28に対する各種がん細胞の感受性と脱リン酸化酵素DUSPの関わり
    藤原大輝; 水野綾美; 神田勇輝; 濵田直弥; 髙崎輝恒; 佐藤亮介; 杉浦麗子
    第70回 日本薬学会関西支部大会  2020/10
  • DEAD-box型RNA helicase DDX3/Ded1はPKC/Pck2をSGへ移行する働きを持つ
    冨本 尚史; 神田 勇輝; Tsai Chun An; 佐藤 亮介; 高崎 輝恒; 杉浦 麗子
    日本生化学会大会プログラム・講演要旨集  2020/09  (公社)日本生化学会
  • 新規ERKシグナル調節薬ACA-28が多様なERK活性化癌細胞に対してERK依存的細胞死を引き起こす分子機構についての解析  [Not invited]
    濵田直弥; 佐藤亮介; 高崎輝恒; 田邉元三; 杉浦麗子
    第136回日本薬理学会近畿部会  2019/11
  • オートファジー関連因子Atg1のMAPK経路およびCa2+/カルシニューリンシグナル制御因子としての新たな働き  [Not invited]
    嶋田絵理香; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第136回日本薬理学会近畿部会  2019/11
  • 新規抗がん剤候補化合物ACA-28依存的なアポトーシス誘導機構におけるMAPK Phosphatase DUSP6の役割  [Not invited]
    水野綾美; 宮本理穂; 神田勇輝; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第136回日本薬理学会近畿部会  2019/11
  • 新規ERK活性調節剤ACA-28によるメラノーマ細胞特異的細胞死誘導機構の解析  [Not invited]
    當内健太; 森梓; 萩原加奈子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第69回日本薬学会関西支部総会・大会  2019/10
  • α-EndosulfineホモログIgo1が酸化ストレス耐性をどのように獲得するのか ーリン酸化依存的な調節機構についてー  [Not invited]
    田原彩花; 當内健太; 鳥居礼奈; 萩原加奈子; 佐藤亮介; 高崎輝恒; Dieter Wolf; 杉浦麗子
    第69回日本薬学会関西支部総会・大会  2019/10
  • PKCがストレス顆粒へ移行するメカニズムの解析 −PKCのキナーゼ活性やMAPKシグナルがPKCのストレス顆粒移行に与える影響ー  [Not invited]
    冨本尚史; 神田勇輝; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第69回日本薬学会関西支部総会・大会  2019/10
  • PKCがストレス顆粒へ移行するメカニズムの探索  [Not invited]
    冨本尚史; 神田勇輝; 佐藤亮介; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第52回研究報告会  2019/09
  • 分裂酵母の酸化ストレス応答におけるダウン症責任因子DSCR1/RCAN1ホモログの新たな役割  [Not invited]
    高崎輝恒; 松村綾華; 真鍋涼; 佐藤亮介; 杉浦麗子
    酵母遺伝学フォーラム第52回研究報告会  2019/09
  • RNA結合タンパク質Pumilioによるイノシトールリン脂質代謝経路の制御  [Not invited]
    佐藤亮介; 田中千晶; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第52回研究報告会  2019/09
  • The KH-type RNA-binding protein Rnc1 regulates stress granule assembly, dependently or independently of its RNA-binding activity  [Not invited]
    Ryosuke Satoh; Aki Kawasaki; Nobuki Hara; Teruaki Takasaki; Reiko Sugiura
    10th International Fission Yeast Meeting (pombe 2019)  2019/07
  • Chemical genetic screen in fission yeast identified ACA-28 and its potent derivative compound, which preferentially kill several cancer cells  [Not invited]
    Naoya Hamada; Ryosuke Satoh; Genzoh Tanabe; Fumihiro Ishikawa; Teruaki Takasaki; Reiko Sugiura
    10th International Fission Yeast Meeting (pombe 2019)  2019/07
  • The role of autophagy-related factors and calcineurin in the mechanisms of Ca2+ homeostasis in nutrient-rich and starved conditions  [Not invited]
    Erika Shimada; Taisei Sugiyama; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    10th International Fission Yeast Meeting (pombe 2019)  2019/07
  • Phospho-regulation of α-Endosulfine homolog Igo1 in oxidative stress responses  [Not invited]
    Ayaka Tahara; Kenta Touchi; Reina Torii; Kanako Hagihara; Azusa Mori; Ryosuke Satoh; Teruaki Takasaki; Dieter Wolf; Reiko Sugiura
    10th International Fission Yeast Meeting (pombe 2019)  2019/07
  • The importance of the DUSPs (dual-specificity phosphatases) in mediating the biological effect of ACA-28, a novel MAPK signalling modulator identified in the chemical genetic screen using fission yeast  [Not invited]
    Ayami Mizuno; Yuki Kanda; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    10th International Fission Yeast Meeting (pombe 2019)  2019/07
  • RNA結合タンパク質Rnc1のストレス顆粒局在機構  [Not invited]
    佐藤亮介; 原伸樹; 川崎有記; 崎輝恒; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • 酸化ストレス応答におけるPumilioファミリータンパク質Puf4のリン酸化修飾とその生理的役割  [Not invited]
    稲荷正大; 田中千晶; 甲斐千夏; 田中妙美; 佐藤亮介; 高崎輝恒; Dieter A Wolf; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • 酸化ストレス条件下におけるα-EndosulfineホモログIgo1のリン酸化制御  [Not invited]
    田原彩花; 當内健太; 鳥居礼奈; 萩原加奈子; 佐藤亮介; 高崎輝恒; Dieter A Wolf; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • α-EndosulfineホモログIgo1は酸化ストレス依存的なストレス応答MAPK経路の活性化に関与する  [Not invited]
    當内健太; 田原彩花; 鳥居礼奈; 萩原加奈子; 佐藤亮介; 高崎輝恒; Dieter A Wolf; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • RNA結合タンパク質Rnc1のストレス顆粒への移行率は自身のリン酸化レベルと相関する  [Not invited]
    原伸樹; 佐藤亮介; 川崎有記; 高崎輝恒; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • RNA結合タンパク質Rnc1のRNA結合能依存的な凝集機構  [Not invited]
    川崎有記; 佐藤亮介; 原伸樹; 高崎輝恒; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • ERKシグナル調節薬ACA-28とその高活性アナログのがん細胞に対するアポトーシス誘導活性  [Not invited]
    田 直弥; 佐藤亮介; 高崎輝恒; 田邉元三; 石川文洋; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • 新規抗がん剤候補化合物ACA-28依存的なアポトーシス誘導機構におけるMAPキナーゼホスファターゼDUSP6の役割  [Not invited]
    水野綾美; 宮本理穂; 神田勇輝; 崎輝恒; 佐藤亮介; 杉浦麗子
    未来創薬医療イノベーションシンポジウム “Beyond the Genome” ~New Horizons for Health and Diseases~  2019/03
  • Hsp90によるMAPKシグナル制御機構の解析  [Not invited]
    池畑拓実; 大谷夏実; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第134回日本薬理学会近畿部会_  2018/11
  • MAPKシグナルはRNA顆粒形成を介してProtein Kinase Cの活性を空間的に制御する  [Not invited]
    神田勇輝; 永井善紀; 田中妙美; 土屋葵子; 水野綾美; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第41回日本分子生物学会年会  2018/11
  • カルシニューリン制御因子Rcn1の新たな役割 ~酸化ストレス応答経路におけるネガティブフィードバック作用~  [Not invited]
    高崎輝恒; 佐藤亮介; 杉浦麗子
    第41回日本分子生物学会年会  2018/11
  • RNA結合タンパク質Rnc1のRNA結合能依存的/非依存的なストレス顆粒制御機構  [Not invited]
    第41回日本分子生物学会年会  2018/11
  • ACA-28, an ERK MAPK signaling modulator, influences DUSP6 expression  [Not invited]
    Yuki Kanda; Ayami Mizuno; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    Workshop on Frontiers in Phosphatase Research and Drug Discovery (ICPP13)  2018/10
  • A novel role for the regulator of calcineurin Rcn1 in negative feedback regulation of the stress-activated MAPK signaling  [Not invited]
    Teruaki Takasaki; Ryosuke Satoh; Reiko Sugiura
    Workshop on Frontiers in Phosphatase Research and Drug Discovery (ICPP13)  2018/10
  • A role of α-Endosulfine homolog Igo1 in oxxdative stress responses  [Not invited]
    Ayaka Tahara; Kenta touchi; Reina Torii; Kanako Hagihara; Ryosuke Satoh; Teruaki Takasaki; Dieter Wolf; Reiko Sugiura
    Workshop on Frontiers in Phosphatase Research and Drug Discovery (ICPP13)  2018/10
  • DUSPホモログPmp1のストレス依存的細胞内局在変化とストレス顆粒の関わり  [Not invited]
    水野綾美; 神田勇輝; 崎輝恒; 佐藤亮介; 杉浦麗子
    第68回日本薬学会近畿支部総会・大会  2018/10
  • ストレス応答MAPKシグナルの調節におけるα-EndosulfineホモログIgo1の役割  [Not invited]
    當内健太; 廣井 遥; 田原彩花; 鳥居礼奈; 萩原加奈子; 佐藤亮介; 高崎輝恒; Dieter Wolf; 杉浦麗子
    第68回日本薬学会近畿支部総会・大会  2018/10
  • ERK依存的細胞死誘導剤ACA-28のトリプルネガティブ乳癌に対する効果  [Not invited]
    田直弥; 川崎有記; 佐藤亮介; 高崎輝恒; 田邉元三; 石川文洋; 杉浦麗子
    第68回日本薬学会近畿支部総会・大会  2018/10
  • α-EndosulfineホモログIgo1の酸化ストレス応答におけるリン酸化依存的な役割  [Not invited]
    田原彩花; 廣井遥; 當内健太; 萩原加奈子; 佐藤亮介; 高崎輝恒; 杉浦麗子; Dieter Wolf
    第91回日本生化学会大会  2018/09
  • α-EndosulfineホモログIgo1はストレス応答MAPKシグナルの調節に関わる  [Not invited]
    當内健太; 廣井遥; 田原彩花; 鳥居礼奈; 萩原加奈子; 佐藤亮介; 高崎輝恒; 杉浦麗子; Dieter Wolf
    第91回日本生化学会大会  2018/09
  • オートファジー関連因子Atg1とMAPKおよびCa2+/カルシニューリンシグナルの機能的関わり  [Not invited]
    嶋田絵理香; 神田勇輝; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第91回日本生化学会大会  2018/09
  • ERK依存的細胞死誘導剤ACA-28の高活性アナログによるがん細胞増殖抑制  [Not invited]
    田直弥; 川崎有記; 佐藤亮介; 高崎輝恒; 田邉元三; 石川文洋; 杉浦麗子
    第91回日本生化学会大会  2018/09
  • DEAD box型RNA ヘリケースDed1によるPKC/MAPK シグナル制御機構  [Not invited]
    土屋葵子; 神田勇輝; 永井善紀; 田中妙美; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第91回日本生化学会大会  2018/09
  • RNA結合タンパク質Rnc1の空間制御を介したMAPKシグナル調節機構とストレス顆粒形成制御  [Not invited]
    佐藤亮介; 原伸樹; 川崎有記; 高崎輝恒; 杉浦麗子
    第91回日本生化学会大会  2018/09
  • DUSPホモログPmp1 のストレス依存的細胞内局在変化とMAPKシグナル制御との関わり  [Not invited]
    水野綾美; 神田勇輝; 高崎輝恒; 佐藤亮介; 杉浦麗子
    第91回日本生化学会大会  2018/09
  • DUSPホモログPmp1のストレス依存的細胞内局在変化とMAPKシグナル制御との関わり
    水野 綾美; 神田 勇輝; 高崎 輝恒; 佐藤 亮介; 杉浦 麗子
    日本生化学会大会プログラム・講演要旨集  2018/09  (公社)日本生化学会
  • RNA granuleを介したDEAD box型RNA helicase Ded1によるPKC/MAPKシグナルの新規制御機構の提唱  [Not invited]
    神田勇輝; 永井善紀; 田中妙美; 土屋葵子; 池田智里; 水野綾美; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第20回日本RNA学会年会  2018/07
  • 酸化ストレス応答におけるPumilioファミリータンパク質Puf4のリン酸化修飾とその生理的役割  [Not invited]
    稲荷正大; 田中千晶; 甲斐千夏; 佐藤亮介; 高崎輝恒; Dieter A Wolf; 杉浦麗子
    第20回日本RNA学会年会  2018/07
  • 酸化ストレス耐性におけるα-EndosulfineホモログIgo1の働き  [Not invited]
    田原彩花; 當内健太; 鳥居礼奈; 萩原加奈子; 高崎輝恒; 佐藤亮介; Dieter Wolf; 杉浦麗子
    第20回日本RNA学会年会  2018/07
  • RNA結合タンパク質Rnc1のRNA結合能依存的/非依存的なストレス顆粒局在機構  [Not invited]
    佐藤亮介; 原伸樹; 川崎有記; 高崎輝恒; 杉浦麗子
    第20回日本RNA学会年会  2018/07
  • RNA結合タンパク質の時間・空間的制御を介したMAPKシグナル調節機構〜RNA結合タンパク質の局在制御を標的としたMAPKシグナル調節薬の創薬基盤〜  [Not invited]
    佐藤亮介; 萩原加奈子; 高崎輝恒; 杉浦麗子
    日本薬学会第138年会  2018/03
  • DEAD box型RNA helicase Ded1はPKC/MAPKシグナルを制御する 〜RNA granuleを介するPKC/MAPKシグナルの空間的制御メカニズム〜  [Not invited]
    永井善紀; 神田勇輝; 松本紗希; 犬塚夏実; 池田智里; 土屋葵子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    日本薬学会第138年会  2018/03
  • Ca2+ホメオスタシスを介するオートファジー制御因子Atg1とMAPK経路との関わり  [Not invited]
    嶋田絵理香; 萩原加奈子; 高崎輝恒; 佐藤亮介; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • RNA granuleを介したDEAD box型RNA helicase Ded1によるPKC/MAPKシグナル制御機構の提唱  [Not invited]
    神田勇輝; 犬塚夏実; 松本紗希; 池田智里; 永井善紀; 土屋葵子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • Hsp90とMAPKシグナル伝達経路構成因子のクロストーク機構  [Not invited]
    池畑拓実; 大谷夏実; 萩原加奈子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • EndosulfineホモログIgo1の酸化ストレス応答における役割  [Not invited]
    田原彩花; 萩原加奈子; 石田紘基; 廣井遥; 佐藤亮介; 高崎輝恒; Dieter Wolf; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • 分裂酵母Pumilioの酸化ストレス応答における役割  [Not invited]
    稲荷正大; 萩原加奈子; 原伸樹; 田中千晶; 佐藤亮介; 高崎輝恒; Wolf Dieter A; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • αシヌクレイン凝集体が引き起こす細胞障害メカニズムの解析:分裂酵母モデル生物を用いた細胞内輸送システムとの関わり  [Not invited]
    高崎輝恒; 吉本佐紀; 萩原加奈子; 佐藤亮介; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • ケミカルゲノミクスを用いたFTY720感受性遺伝子の網羅的探索とROS/カルシウムシグナルの関わり  [Not invited]
    萩原加奈子; 石田紘基; 木下佳那子; 亀岡佳則; 北條志穂美; 佐藤亮介; 高崎輝恒; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • RNA結合タンパク質のMAPK依存的なリン酸化の役割 〜RNA結合能と細胞内局在の二重制御〜  [Not invited]
    佐藤亮介; 萩原加奈子; 深尾亜喜良; 藤原俊伸; 平井晋哉; 谷時雄; 高崎輝恒; 杉浦麗子
    2017年度生命科学系学会合同年次大会(ConBio2017)  2017/12
  • The DEAD box RNA helicase Ded1 negatively regulates PKC/MAPK signaling via RNA granule  [Not invited]
    Yuki Kanda; Yoshinori Nagai; Kiko Tsuchiya; Ryosuke Satoh; Teruaki Takasaki; Reiko Sugiura
    The 3rd Japan-Taiwan Bilateral Conference on Protein Phosphatase & The 8th Japanese Conference on Protein Phosphatase  2017/11
  • THE DEAD BOX RNA HELICASE DED1 NEGATIVELY REGULATES PKC/MAPK SIGNALING VIA RNA GRANULES  [Not invited]
    Yuki Kanda; Saki Matsumoto; Natsumi Inutsuka; Chisato Ikeda; Yoshinori Nagai; Kiko Tsuchiya; Teruaki Takasaki; Ryosuke Satoh; Reiko Sugiura
    RNA Biology 2017 ~Cutting Edge Developments in RNA Biology for the Control of Gene Expression~  2017/11
  • ”キャビコール誘導体ACA-28”は、がん細胞特異的にERK依存的細胞死を誘導する革新的抗がん剤シーズである  [Not invited]
    杉浦麗子; 佐藤亮介; 松浦一貴; 萩原加奈子; 神田勇輝; 石川文洋; 田邉元三; 村岡修; 高崎輝恒
    第35回メディシナルケミストリーシンポジウム  2017/10
  • S1P受容体調節剤FTY720を介するシグナル伝達機構の解明 -FTY720添加のもたらすCa2+/ROS/Feシグナルの変化と新たな生理活性-  [Not invited]
    萩原加奈子; 亀岡佳則; 北條志穂美; 近重裕次; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第67回日本薬学会近畿支部総会・大会  2017/10
  • EndosulfineホモログIgo1が酸化ストレスにどのように応答するのか -ROSシグナル応答に関わる分子のリン酸化による調節メカニズム-  [Not invited]
    田原彩花; 萩原加奈子; 石田紘基; 廣井遥; 佐藤亮介; 高崎輝恒; Dieter Wolf; 杉浦麗子
    第67回日本薬学会近畿支部総会・大会  2017/10
  • RNA 結合タンパク質の時間・空間的制御を介したMAPKシグナル調節機構 -RNA結合タンパク質の局在制御機構と創薬への応用-  [Not invited]
    佐藤亮介; 萩原加奈子; 高崎輝恒; 杉浦麗子
    第67回日本薬学会近畿支部総会・大会  2017/10
  • MAPKシグナル制御におけるDEAD box型RNA helicase Ded1の役割 -RNA granuleを介するPKC/MAPKシグナルの空間的制御メカニズム-  [Not invited]
    永井善紀; 神田勇輝; 松本紗希; 犬塚夏実; 池田智里; 土屋葵子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    第67回日本薬学会近畿支部総会・大会  2017/10
  • Ca2+ホメオスタシスを介するオートファジー遺伝子とMAPKシグナル経路の関わり  [Not invited]
    嶋田絵理香; 萩原加奈子; 高崎輝恒; 佐藤亮介; 杉浦麗子
    第67回日本薬学会近畿支部総会・大会  2017/10
  • Ca2+ホメオスタシスを介するオートファジー遺伝子とMAPKシグナル経路の関わり  [Not invited]
    嶋田絵理香; 萩原加奈子; 高崎輝恒; 佐藤亮介; 杉浦麗子
    酵母遺伝学フォーラム第50回研究報告会  2017/09
  • 酵母遺伝学の創薬への応用:ERK MAPKシグナル経路(パスウェイ) 標的薬ACA-28の発見と新たながん治療戦略  [Not invited]
    杉浦麗子; 佐藤亮介; 松浦一貴; 萩原加奈子; 神田勇輝; 高崎輝恒
    酵母遺伝学フォーラム第50回研究報告会  2017/09
  • RNA結合タンパク質Rnc1の空間制御機構とMAPKシグナルの関わり  [Not invited]
    佐藤亮介; 原伸樹; 萩原加奈子; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第50回研究報告会  2017/09
  • DEAD box型RNAヘリケースDed1によるMAPKシグナル抑制機構  [Not invited]
    永井善紀; 神田勇輝; 松本紗希; 犬塚夏実; 池田智里; 土屋葵子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第50回研究報告会  2017/09
  • MAPKシグナル抑制因子であるRNA結合タンパク質Rnc1とストレス顆粒との関係  [Not invited]
    原伸樹; 佐藤亮介; 萩原加奈子; 高崎輝恒; 杉浦麗子
    酵母遺伝学フォーラム第50回研究報告会  2017/09
  • RNA結合タンパク質Pumiliioとイノシトールリン脂質代謝との機能的関係  [Not invited]
    稲荷正大; 萩原加奈子; 原伸樹; 田中千晶; 佐藤亮介; 高崎輝恒; 杉浦麗子
    近畿大学大学院サイエンスネットワーク2017「第7回院生サミット」  2017/09
  • Hsp90とMAPKシグナル伝達経路構成因子のクロストーク機構  [Not invited]
    池畑拓実; 大谷夏実; 佐藤亮介; 高崎輝恒; 杉浦麗子
    近畿大学大学院サイエンスネットワーク2017「第7回院生サミット」  2017/09
  • DEAD box型RNA helicase Ded1によるPKC/MAPKシグナル制御機構の提唱  [Not invited]
    神田勇輝; 犬塚夏実; 松本紗希; 池田智里; 永井善紀; 土屋葵子; 佐藤亮介; 高崎輝恒; 杉浦麗子
    近畿大学大学院サイエンスネットワーク2017「第7回院生サミット」  2017/09
  • ACA-28によるERK MAPKシグナルを介したメラノーマ特異的細胞増殖抑制機構  [Not invited]
    松浦一貴; 佐藤亮介; 萩原加奈子; 神田勇輝; 高崎輝恒; 杉浦麗子
    近畿大学大学院サイエンスネットワーク2017「第7回院生サミット」  2017/09
  • Duchenne 型筋ジストロフィーの尿中タイチン濃度は健常人より 100 倍以上高値である
    粟野 宏之; 松本 真明; 永井 正志; 白川 卓; 高崎 輝恒; 丸山 順裕; 鍋島 陽一; 松尾 雅文
    精神・神経疾患研究開発費 『筋ジストロフィーのエビデンス創出を目的とした 臨床研究と体制整備』班 平成 28 年度班会議  2016/11
  • Chromodomain protein MRG-1 is required for global repression of Pol II-dependent transcription in the primordial germ cells in C. elegans  [Not invited]
    Takashi Miwa; Teruaki Takasaki; Kunio Inoue; Hiroshi Sakamoto
    JSDB Special Symposium: Frontier of Developmental Biology Hosted by JSDB  2016/02  東京大学(東京都)
  • 線虫C. elegansの生殖細胞形成に必須なクロマチン制御因子群の始原生殖細胞への限局機構の解析  [Not invited]
    巳波 孝至; INOUE KUNIO; SAKAMOTO HIROSHI; TAKASAKI TERUAKI
    第38回日本分子生物学会  2015/12  神戸国際展示場
  • 線虫に学ぶ生殖細胞の運命決定様式~生殖質とヒストン修飾の二重制御~  [Invited]
    TAKASAKI TERUAKI
    筑波大学TARA公開セミナー  2015/11  筑波大学TARAセンター(茨城県)
  • 線虫C.elegansの始原生殖細胞成熟過程におけるクロマチン制御機構の研究  [Invited]
    巳波 孝至; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    関西地区線虫勉強会ジョイントミーティング  2015/10  関西学院大学梅田キャンパス(大阪府)
  • 線虫C.elegansの生殖細胞形成に必須なクロマチン制御因子群の始原生殖細胞への限局機構の解析  [Not invited]
    巳波 孝至; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    第17回RNA学会年会  2015/07  ホテルライフォート札幌(北海道)
  • 線虫C.elegansにおけるクロモドメイン蛋白質MRG-1の始原生殖細胞への限局メカニズムの解析  [Not invited]
    巳波 孝至; INOUE KUNIO; SAKAMOTO HIROSHI; TAKASAKI TERUAKI
    第37回日本分子生物学会  2014/11  パシフィコ横浜
  • 線虫C.elegansにおける、クロモドメイン蛋白質MRG-1の始原生殖細胞への限局メカニズムの解析  [Not invited]
    巳波 孝至; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    第5回サイエンスフロンティア研究発表会  2014/10  神戸大学
  • The mechanism for enrichment of a chromodomain protein MRG-1 into the primordial germ cells in C. elegans  [Not invited]
    Takashi Miwa; Kunio Inoue; Hiroshi Sakamoto; Teruaki Takasaki
    C. elegans Development, Cell Biology and Gene Expression Meeting in Association with The 6th Asia-Pacific C. elegans Meeting  2014/07  奈良県新公会堂
  • Analysis of the mechanism to enrich a chromodomain protein MRG-1 into the primordial germ cells in C.elegans  [Invited]
    Takashi Miwa; INOUE KUNIO; SAKAMOTO HIROSHI; TAKASAKI TERUAKI
    第47回日本発生生物学会  2014/05  ウインクあいち、愛知県名古屋市
  • MRG-1 acts as an epigenome interpreter of Lys36 methylation on histone H3 in C. elegans germline development  [Invited]
    Teruaki Takasaki; Andreas Rechtsteiner; Thea Egelhofer; Jeremy Kreher; Erina Shigeyama; Hiroshi Sakamoto; Susan Strome
    第47回日本発生生物学会  2014/05  ウインクあいち、愛知県名古屋市
  • Analysis of the mechanism to enrich a chromodomain protein MRG-1 into the primordial germ cells in C. elegans  [Not invited]
    Takashi Miwa; Kunio Inoue; Hiroshi Sakamoto; Teruaki Takasaki
    第47回日本発生生物学会  2014/05  ウインクあいち、愛知県名古屋市
  • 線虫C.elegansにおける生殖細胞形成に関与するクロモドメインタンパクMRG-1の局在機構の解析  [Not invited]
    巳波 孝至; TAKASAKI TERUAKI; SAKAMOTO HIROSHI
    関西地区線虫勉強会  2014/01  関西学院大学梅田キャンパス
  • 線虫C.elegans生殖細胞におけるスプライシング関連因子SPK-1の機能解析  [Not invited]
    土橋 匠; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    関西地区線虫勉強会ジョイントミーティング  2013/10  関西学院大学梅田キャンパス
  • 線虫C.elegans生殖細胞におけるスプライシング関連タンパク質リン酸化酵素SPK-1の機能解析  [Not invited]
    土橋 匠; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    RNAフロンティアミーティング2013  2013/09  ラフォーレ修善寺
  • 線虫C.elegansにおける生殖細胞形成に関与するクロマチンリモデリング因子群の局在機構の解析  [Not invited]
    巳波 孝至; TAKASAKI TERUAKI; INOUE KUNIO; SAKAMOTO HIROSHI
    RNAフロンティアミーティング  2013/09  ラフォーレ修善寺
  • MRG-1 acts as an epigenome interpreter of Lys36 methylation on histone H3  [Not invited]
    TAKASAKI TERUAKI; Thea Egelhofer; Andreas Rechtsteiner; SAKAMOTO HIROSHI; Susan Strome
    The 19th International C.elegans Meeting  2013  カリフォルニア大学ロサンゼルス校
  • 生殖細胞と体細胞の違いを生み出すC.elegansのヒストン修飾制御機構  [Not invited]
    TAKASAKI TERUAKI
    関西地区線虫勉強会ジョイントミーティング  2013/01  関西学院大学梅田キャンパス
  • 生殖細胞と体細胞の違いを生み出す線虫C.elegansのヒストン修飾制御機構  [Not invited]
    TAKASAKI TERUAKI; Thea Egelhofer; Andreas Rechtsteiner; SAKAMOTO HIROSHI; Susan Strome
    第85回日本生化学会大会  2012/12  福岡国際会議場
  • 線虫生殖腺におけるスプライシング関連因子SPK-1の解析  [Not invited]
    土橋 匠; TAKASAKI TERUAKI; SAKAMOTO HIROSHI
    関西地区線虫勉強会ジョイントミーティング  2012/10  関西学院大学梅田キャンパス
  • 線虫C.elegansの生殖細胞分化に関わるエピジェネティック制御  [Not invited]
    茂山 恵里那; TAKASAKI TERUAKI; SAKAMOTO HIROSHI
    関西地区線虫勉強会ジョイントミーティング  2012/10  関西学院大学梅田キャンパス
  • 線虫C.elegansの生殖細胞分化能を規定するヒストン修飾制御機構  [Not invited]
    TAKASAKI TERUAKI; Thea Egelhofer; Andreas Rechtsteiner; Susan Strome
    第6回日本エピジェネティクス研究会年会  2012/05  学術総合センター(東京)
  • Epigenetics in C.elegans germline development  [Not invited]
    TAKASAKI Teruaki
    関西地区線虫勉強会ジョイントミーティング  2012/03  大阪  関西学院大学

Research Themes

  • Japan Society for the Promotion of Science:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)
    Date (from‐to) : 2020/04 -2023/03 
    Author : 高崎 輝恒
     
    本研究は、パーキンソン病発症の原因として考えられているαシヌクレインタンパク質の凝集を抑制するメカニズムの解明を目指すものである。αシヌクレインタンパク質は本来は可溶性のタンパク質であり、αシヌクレインタンパク質の凝集形成には、遺伝的要素よりも老化による影響が強いと考えられている。しかしながら、αシヌクレインタンパク質は健常者においても豊富に発現しているタンパク質であり、なぜ凝集化が始まるのかは依然として解明されておらず、原因究明が急がれている。 本研究課題の主軸は、分裂酵母を遺伝子改変して作成したパーキンソン病モデル細胞に対し、ヒト神経細胞から作成したcDNAライブラリを用いて、αシヌクレインタンパク質の凝集抑制因子を探索するところにあるが、残念ながら現時点では良好なスクリーニング結果は得られていない。 そこで、凝集抑制因子のスクリーニング感度を高める培養条件等を検討したところ、バルプロ酸添加培地において、パーキンソン病モデル酵母の細胞障害(増殖遅延)が顕著に増悪することが本年度の解析によって新たに明らかとなった。バルプロ酸の使用が、パーキンソン病の進行を早める可能性を示唆する新規の知見であり、大変興味深いと考えている。今後は、バルプロ酸添加培地を活用して、当初の計画通りシヌクレイン凝集抑制因子のスクリーニングを進めるとともに、初年度に見出した凝集抑制能をもつ薬剤の作用機序、および、タンパク質の折り畳みに関わる分子シャペロンHsp90タンパク質とシヌクレインタンパク質の凝集性との関わりついても解析を進めていく予定である。
  • 転写伸長促進機構を分子基盤とした生殖細胞の特性形成メカニズム
    科学研究費補助金/若手研究(B):
    Date (from‐to) : 2016/04 -2017/03 
    Author : 高崎 輝恒
  • 科学研究費補助金/若手研究(B)
    Date (from‐to) : 2012/04 -2014/03 
    Author : 高崎 輝恒

Industrial Property Rights

  • 特許7295545:アポトーシス誘導剤と癌治療剤  
    杉浦 麗子, 高崎 輝恒, 佐藤 亮介, 村岡 修, 田邉 元三