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MIYAMOTO Masaaki
Institute for Academic Research and Co-Creative Innovation
Professor

Researcher basic information

■ Research Keyword
  • Molecular Biology
  • Cell Biology
■ Research Areas
  • Life sciences / Genomics
  • Life sciences / Molecular biology
  • Life sciences / Cell biology
■ Committee History
  • 大学等放射線施設協議会, 理事
  • 日本放射線安全管理学会 編集委員

Research activity information

■ Paper
  • Hiroki Yasuda, Hikaru Yamamoto, Kenji Hanamura, Mona Mehruba, Toshio Kawamata, Hiromi Morisaki, Masaaki Miyamoto, Shinji Takada, Tomoaki Shirao, Yoshitaka Ono, Hideyuki Mukai
    AbstractAbnormal metabotropic glutamate receptor (mGluR) activity could cause brain disorders; however, its regulation has not yet been fully understood. Here, we report that protein kinase N1 (PKN1), a protein kinase expressed predominantly in neurons in the brain, normalizes group 1 mGluR function by upregulating a neuronal glutamate transporter, excitatory amino acid transporter 3 (EAAT3), and supports silent synapse activation. Knocking out PKN1a, the dominant PKN1 subtype in the brain, unmasked abnormal input-nonspecific mGluR-dependent long-term depression (mGluR-LTD) and AMPA receptor (AMPAR) silencing in the developing hippocampus. mGluR-LTD was mimicked by inhibiting glutamate transporters in wild-type mice. Knocking out PKN1a decreased hippocampal EAAT3 expression and PKN1 inhibition reduced glutamate uptake through EAAT3. Also, synaptic transmission was immature; there were more silent synapses and fewer spines with shorter postsynaptic densities in PKN1a knockout mice than in wild-type mice. Thus, PKN1 plays a critical role in regulation of synaptic maturation by upregulating EAAT3 expression.
    Springer Science and Business Media LLC, Dec. 2020, Communications Biology, 3(1) (1)
    [Refereed]
    Scientific journal

  • Yuta Tsukamoto, Satoshi Kagiwada, Sayuri Shimazu, Kaoru Takegawa, Tetsuko Noguchi, Masaaki Miyamoto
    Mar. 2015, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 458(4) (4), 802 - 809, English
    [Refereed]
    Scientific journal

  • Tetsuro Mimura, Mari Mimura, Daisuke Kobayashi, Chiyo Komiyama, Hitoshi Sekimoto, Masaaki Miyamoto, Akira Kitamura
    Jan. 2014, Journal of Plant Research, 127(1) (1), 5 - 10, English
    [Refereed]
    Scientific journal

  • Radioactive pollution and accumulation of radionuclides in wild plants in Fukushima. In JPR Sympoium “Current status and future control of cesium contamination in plants and algae in Fukushima”
    Mimura Tetsuro, Mimura Mari, Kobayashi Daisuke, Komiyama Chiyo, Sekimoto Hisashi, Miyamoto Masaaki, Kitamura Akira
    Jan. 2014, Journal of Plant Research, English
    [Refereed]
    Scientific journal

  • Tetsuro Mimura, Mari Mimura, Chiyo Komiyama, Masaaki Miyamoto, Akira Kitamura
    Jan. 2014, JOURNAL OF PLANT RESEARCH, 127(1) (1), 91 - 97, English
    [Refereed]
    Scientific journal

  • Yuta Tsukamoto, Chisako Katayama, Miki Shinohara, Akira Shinohara, Shohei Maekawa, Masaaki Miyamoto
    Nov. 2013, Biochemical and Biophysical Research Communications, 441(4) (4), 867 - 872, English
    [Refereed]
    Scientific journal

  • Motomichi Doi, Hideki Minematsu, Yukihiko Kubota, Kiyoji Nishiwaki, Masaaki Miyamoto
    Aug. 2013, Development (Cambridge), 140(16) (16), 3435 - 3444, English
    [Refereed]
    Scientific journal

  • M. Doi, H. Minematsu, Y. Kubota, K. Nishiwaki, M. Miyamoto
    2013, Development, 140(16) (16), 3435 - 44, English
    [Refereed]
    Scientific journal

  • Shinki Iwashita, Yoshie Hiramatsu, Takayuki Otani, Chie Amano, Masahiko Hirai, Kazunori Oie, Eiji Yuba, Kenji Kono, Masaaki Miyamoto, Koichi Igarashi
    Nov. 2012, JOURNAL OF BIOMATERIALS APPLICATIONS, 27(4) (4), 445 - 456, English
    [Refereed]
    Scientific journal

  • Toshiyuki Nakamura, Takahiro Tokushima, Kyuichi Kawabata, Norio Yamamoto, Masaaki Miyamoto, Hitoshi Ashida
    May 2012, ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 521(1-2) (1-2), 71 - 76, English
    [Refereed]
    Scientific journal

  • Yoshio Takahata, Masao Inoue, Kwang Kim, Yota Iio, Masaaki Miyamoto, Ryoji Masui, Yasushi Ishihama, Seiki Kuramitsu
    May 2012, PROTEOMICS, 12(9) (9), 1414 - 1430, English
    [Refereed]
    Scientific journal

  • Mai Nakase, Yuta Tsukamoto, Akira Hosomi, Tomo Matsuda, Masaaki Miyamoto, Kaoru Takegawa
    Apr. 2012, BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, 76(4) (4), 652 - 659, English
    [Refereed]
    Scientific journal

  • Masaaki Miyamoto, Shinki Iwashita, Satomi Yamaguchi, Yoshitaka Ono
    Sep. 2009, MOLECULAR AND CELLULAR BIOCHEMISTRY, 329(1-2) (1-2), 175 - 179, English
    [Refereed]
    Scientific journal

  • S Iwashita, M Fujii, H Mukai, Y Ono, M Miyamoto
    Aug. 2004, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 320(4) (4), 1063 - 1068, English
    [Refereed]
    Scientific journal

  • N Iwaki, K Karatsu, M Miyamoto
    Dec. 2003, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 312(2) (2), 414 - 420, English
    [Refereed]
    Scientific journal

  • Mutational analysis of the regulatory mechanism of PKN: the regulatory region of PKN contains an arachidonic acid-sensitive autoinhibitory domain.
    C Yoshinaga, H Mukai, M Toshimori, M Miyamoto, Y Ono
    PKN is a fatty acid- and Rho GTPase-activated protein kinase whose catalytic domain in the carboxyl terminus is homologous to those of protein kinase C (PKC) family members. The amino terminal region of PKN is suggested to function as a regulatory domain, since tryptic cleavage or the binding of Rho GTPase to this region results in protein kinase activation of PKN. The structural basis for the regulation of PKN was investigated by analyzing the activity of a series of deletion/site-directed mutants expressed in insect cells. The amino-terminally truncated form of PKN (residue 455-942) showed low basal activity similar to that of the wild-type enzyme, and was arachidonic acid-dependent. However, further deletion (residue 511-942) resulted in a marked increase in the basal activity and a decrease in the arachidonic acid dependency. A (His)(6)-tagged protein comprising residues 455-511 of PKN (designated His-Ialpha) inhibited the kinase activity of the catalytic fragment of PKN in a concentration-dependent manner in competition with substrate (K(i) = 0.6+/-0.2 microM). His-Ialpha also inhibited the activity of the catalytic fragment of PRK2, an isoform of PKN, but had no inhibitory effect on protein kinase A or protein kinase Cdelta. The IC(50) value obtained in the presence of 40 microM arachidonic acid was two orders of magnitude greater than that in the absence of the modifier. These results indicate that this protein fragment functions as a specific inhibitor of PKN and PRK2, and that arachidonic acid relieves the catalytic activity of wild-type PKN from autoinhibition by residues 455-511 of PKN. Autophosphorylation of wild-type PKN increased the protein kinase activity, however, substitution of Thr64, Ser374, or Thr531 in the regulatory region of PKN with alanine, abolished this effect. Substitution of Thr774 in the activation loop of the catalytic domain of PKN with alanine completely abolished the protein kinase activity. These results suggest that these phosphorylation sites are also important in the regulation of the PKN kinase activity. Potential differences in the mechanism of activation between the catalytic regions of PKN and PRK2 are also discussed.
    Sep. 1999, Journal of biochemistry, 126(3) (3), 475 - 84, English, International magazine
    [Refereed]
    Scientific journal

  • Characterization of a novel giant scaffolding protein, CG-NAP, that anchors multiple signaling enzymes to centrosome and the golgi apparatus.
    M Takahashi, H Shibata, M Shimakawa, M Miyamoto, H Mukai, Y Ono
    A novel 450-kDa coiled-coil protein, CG-NAP (centrosome and Golgi localized PKN-associated protein), was identified as a protein that interacted with the regulatory region of the protein kinase PKN, having a catalytic domain homologous to that of protein kinase C. CG-NAP contains two sets of putative RII (regulatory subunit of protein kinase A)-binding motif. Indeed, CG-NAP tightly bound to RIIalpha in HeLa cells. Furthermore, CG-NAP was coimmunoprecipitated with the catalytic subunit of protein phosphatase 2A (PP2A), when one of the B subunit of PP2A (PR130) was exogenously expressed in COS7 cells. CG-NAP also interacted with the catalytic subunit of protein phosphatase 1 in HeLa cells. Immunofluorescence analysis of HeLa cells revealed that CG-NAP was localized to centrosome throughout the cell cycle, the midbody at telophase, and the Golgi apparatus at interphase, where a certain population of PKN and RIIalpha were found to be accumulated. These data indicate that CG-NAP serves as a novel scaffolding protein that assembles several protein kinases and phosphatases on centrosome and the Golgi apparatus, where physiological events, such as cell cycle progression and intracellular membrane traffic, may be regulated by phosphorylation state of specific protein substrates.
    Jun. 1999, The Journal of biological chemistry, 274(24) (24), 17267 - 74, English, International magazine
    [Refereed]
    Scientific journal

  • Proteolytic activation of PKN by caspase-3 or related protease during apoptosis.
    M Takahashi, H Mukai, M Toshimori, M Miyamoto, Y Ono
    PKN, a fatty acid- and Rho-activated serine/threonine kinase having a catalytic domain highly homologous to protein kinase C (PKC), was cleaved at specific sites in apoptotic Jurkat and U937 cells on Fas ligation and treatment with staurosporin or etoposide, respectively. The cleavage of PKN occurred with a time course similar to that of PKCdelta, a known caspase substrate. This proteolysis was inhibited by a caspase inhibitor, acetyl-Asp-Glu-Val-Asp-aldehyde. The cleavage fragments were generated in vitro from PKN by treatment with recombinant caspase-3. Site-directed mutagenesis of specific aspartate residues prevented the appearance of these fragments. These results indicate that PKN is cleaved by caspase-3 or related protease during apoptosis. The major proteolysis took place between the amino-terminal regulatory domain and the carboxyl-terminal catalytic domain, and it generated a constitutively active kinase fragment. The cleavage of PKN may contribute to signal transduction, eventually leading to apoptosis.
    Sep. 1998, Proceedings of the National Academy of Sciences of the United States of America, 95(20) (20), 11566 - 71, English, International magazine
    [Refereed]
    Scientific journal

  • res2+, a new member of the cdc10+/SWI4 family, controls the 'start' of mitotic and meiotic cycles in fission yeast.
    M Miyamoto, K Tanaka, H Okayama
    In the fission yeast Schizosaccharomyces pombe, the cdc10+ and res1+ genes play a crucial role in the start of mitotic and meiotic cycles. They encode structurally related transcriptional complex proteins and regulate some S phase-specific genes. Here we report the identification of a new member of this family named as res2+. res2+ has been isolated as a multicopy suppressor of a res1- null mutant and specifies a 73 kDa protein, which has two copies of the Swi/ankyrin motif and shares the highest sequence and structure similarity with the Res1 protein. res2+ is largely redundant in function with res1+ and is required for the initiation of mitotic and premeiotic DNA synthesis, but has an additional role in meiotic division. Unlike res1+, res2+ is highly induced during conjugation and strongly depends on cdc10+ for its activity. We conclude that the fission yeast contains two functionally overlapping parallel 'start' systems, Res1-Cdc10 and Res2-Cdc10, the former of which plays a major role in mitotic cycle whereas the latter in meiotic cycle.
    Apr. 1994, The EMBO journal, 13(8) (8), 1873 - 80, English, International magazine
    [Refereed]
    Scientific journal

  • Molecular cloning of a novel cytokine cDNA encoding the ninth member of the fibroblast growth factor family, which has a unique secretion property.
    M Miyamoto, K Naruo, C Seko, S Matsumoto, T Kondo, T Kurokawa
    Glia-activating factor (GAF) is a novel heparin-binding growth factor purified from the culture supernatant of a human glioma cell line. It shows a spectrum of activity slightly different from those of other known growth factors. We have isolated the cDNA which encodes human GAF. A homology search revealed that GAF would be the ninth member of the FGF family, and we therefore call it FGF-9. The human FGF-9 cDNA cloned by using oligonucleotide probes encoded a polypeptide consisting of 208 amino acids. Sequence similarity to other members of the FGF family was estimated to be around 30%. Two cysteine residues and other consensus sequences in family members were also well conserved in the FGF-9 sequence. FGF-9 was found to have no typical signal sequence in its N terminus like those in acidic FGF and basic FGF. Acidic FGF and basic FGF are known not to be secreted from cells in a conventional manner. However, FGF-9 was found to be secreted from cells after synthesis despite its lack of a typical signal sequence. It could be detected exclusively in the culture medium of cDNA-transfected COS cells. The amino acid sequence of proteins purified from culture supernatant of the CHO cell line, which was cDNA transfected and selected as a high producer of FGF-9, showed that no peptides were cleaved from the N terminus except the initiation methionine. The rat FGF-9 cDNA was also cloned, and the structural analysis indicated that the PGF-9 gene is highly conserved. Expression of the FGF-9 gene could be detected in the brain and kidney of the adult rat. Restricted gene expression in organs and the unique secretion nature of the protein suggest that FGF-9 plays a physiological role which differs from those of well-characterized acidic FGF and basic FGF.
    Jul. 1993, Molecular and cellular biology, 13(7) (7), 4251 - 9, English, International magazine
    [Refereed]
    Scientific journal

  • Absence of the type I IFN system in EC cells: transcriptional activator (IRF-1) and repressor (IRF-2) genes are developmentally regulated.
    H Harada, K Willison, J Sakakibara, M Miyamoto, T Fujita, T Taniguchi
    Interferons (IFNs) are a heterogeneous family of cytokines that exhibits multiple biological activities. Upon viral infection, expression of type I IFNs (i.e., IFN-alpha and IFN-beta) is induced in a variety of differentiated cells but not in cells of embryonal origin. IRF-1 and IRF-2, which bind to the same cis-elements within the promoters of type I IFN and IFN-inducible MHC class I genes, were identified previously. Here we demonstrate that the expression of both IRF and IFN genes is developmentally regulated in mouse EC cells; these genes become functional only after cell differentiation. Furthermore, cDNA-directed IRF-1 produced in undifferentiated but not differentiated EC cells efficiently activates the transfected IFN-alpha and IFN-beta and endogenous IFN-alpha genes, whereas IRF-2 represses the IRF-1 effects. These findings emphasize the dual function of the IRF-responsive cis-elements as positive and negative regulators, since they can be occupied by transcriptionally active or inactive IRF molecules. This type of regulatory mechanism might operate in other cytokine systems.
    Oct. 1990, Cell, 63(2) (2), 303 - 12, English, International magazine
    [Refereed]
    Scientific journal

  • Structurally similar but functionally distinct factors, IRF-1 and IRF-2, bind to the same regulatory elements of IFN and IFN-inducible genes.
    H Harada, T Fujita, M Miyamoto, Y Kimura, M Maruyama, A Furia, T Miyata, T Taniguchi
    Viral infections commonly induce expression of type I interferon (IFN) genes. The induction is transient and involves transcriptional activation wherein a positive factor, IRF-1, binds to upstream regulatory cis elements. In the present study we report the isolation of a cDNA encoding a novel factor, termed IRF-2, that interacts with the same nucleotide sequence elements as IRF-1. Both genes are inducible not only by virus but also by IFN. Unlike IRF-1, IRF-2 does not function as an activator; rather, it suppresses the function of IRF-1 under certain circumstances. Our results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.
    Aug. 1989, Cell, 58(4) (4), 729 - 39, English, International magazine
    [Refereed]
    Scientific journal

  • Involvement of a cis-element that binds an H2TF-1/NF kappa B like factor(s) in the virus-induced interferon-beta gene expression.
    T Fujita, M Miyamoto, Y Kimura, J Hammer, T Taniguchi
    Interferon-beta (IFN-beta) gene is transcriptionally activated following virus infection of various cell types such as fibroblasts. In the previous studies, regulatory DNA sequences that mediate the virus-induced transcriptional activation have been identified within the 5'-flanking region (up to around -117 respect to the CAP site) of the human IFN-beta gene. The sequences contain binding sites (-100 to -61) for a transcriptional activator, IRF-1, the gene of which is also virus-inducible. In the present study, we focused on an additional cis-element, located between the IRF-1 binding sites and TATA box. Interestingly, the element coincides with the previously identified elements for the transcription factors H2TF-1 and NF kappa B. The element, when tandemly repeated, functions in activating the distal gene expression in either constitutive or virus-inducible manner depending on the cell type. The results suggest the importance of cooperation between IRF-1 and H2TF-1/NF kappa B-like factor in the maximal IFN-beta gene induction.
    May 1989, Nucleic acids research, 17(9) (9), 3335 - 46, English, International magazine
    [Refereed]
    Scientific journal

  • Induction of endogenous IFN-alpha and IFN-beta genes by a regulatory transcription factor, IRF-1.
    T Fujita, Y Kimura, M Miyamoto, E L Barsoumian, T Taniguchi
    Interferons (IFNs) have an important role in cell growth and differentiation. The most well-known function of IFNs is their antiviral activity; viral infections result in induction of the transcription of the IFN-alpha and IFN-beta genes. Recently we isolated the gene encoding a transcription factor, IRF-1, that may play a part in the induction of IFN genes. Interestingly, the IRF-1 gene itself is virus-inducible, suggesting the importance of de novo production of IRF-1 in IFN gene induction. Here we show that high-level expression of the cloned mouse IRF-1 gene in monkey COS cells results in the induction of endogenous IFN-alpha and IFN-beta genes without viral stimulation. Furthermore, we demonstrate the induction of these genes by an IRF-1/yeast GAL4 chimaeric transcription factor. This may be the first demonstration of the specific induction of silent chromosomal genes by transfection of a single transcription factor gene in mammalian cells.
    Jan. 1989, Nature, 337(6204) (6204), 270 - 2, English, International magazine
    [Refereed]
    Scientific journal

  • Evidence for a nuclear factor(s), IRF-1, mediating induction and silencing properties to human IFN-beta gene regulatory elements.
    T Fujita, J Sakakibara, Y Sudo, M Miyamoto, Y Kimura, T Taniguchi
    Transcription of the human interferon-beta (IFN-beta) gene is induced by a variety of agents such as viruses, dsRNA and some cytokines. In this study, we describe a nuclear factor, termed interferon regulatory factor-1 (IRF-1), that is involved in the transcription of IFN-beta and possibly other genes. We demonstrate that IRF-1 functions in virus-induced transcription by interacting with previously identified, IFN-beta regulatory DNA elements. Our data suggest that IRF-1 participates in the transient formation of an induction-specific complex(es) with the regulatory elements. IRF-1 may also be involved in silencing the function of the SV40 enhancer juxtaposed to the regulatory elements in uninduced cells.
    Nov. 1988, The EMBO journal, 7(11) (11), 3397 - 405, English, International magazine
    [Refereed]
    Scientific journal

  • Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-beta gene regulatory elements.
    M Miyamoto, T Fujita, Y Kimura, M Maruyama, H Harada, Y Sudo, T Miyata, T Taniguchi
    Expression of the interferon-beta (IFN-beta) gene is induced by a variety of agents, including viruses. Evidence has been provided that a mouse nuclear factor, termed interferon regulatory factor-1 (IRF-1), specifically binds to the upstream regulatory region of the human IFN-beta gene and mediates virus-induced transcription of the gene. In this study, we describe the molecular cloning and characterization of the mouse and human cDNAs encoding IRF-1. Our results suggest that IRF-1 is also involved in the regulation of other genes such as IFN-alpha and MHC class I genes. Surprisingly, IRF-1 gene expression is dramatically induced by Newcastle disease virus in mouse L929 cells and by Concanavalin A in spleen cells. We show here that the IRF-1 gene possesses virus-inducible promoter.
    Sep. 1988, Cell, 54(6) (6), 903 - 13, English, International magazine
    [Refereed]
    Scientific journal

■ MISC
  • The small GTPase Rab5 controls cell morphology, sexual development, ion-stress response and vacuolar formation in fission yeast
    Masaaki Miyamoto, Yuta Tsukamoto, Chisako Katayama, Miki Shinohara, Akira Shinohara, Shohei Maekawa
    Apr. 2014, FASEB JOURNAL, 28(1) (1), English
    Summary international conference

  • サウスウエスタンブロット法によるクローニング
    MIYAMOTO Masaaki
    Nov. 2010, 新遺伝子工学ハンドブック, p66-70, Japanese
    [Refereed]
    Introduction scientific journal

  • Motomichi Doi, Hideki Minematsu, Yukihiko Kubota, Kiyoji Nishiwaki, Masaaki Miyamoto
    2009, NEUROSCIENCE RESEARCH, 65, S97 - S97, English
    Summary international conference

  • 【新遺伝子工学ハンドブック】遺伝子クローニング 発現クローニング サウスウエスタンブロット法によるクローニング
    宮本 昌明
    (株)羊土社, Sep. 1999, 実験医学, 別冊(新遺伝子工学ハンドブック) (新遺伝子工学ハンドブック), 23 - 27, Japanese

  • 遺伝子クローニング cDNAクローニング サウスウエスタンブロット法によるクローニング
    宮本 昌明
    (株)羊土社, Apr. 1996, 実験医学, 別冊(新遺伝子工学ハンドブック) (新遺伝子工学ハンドブック), 44 - 49, Japanese

  • 遺伝子細胞工学の基礎技術 遺伝子発現調節の解析方法 サウスウエスタンブロット法
    宮本 昌明
    (株)日本臨床社, Sep. 1994, 日本臨床, 52(特別 臨床分子生物学) (特別 臨床分子生物学), 377 - 380, Japanese

  • 遺伝子工学最新技術 サウスウエスタンプロットによるクローニング
    宮本 昌明, 藤田 尚志
    (株)羊土社, Dec. 1989, 実験医学, 7(17) (17), 2055 - 2058, Japanese

■ Books And Other Publications
  • 新遺伝子工学ハンドブック「サウスウエスタン法によるクローニング」
    宮本 昌明
    Joint work, 羊土社, Jul. 2003, Japanese
    Scholarly book

  • サウスウエスタン法によるcDNAクローニング
    宮本昌明, 谷口維紹
    Joint work, 新生化学実験講座 核酸III 組み換えDNA技術, 東京化学同人, 1992

■ Lectures, oral presentations, etc.
  • Exploration of Rab5 effectors in fission yeast
    Miyamoto, M, Matsumoto, A, Kusakabe, R, Shimazu, S, Kashiwazaki, J
    10th International Fission Yeast Meeting, English
    Poster presentation

  • Identification of Rab5 effectors in fission yeast
    松本 中, 日下部 良子, 嶋津 小百合, 塚本 雄太, 柏崎 隼, 宮本 昌明
    ConBio2017, Dec. 2017, English, 神戸, International conference
    Poster presentation

  • 多機能酵素ヌクレオシド二リン酸キナーゼのDNA結合活性
    佐古 千菜美, 宮本 昌明, 赤沼 哲史, 増井 良治
    ConBio2017, Dec. 2017, Japanese, 神戸, International conference
    Poster presentation

  • Vps901 and Vps902, VPS9 domain-containing proteins, cooperate in the regulation of Rab5 GTPase signaling in fission yeast
    塚本 雄太, 鍵和田 聡, 竹川 薫, 野口 哲子, MIYAMOTO MASAAKI
    The 12th International Congress of Cell Biology, Jul. 2016, English, Prague, Czech Republic, International conference
    Poster presentation

  • VPS9 domain proteins cooperatively regulate Rab5 signaling in fission yeast
    Tsukamoto Y, Kagiwada S, Shimazu S, Takegawa K, Noguchi T, MIYAMOTO MASAAKI
    第67回 日本細胞生物学会大会, Jul. 2015, English, 東京, Domestic conference
    Poster presentation

  • Two VPS9 proteins cooperate in the regulation of Rab5 signaling in fission yeast
    Tsukamoto Y, Kagiwada S, Shimazu S, Takegawa K, Noguchi T, MIYAMOTO MASAAKI
    The Eighth International Fission Yeast Meeting, Jun. 2015, English, Kobe, International conference
    Poster presentation

  • Analyses of downstream effector of Rab5 in fission yeast
    Tsukamoto Y, Miyamoto M
    第37 回 日本分子生物学会年会, Nov. 2014, English, Domestic conference
    Poster presentation

  • Ypt5, Rab5 homologue in fission yeast, is involved in cellular functions such as membrane transport (Poster)
    Tsukamoto Y, Katayama C, Matsumoto A, SHimazu S, Miyamoto M
    第87回 日本生化学会大会, 2014, English, Domestic conference
    Poster presentation

  • The small GTPase Rab5 controls cell morphology, sexual development, ion-stress response and vacuolar formation in fission yeast
    MIyamoto M, Tsukamoto Y, Katayama C, Shinohara M, SHiNohara A, Maekawa S
    ASBMB Experimental Biology, 2014, English, International conference
    Poster presentation

  • Candidates for downstream effector of Rab5 have different roles in sexual differentiation, response to ion stress, and vacuole formation in fission yeast
    Tsukamoto Y, MIyamoto M
    第66回 日本細胞生物学会大会, 2014, English, Domestic conference
    Oral presentation

  • 分裂酵母におけるYpt5(Rab5)エフェクター候補であるPep7の解析
    Tsukamoto Y, Miyamoto Masaaki
    第65回日本細胞生物学会大会, 2013, Japanese, 名古屋, Domestic conference
    Oral presentation

  • 分裂酵母におけるRab5とVPS9タンパク質の解析
    Tsukamoto Y, Katayama C, Matsuda T, Tsuji H, Miyamoto Masaaki
    第36回日本分子生物学会年会, 2013, Japanese, 神戸, Domestic conference
    Oral presentation

  • Analyses of Vps901 and Vps902, VPS- domain-containing proteins in fission yeast
    Tsukamoto Y, Matsuda T, Tsuji H, Goto T, Miyamoto Masaaki
    EMBO Conference, 7th International Fission Yeast Meeting, 2013, English, London, UK, International conference
    Oral presentation

  • Analyses of Ypt5, Rab5 homologue in fission yeast, and its downstream effector
    Yuta Tsukamoto, Chisako Katayama, MIYAMOTO MASAAKI
    第85回日本生化 学会大会, Dec. 2012, Japanese, 福岡, Domestic conference
    Poster presentation

  • 福島における植物の放射性物質被曝状況と動態
    MIMURA TETSURO, 三村 真理, MIYAMOTO MASAAKI, 小宮山 千代, 北村 晃, 松崎 昭夫, 関本 均, 藤原 徹
    日本植物学会第76回大会, Sep. 2012, Japanese, 姫路, Domestic conference
    Oral presentation

  • Rab5 signaling pathway in fission yeast cells.
    Miyamoto Masaaki, Tsukamoto Y, Katayama C, Goto T
    Cold Spring Harbor Asia Conferences, Small GTPases at different scales, Sep. 2012, English, China, International conference
    Oral presentation

  • Rab5 signaling pathway in fission yeast cells
    MIYAMOTO MASAAKI, Yuta Tsukamoto, Chisako Katayama, Takuya Goto
    Cold Spring Harbor Asia Conferences, Small GTPases at Different Scales: Proteins, Membranes, Cells, Sep. 2012, English, Suzhou, China, International conference
    Oral presentation

  • Analysis of Rab5 in fission yeast.
    Tsukamoto Y, Katayama C, Miyamoto Masaaki
    第64回 日本細胞生物学会合同大会・ 第45回 日本発生生物学会, May 2012, English, Domestic conference
    Oral presentation

  • Analysis of Rab5 in fission yeast
    Yuta Tsukamoto, Chisako Katayama, MIYAMOTO MASAAKI
    第45回日本発生 生物学会・第64回日本細胞生物学会合同大会, May 2012, English, 神戸, Domestic conference
    Public symposium

  • Identification of phosphoprotein and structural analysis of the phosphorylation site in Thermus thermophilus HB8
    Takahata Y, InoueM, Kim K, Iio Y, MIYAMOTO Masaaki, Masui R, Ishihama Y, Kuramitsu S
    17th Lorne Proteomics Symposium, Feb. 2012, English, The Australasian Proteomics Society, Lorne, Australia, International conference
    Poster presentation

  • Analysis of Ypt5, a homologue of Rab5 in fission yeast, and downstream effector of Ypt5
    Tsukamoto Y, MIYAMOTO Masaaki
    第34回日本分子生物学会年会, Dec. 2011, Japanese, 日本分子生物学会, 横浜, Domestic conference
    Oral presentation

  • Analysis of signaling mechanism through Rab5 in fission yeast
    Tsukamoto Y, MIYAMOTO Masaaki
    第84回日本生化学会大会, Sep. 2011, Japanese, 日本生化学会, 京都, Domestic conference
    Oral presentation

  • Ypt5, Rab5 homologue, is involved in the regulation of cell morphology and membrane fusion
    MIYAMOTO Masaaki, Tsukamoto Y, Katayama C
    6th International Fission Yeast Meeting, Jun. 2011, English, 6th International Fission Yeast Meeting Organizing Committee, Boston, USA, International conference
    Poster presentation

  • Two VPS9 domain-containing factors in fission yeast
    Tsukamoto Y, Matsuda T, Tsuji H, Takegawa K, MIYAMOTO Masaaki
    第63回日本細胞生物学会大会, Jun. 2011, English, 日本細胞生物学会, 北海道, Domestic conference
    Poster presentation

  • Ras-interacting protein 1 homologue RIN-1 is a novel effector protein of CED-10/Rac that regulates neuronal cell and axon growth cone migration
    Doi M, Kubota Y, Minematsu H, Nishiwaki K, MIYAMOTO Masaaki
    第33回日本分子生物学会年会, Dec. 2010, Japanese, 日本分子生物学会, 神戸, Domestic conference
    Oral presentation

  • Rab5 homologue Ypt5, is involved in the regulation of cellular functions in fission yeast
    Katayama C, Tsukamoto Y, MIYAMOTO Masaaki
    第33回日本分子生物学会年会, Dec. 2010, Japanese, 日本分子生物学会, 神戸, Domestic conference
    Poster presentation

  • Ras-interacting protein 1 homologue RIN-1 is a novel effector protein of CED-10/Rac that regulates neuronal cell and axon growth cone migration
    M. Doi, H.Minematsu, Y. Kubota, K. Nishiwaki, MIYAMOTO Masaaki
    4th East Asia C. elegans Meeting, Jul. 2010, English, 4th East Asia C. elegans Meeting Organizing Committee, Tokyo, International conference
    Oral presentation

  • RIN-1, a C. elegans homologue of Ras-interacting protein 1, is the novel effector protein of CED-10/Rac, and regulates the migrations of neuronal cells and axon growth cones.
    M. Doi, H. Minematsu, MIYAMOTO Masaaki
    17th International C. elegans Meeting, Jun. 2009, English, 17th International C. elegans Meeting Organizing Committee, UCLA, USA, International conference
    Oral presentation

  • Ras-interacting protein 1, homologue RIN-1, is a novel effector protein of CED10/Rac that regulates neuronal cell and axon growth cone migration
    Masaaki Miyamoto
    17th International Worm Meeting, Jun. 2009, English, University of California at Los Angeles, International conference
    Poster presentation

  • NM23-H2/Lbc pathway in the regulation of cell shape and migration
    M. Miyamoto, S. Iwashita, Y. Ono
    7th International Congress of the NDP kinase/NM23/awd Family, Sep. 2007, English, A. Mehta, Dundee, UK, International conference
    [Invited]
    Invited oral presentation

  • インテグリンシグナル伝達経路における癌原遺伝子産物Lbcの役割.
    IWASHITA Maki, MIYAMOTO Masaaki
    第28回日本分子生物学会年会, Dec. 2005, Japanese, 福岡市, Domestic conference
    Oral presentation

  • 癌原遺伝子産物Lbcのインテグリンシグナル伝達経路における役割.
    IWASHITA Maki, MIYAMOTO Masaaki
    第64回日本癌学会学術総会, Sep. 2005, Japanese, 札幌, Domestic conference
    Oral presentation

  • Nucleoside diphosphate kinase nm23-H2 binds to RhoGEF Lbc and negatively regulates Rho activity.
    IWASHITA Maki, MIYAMOTO Masaaki
    第58回日本細胞生物学会大会, Jun. 2005, Japanese, 埼玉, Domestic conference
    Oral presentation

  • 癌原遺伝子産物Lbcは癌転移抑制因子nm23-H2と相互作用し、負に制御される.
    IWASHITA Maki, MIYAMOTO Masaaki
    日本生化学会近畿支部例会, May 2005, Japanese, 神戸大学大学院医学系研究科, Domestic conference
    Oral presentation

■ Affiliated Academic Society
  • 日本放射線安全管理学会

  • 日本質量分析学会

  • 日本癌学会

  • 日本細胞生物学会

  • 日本生化学会

  • 日本分子生物学会

■ Research Themes
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