Tokushima University / Educator and Researcher Directory --- Miyake, Masato

Field of Study

○	Molecular Cell Biology

Subject of Study

○	小胞体ストレス応答による細胞機能調節

Book / Paper

Academic Paper (Judged Full Paper):

1.	Jirapat Namkaew, Jun Zhang, Norio Yamakawa, Yoshimasa Hamada, Kazue Tsugawa, Miho Oyadomari, Masato Miyake, Toyomasa Katagiri and Seiichi Oyadomari : Repositioning of mifepristone as an integrated stress response activator to potentiate cisplatin efficacy in non-small cell lung cancer., Cancer Letters, Vol.582, 2023. (Summary) Lung cancer, primarily non-small-cell lung cancer (NSCLC), is a significant cause of cancer-related mortality worldwide. Cisplatin-based chemotherapy is a standard treatment for NSCLC; however, its effectiveness is often limited due to the development of resistance, leading to NSCLC recurrence. Thus, the identification of effective chemosensitizers for cisplatin is of paramount importance. The integrated stress response (ISR), activated by various cellular stresses and mediated by eIF2α kinases, has been implicated in drug sensitivity. ISR activation globally suppresses protein synthesis while selectively promoting the translation of ATF4 mRNA, which can induce pro-apoptotic proteins such as CHOP, ATF3, and TRIB3. To expedite and economize the development of chemosensitizers for cisplatin treatment in NSCLC, we employed a strategy to screen an FDA-approved drug library for ISR activators. In this study, we identified mifepristone as a potent ISR activator. Mifepristone activated the HRI/eIF2α/ATF4 axis, leading to the induction of pro-apoptotic factors, independent of its known role as a synthetic steroid. Our in vitro and in vivo models demonstrated mifepristone's potential to inhibit NSCLC re-proliferation following cisplatin treatment and tumor growth, respectively, via the ISR-mediated cell death pathway. These findings suggest that mifepristone, as an ISR activator, could enhance the efficacy of cisplatin-based therapy for NSCLC, highlighting the potential of drug repositioning in the search for effective chemosensitizers. (Keyword) Humans / Carcinoma, Non-Small-Cell Lung / Cisplatin / Lung Neoplasms / Mifepristone / Drug Repositioning / Signal Transduction / Cell Line, Tumor / Drug Resistance, Neoplasm (Link to Publication Site) ● Publication site (DOI): 10.1016/j.canlet.2023.216509 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38036042 ● Summary page in Scopus @ Elsevier: 2-s2.0-85179100567 (DOI: 10.1016/j.canlet.2023.216509, PubMed: 38036042, Elsevier: Scopus)
2.	Mitsuaki Sobajima, Masato Miyake, Yoshimasa Hamada, Kazue Tsugawa, Miho Oyadomari, Ryota Inoue, Jun Shirakawa, Hiroshi Arima and Seiichi Oyadomari : The multifaceted role of ATF4 in regulating glucose-stimulated insulin secretion., Biochemical and Biophysical Research Communications, Vol.611, 165-171, 2022. (Summary) Stress-inducible transcription factor ATF4 is essential for survival and identity of β-cell during stress conditions. However, the physiological role of ATF4 in β-cell function is not yet completely understood. To understand the role of ATF4 in glucose-stimulated insulin secretion (GSIS), β-cell-specific Atf4 knockout (βAtf4KO) mice were phenotypically characterized. Insulin secretion and mechanistic analyses were performed using islets from control Atf4f/f and βAtf4KO mice to assess key regulators for triggering and amplifying signals for GSIS. βAtf4KO mice displayed glucose intolerance due to reduced insulin secretion. Moreover, βAtf4KO islets exhibited a decrease in both the insulin content and first-phase insulin secretion. The analysis of βAtf4KO islets showed that ATF4 is required for insulin production and glucose-stimulated ATP and cAMP production. The results demonstrate that ATF4 contributes to the multifaceted regulatory process in GSIS even under stress-free conditions. (Keyword) Animals / Glucose / Glucose Intolerance / Insulin / Insulin Secretion / Insulin-Secreting Cells / Islets of Langerhans / Mice / Mice, Knockout (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2022.04.038 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35489203 ● Search Scopus @ Elsevier (PMID): 35489203 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2022.04.038 (DOI: 10.1016/j.bbrc.2022.04.038, PubMed: 35489203)
3.	Masato Miyake, Mitsuaki Sobajima, Kiyoe Kurahashi, Akira Shigenaga, Masaya Denda, Akira Otaka, Tomohide Saio, Naoki Sakane, Hidetaka Kosako and Seiichi Oyadomari : Identification of an endoplasmic reticulum proteostasis modulator that enhances insulin production in pancreatic β cells., Cell Chemical Biology, Vol.29, No.6, 996-1009.e9, 2022. (Summary) Perturbation of endoplasmic reticulum (ER) proteostasis is associated with impairment of cellular function in diverse diseases, especially the function of pancreatic β cells in type 2 diabetes. Restoration of ER proteostasis by small molecules shows therapeutic promise for type 2 diabetes. Here, using cell-based screening, we report identification of a chemical chaperone-like small molecule, KM04794, that alleviates ER stress. KM04794 prevented protein aggregation and cell death caused by ER stressors and a mutant insulin protein. We also found that this compound increased intracellular and secreted insulin levels in pancreatic β cells. Chemical biology and biochemical approaches revealed that the compound accumulated in the ER and interacted directly with the ER molecular chaperone BiP. Our data show that this corrector of ER proteostasis can enhance insulin storage and pancreatic β cell function. (Keyword) Diabetes Mellitus, Type 2 / Endoplasmic Reticulum / Endoplasmic Reticulum Stress / Humans / Insulin / Insulin-Secreting Cells / Proteostasis / Unfolded Protein Response (Tokushima University Institutional Repository) ● Metadata: 116761 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.chembiol.2022.01.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35143772 ● Search Scopus @ Elsevier (PMID): 35143772 ● Search Scopus @ Elsevier (DOI): 10.1016/j.chembiol.2022.01.002 (Tokushima University Institutional Repository: 116761, DOI: 10.1016/j.chembiol.2022.01.002, PubMed: 35143772)
4.	Masato Miyake, Jun Zhang, Akihiro Yasue, Satoshi Hisanaga, Kazue Tsugawa, Hiroshi Sakaue, Miho Oyadomari, Hiroshi Kiyonari and Seiichi Oyadomari : Integrated stress response regulates GDF15 secretion from adipocytes, preferentially suppresses appetite for a high-fat diet and improves obesity., iScience, Vol.24, No.12, 2021. (Summary) The eIF2α phosphorylation-dependent integrated stress response (ISR) is a signaling pathway that maintains homeostasis in mammalian cells exposed to various stresses. Here, ISR activation in adipocytes improves obesity and diabetes by regulating appetite in a non-cell-autonomous manner. Adipocyte-specific ISR activation using transgenic mice decreases body weight and improves glucose tolerance and obesity induced by a high-fat diet (HFD) via preferential inhibition of HFD intake. The transcriptome analysis of ISR-activated adipose tissue reveals that growth differentiation factor 15 (GDF15) expression is induced by the ISR through the direct regulation of the transcription factors ATF4 and DDIT3. Deficiency in the GDF15 receptor GFRAL abolishes the adipocyte ISR-dependent preferential inhibition of HFD intake and the anti-obesity effects. Pharmacologically, 10(E), 12(Z)-octadecadienoic acid induces ISR-dependent GDF15 expression in adipocytes and decreases the intake of the HFD. Based on our findings the specific activation of the ISR in adipocytes controls the non-cell-autonomous regulation of appetite. (Tokushima University Institutional Repository) ● Metadata: 116908 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.isci.2021.103448 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34877504 ● Search Scopus @ Elsevier (PMID): 34877504 ● Search Scopus @ Elsevier (DOI): 10.1016/j.isci.2021.103448 (Tokushima University Institutional Repository: 116908, DOI: 10.1016/j.isci.2021.103448, PubMed: 34877504)
5.	Yu Saitou, Tetsuya Ikemoto, Kazunori Tokuda, Katsuki Miyazaki, Shin-ichiro Yamada, Satoru Imura, Masato Miyake, Yuji Morine, Seiichi Oyadomari and Mitsuo Shimada : Effective three-dimensional culture of hepatocyte-like cells generated from human adipose-derived mesenchymal stem cells., Journal of Hepato-Biliary-Pancreatic Sciences, Vol.28, No.9, 705-715, 2021. (Summary) The aim of this study was to clarify the effectiveness of a new three-dimensional (3D) culture system for hepatocyte-like cells (HLCs) generated from human adipose-derived mesenchymal stem cells (ADSCs). Human ADSCs (2 × 10 ) with or without 0.1 mg/mL human recombinant peptide μ-piece per well were seeded in a 96-well U-bottom plate and then our three-step differentiation protocol was applied for 21 days. At each step, cell morphology and gene expression were investigated. Mature hepatocyte functions were evaluated after HLC differentiation. These parameters were compared between 2D- and 3D-cultured HLCs, and, DNA microarray analysis was also performed. Finally, HLCs were transplanted in to CCl induced acute liver failure model mice. Two-dimensional-cultured HLCs at day 21 did not have a spindle shape and had formed spheroids after day 6, which gradually increased in size for 3D-cultured HLCs. Definitive endoderm, hepatoblast, and hepatocyte genes showed significantly higher expression in the 3D culture group. Three-dimensional-cultured HLCs also had higher albumin expression, CYP3A4 activity, urea synthesis, and ammonium metabolism, and much higher expression of ion transporter, blood coagulation, and cell communication genes. HLC transplantation improved serum liver function, especially in T-Bil levels, and engrafted into immunodeficient mice with HLA class I positive staining. Our new 3D culture protocol is effective to improve hepatocyte functions. Our HLCs might be promising for clinical cell transplantation to treat metabolic disease. (Link to Publication Site) ● Publication site (DOI): 10.1002/jhbp.1024 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34318615 ● Search Scopus @ Elsevier (PMID): 34318615 ● Search Scopus @ Elsevier (DOI): 10.1002/jhbp.1024 (DOI: 10.1002/jhbp.1024, PubMed: 34318615)
6.	Thi Dinh Nguyen, Manh Thuong Le, Tsuyoshi Hattori, Mika Takarada-Iemata, Hiroshi Ishii, Jureepon Roboon, Takashi Tamatani, Takayuki Kannon, Kazuyoshi Hosomichi, Atsushi Tajima, Shusuke Taniuchi, Masato Miyake, Seiichi Oyadomari, Takashi Tanaka, Nobuo Kato, Shunsuke Saito, Kazutoshi Mori and Osamu Hori : The ATF6β-calreticulin axis promotes neuronal survival under endoplasmic reticulum stress and excitotoxicity., Scientific Reports, Vol.11, No.1, 2021. (Summary) homeostasis. (Tokushima University Institutional Repository) ● Metadata: 116629 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-021-92529-w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34158584 ● Search Scopus @ Elsevier (PMID): 34158584 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-021-92529-w (Tokushima University Institutional Repository: 116629, DOI: 10.1038/s41598-021-92529-w, PubMed: 34158584)
7.	Yoshimasa Hamada, Yuji Furumoto, Akira Izutani, Shusuke Taniuchi, Masato Miyake, Miho Oyadomari, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : Nanosecond pulsed electric fields induce the integrated stress response via reactive oxygen species-mediated heme-regulated inhibitor (HRI) activation., PLoS ONE, Vol.15, No.3, e0229948, 2020. (Summary) The integrated stress response (ISR) is one of the most important cytoprotective mechanisms and is integrated by phosphorylation of the α subunit of eukaryotic translation initiation factor 2 (eIF2α). Four eIF2α kinases, heme-regulated inhibitor (HRI), double-stranded RNA-dependent protein kinase (PKR), PKR-like endoplasmic reticulum kinase (PERK), and general control nonderepressible 2 (GCN2), are activated in response to several stress conditions. We previously reported that nanosecond pulsed electric fields (nsPEFs) are a potential therapeutic tool for ISR activation. In this study, we examined which eIF2α kinase is activated by nsPEF treatment. To assess the responsible eIF2α kinase, we used previously established eIF2α kinase quadruple knockout (4KO) and single eIF2α kinase-rescued 4KO mouse embryonic fibroblast (MEF) cells. nsPEFs 70 ns in duration with 30 kV/cm electric fields caused eIF2α phosphorylation in wild-type (WT) MEF cells. On the other hand, nsPEF-induced eIF2α phosphorylation was completely abolished in 4KO MEF cells and was recovered by HRI overexpression. CM-H2DCFDA staining showed that nsPEFs generated reactive oxygen species (ROS), which activated HRI. nsPEF-induced eIF2α phosphorylation was blocked by treatment with the ROS scavenger N-acetyl-L-cysteine (NAC). Our results indicate that the eIF2α kinase HRI is responsible for nsPEF-induced ISR activation and is activated by nsPEF-generated ROS. (Tokushima University Institutional Repository) ● Metadata: 114915 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0229948 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32155190 ● Search Scopus @ Elsevier (PMID): 32155190 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0229948 (Tokushima University Institutional Repository: 114915, DOI: 10.1371/journal.pone.0229948, PubMed: 32155190)
8.	Hironori Kato, Kohki Okabe, Masato Miyake, Kazuki Hattori, Tomohiro Fukaya, Kousuke Tanimoto, Shi Beini, Mariko Mizuguchi, Satoru Torii, Satoko Arakawa, Masaya Ono, Yusuke Saito, Takashi Sugiyama, Takashi Funatsu, Katsuaki Sato, Shigeomi Shimizu, Seiichi Oyadomari, Hidenori Ichijo, Hisae Kadowaki and Hideki Nishitoh : ER-resident sensor PERK is essential for mitochondrial thermogenesis in brown adipose tissue., Life Science Alliance, Vol.3, No.3, e201900576, 2020. (Summary) Mitochondria play a central role in the function of brown adipocytes (BAs). Although mitochondrial biogenesis, which is indispensable for thermogenesis, is regulated by coordination between nuclear DNA transcription and mitochondrial DNA transcription, the molecular mechanisms of mitochondrial development during BA differentiation are largely unknown. Here, we show the importance of the ER-resident sensor PKR-like ER kinase (PERK) in the mitochondrial thermogenesis of brown adipose tissue. During BA differentiation, PERK is physiologically phosphorylated independently of the ER stress. This PERK phosphorylation induces transcriptional activation by GA-binding protein transcription factor α subunit (GABPα), which is required for mitochondrial inner membrane protein biogenesis, and this novel role of PERK is involved in maintaining the body temperatures of mice during cold exposure. Our findings demonstrate that mitochondrial development regulated by the PERK-GABPα axis is indispensable for thermogenesis in brown adipose tissue. (Tokushima University Institutional Repository) ● Metadata: 115577 (Link to Publication Site) ● Publication site (DOI): 10.26508/lsa.201900576 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32029570 ● Search Scopus @ Elsevier (PMID): 32029570 ● Search Scopus @ Elsevier (DOI): 10.26508/lsa.201900576 (Tokushima University Institutional Repository: 115577, DOI: 10.26508/lsa.201900576, PubMed: 32029570)
9.	Keisuke Kitakaze, Shusuke Taniuchi, Eri Kawano, Yoshimasa Hamada, Masato Miyake, Miho Oyadomari, Hirotatsu Kojima, Hidetaka Kosako, Tomoko Kuribara, Suguru Yoshida, Takamitsu Hosoya and Seiichi Oyadomari : Cell-based HTS identifies a chemical chaperone for preventing ER protein aggregation and proteotoxicity., eLife, Vol.8, e43302, 2019. (Summary) ]benzothiazole derivatives (IBTs) as chemical chaperones in a cell-based high-throughput screen. Biochemical and chemical biology approaches revealed that IBT21 directly binds to unfolded or misfolded proteins and inhibits protein aggregation. Finally, IBT21 prevented cell death caused by chemically induced ER stress and by a proteotoxin, an aggression-prone prion protein. Taken together, our data show the promise of IBTs as potent chemical chaperones that can ameliorate diseases resulting from protein aggregation under ER stress. (Tokushima University Institutional Repository) ● Metadata: 115090 (Link to Publication Site) ● Publication site (DOI): 10.7554/eLife.43302 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31843052 ● Search Scopus @ Elsevier (PMID): 31843052 ● Search Scopus @ Elsevier (DOI): 10.7554/eLife.43302 (Tokushima University Institutional Repository: 115090, DOI: 10.7554/eLife.43302, PubMed: 31843052)
10.	Satoshi Hisanaga, Masato Miyake, Shusuke Taniuchi, Miho Oyadomari, Masatoshi Morimoto, Ryosuke Sato, Jun Hirose, Hiroshi Mizuta and Seiichi Oyadomari : PERK-mediated translational control is required for collagen secretion in chondrocytes., Scientific Reports, Vol.8, No.1, 773, 2018. (Summary) mice displayed reduced collagen in articular cartilage but no differences in chondrocyte proliferation or apoptosis compared to the findings in wild-type mice. PERK inhibition increases misfolded protein levels in the ER, which largely hinder ER-to-Golgi transport. These results suggest that the translational control mediated by PERK is a critical determinant of ECM secretion in chondrocytes. (Tokushima University Institutional Repository) ● Metadata: 112406 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-19052-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29335505 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057222869 (Tokushima University Institutional Repository: 112406, DOI: 10.1038/s41598-017-19052-9, PubMed: 29335505, Elsevier: Scopus)
11.	Carina Fischer, Takahiro Seki, Sharon Lim, Masaki Nakamura, Patrik Andersson, Yunlong Yang, Jennifer Honek, Yangang Wang, Yanyan Gao, Fang Chen, J Nilesh Samani, Jun Zhang, Masato Miyake, Seiichi Oyadomari, Akihiro Yasue, Xuri Li, Yun Zhang, Yizhi Liu and Yihai Cao : A miR-327-FGF10-FGFR2-mediated autocrine signaling mechanism controls white fat browning., Nature Communications, Vol.8, No.1, 2079, 2017. (Summary) Understanding the molecular mechanisms regulating beige adipocyte formation may lead to the development of new therapies to combat obesity. Here, we report a miRNA-based autocrine regulatory pathway that controls differentiation of preadipocytes into beige adipocytes. We identify miR-327 as one of the most downregulated miRNAs targeting growth factors in the stromal-vascular fraction (SVF) under conditions that promote white adipose tissue (WAT) browning in mice. Gain- and loss-of-function experiments reveal that miR-327 targets FGF10 to prevent beige adipocyte differentiation. Pharmacological and physiological -adrenergic stimulation upregulates FGF10 levels and promotes preadipocyte differentiation into beige adipocytes. In vivo local delivery of miR-327 to WATs significantly compromises the beige phenotype and thermogenesis. Contrarily, systemic inhibition of miR-327 in mice induces browning and increases whole-body metabolic rate under thermoneutral conditions. Our data provide mechanistic insight into an autocrine regulatory signaling loop that regulates beige adipocyte formation and suggests that the miR-327-FGF10-FGFR2 signaling axis may be a therapeutic targets for treatment of obesity and metabolic diseases. (Tokushima University Institutional Repository) ● Metadata: 112463 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41467-017-02158-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29233981 ● Search Scopus @ Elsevier (PMID): 29233981 ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-017-02158-z (Tokushima University Institutional Repository: 112463, DOI: 10.1038/s41467-017-02158-z, PubMed: 29233981)
12.	Masato Miyake, Masashi Kuroda, Hiroshi Kiyonari, Kenji Takehana, Satoshi Hisanaga, Masatoshi Morimoto, Jun Zhang, Miho Oyadomari, Hiroshi Sakaue and Seiichi Oyadomari : Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice., PLoS ONE, Vol.12, No.6, e0179955, 2017. (Summary) As a novel model of muscle wasting, HSA-Fv2E-PERK Tg mice provide a convenient tool for studying the pathogenesis of muscle loss and for assessing putative therapeutics. (Tokushima University Institutional Repository) ● Metadata: 114340 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0179955 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28644884 ● Search Scopus @ Elsevier (PMID): 28644884 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0179955 (Tokushima University Institutional Repository: 114340, DOI: 10.1371/journal.pone.0179955, PubMed: 28644884)
13.	Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara : The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes. (Tokushima University Institutional Repository) ● Metadata: 110925 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37739 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917 ● Search Scopus @ Elsevier (PMID): 28502917 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739 (Tokushima University Institutional Repository: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917)
14.	Shusuke Taniuchi, Masato Miyake, Kazue Tsugawa, Miho Oyadomari and Seiichi Oyadomari : Integrated stress response of vertebrates is regulated by four eIF2α kinases., Scientific Reports, Vol.6, 32886, 2016. (Summary) The integrated stress response (ISR) is a cytoprotective pathway initiated upon phosphorylation of the eukaryotic translation initiation factor 2 (eIF2α) residue designated serine-51, which is critical for translational control in response to various stress conditions. Four eIF2α kinases, namely heme-regulated inhibitor (HRI), protein kinase R (PKR), PKR-like endoplasmic reticulum kinase, (PERK) and general control non-depressible 2 (GCN2), have been identified thus far, and they are known to be activated by heme depletion, viral infection, endoplasmic reticulum stress, and amino acid starvation, respectively. Because eIF2α is phosphorylated under various stress conditions, the existence of an additional eIF2α kinase has been suggested. To validate the existence of the unidentified eIF2α kinase, we constructed an eIF2α kinase quadruple knockout cells (4KO cells) in which the four known eIF2α kinase genes were deleted using the CRISPR/Cas9-mediated genome editing. Phosphorylation of eIF2α was completely abolished in the 4KO cells by various stress stimulations. Our data suggests that the four known eIF2α kinases are sufficient for ISR and that there are no additional eIF2α kinases in vertebrates. (Tokushima University Institutional Repository) ● Metadata: 112371 (Link to Publication Site) ● Publication site (DOI): 10.1038/srep32886 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27633668 ● Search Scopus @ Elsevier (PMID): 27633668 ● Search Scopus @ Elsevier (DOI): 10.1038/srep32886 (Tokushima University Institutional Repository: 112371, DOI: 10.1038/srep32886, PubMed: 27633668)
15.	Masato Miyake, Akitoshi Nomura, Atsushi Ogura, Kenji Takehana, Yoshihiro Kitahara, Kazuna Takahara, Kazue Tsugawa, Chinobu Miyamoto, Naoko Miura, Ryosuke Sato, Kiyoe Kurahashi, P Heather Harding, Miho Oyadomari, David Ron and Seiichi Oyadomari : Skeletal muscle-specific eukaryotic translation initiation factor 2 phosphorylation controls amino acid metabolism and fibroblast growth factor 21-mediated non-cell-autonomous energy metabolism., The FASEB journal, Vol.30, No.2, 798-812, 2015. (Summary) The eukaryotic translation initiation factor 2 (eIF2) phosphorylation-dependent integrated stress response (ISR), a component of the unfolded protein response, has long been known to regulate intermediary metabolism, but the details are poorly worked out. We report that profiling of mRNAs of transgenic mice harboring a ligand-activated skeletal muscle-specific derivative of the eIF2 protein kinase R-like ER kinase revealed the expected up-regulation of genes involved in amino acid biosynthesis and transport but also uncovered the induced expression and secretion of a myokine, fibroblast growth factor 21 (FGF21), that stimulates energy consumption and prevents obesity. The link between the ISR and FGF21 expression was further reinforced by the identification of a small-molecule ISR activator that promoted Fgf21 expression in cell-based screens and by implication of the ISR-inducible activating transcription factor 4 in the process. Our findings establish that eIF2 phosphorylation regulates not only cell-autonomous proteostasis and amino acid metabolism, but also affects non-cell-autonomous metabolic regulation by induced expression of a potent myokine.-Miyake, M., Nomura, A., Ogura, A., Takehana, K., Kitahara, Y., Takahara, K., Tsugawa, K., Miyamoto, C., Miura, N., Sato, R., Kurahashi, K., Harding, H. P., Oyadomari, M., Ron, D., Oyadomari, S. Skeletal muscle-specific eukaryotic translation initiation factor 2 phosphorylation controls amino acid metabolism and fibroblast growth factor 21-mediated non-cell-autonomous energy metabolism. (Tokushima University Institutional Repository) ● Metadata: 115105 (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.15-275990 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26487695 ● Summary page in Scopus @ Elsevier: 2-s2.0-84958811791 (Tokushima University Institutional Repository: 115105, DOI: 10.1096/fj.15-275990, PubMed: 26487695, Elsevier: Scopus)
16.	H Takahashi, K Sato, T Yamaguchi, Masato Miyake, H Watanabe, Y Nagasawa, E Kitagawa, S Terada, M Urakawa, M T. Rose, C D. McMahon, K Watanabe, S Ohwada, T Gotoh and H Aso : Myostatin alters glucose transporter-4 (GLUT4) expression in bovine skeletal muscles and myoblasts isolated from double-muscled (DM) and normal-muscled (NM) Japanese shorthorn cattle., Domestic Animal Endocrinology, Vol.48, 62-68, 2014. (Summary) The purpose of this study was to determine whether myostatin alters glucose transporter-4 (GLUT4) expression in bovine skeletal muscles and myoblasts isolated from double-muscled (DM) and normal-muscled (NM) Japanese Shorthorn cattle. Plasma concentrations of glucose were lower in DM cattle than in NM cattle (P < 0.01). The expression of GLUT4 messenger RNA (mRNA) in the skeletal muscle ex vivo and in myoblasts at 72 h after differentiation in vitro was higher in DM cattle than in NM cattle (P < 0.01). In contrast, the NM and DM cattle did not differ with respect to skeletal muscle expression of GLUT1 and myocyte enhancer factor-2c (MEF2c), a transcription factor of GLUT4. In differentiated myoblasts, the expression of GLUT1, GLUT4, and MEF2c mRNAs was greater in DM cattle than in NM cattle (P < 0.01). In the presence and absence of insulin, glucose uptake in myoblasts was increased in DM cattle relative to that of NM cattle (P < 0.01). The addition of myostatin decreased the expression of GLUT4 and MEF2c mRNAs in DM myoblasts (P < 0.05). Results of the present study suggest that myostatin inhibits the expression of GLUT4 mRNA possibly via MEF2c and that the greater ability of the DM cattle to produce muscle relative to the NM cattle may be due to their greater sensitivity to insulin and greater use of glucose. (Keyword) Animals / Blood Glucose / Cattle / Gene Expression Regulation / Glucose Tolerance Test / Glucose Transporter Type 4 / Insulin / Muscle, Skeletal / Myoblasts / Myostatin / RNA, Messenger (Link to Publication Site) ● Publication site (DOI): 10.1016/j.domaniend.2014.01.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24906930 ● Search Scopus @ Elsevier (PMID): 24906930 ● Search Scopus @ Elsevier (DOI): 10.1016/j.domaniend.2014.01.007 (DOI: 10.1016/j.domaniend.2014.01.007, PubMed: 24906930)
17.	Shunsuke Iwasaki, Masato Miyake, Shinichiro Hayashi, Hitoshi Watanabe, Yuya Nagasawa, Shunsuke Terada, Kouichi Watanabe, Shyuichi Ohwada, Haruki Kitazawa, Michael T. Rose and Hisashi Aso : Effect of myostatin on chemokine expression in regenerating skeletal muscle cells., Cells, Tissues, Organs, Vol.198, No.1, 66-74, 2013. (Summary) Transforming growth factor- (TGF-) is implicated in the regulatory expression of chemokines that control multiple steps in myogenesis. However, it remains to be established whether myostatin, a member of the TGF- superfamily, affects chemokine expression in skeletal muscle. We investigated the effects of myostatin on the expression of mRNAs and proteins for 4 chemokines (CXCL1, CXCL2, CXCL6, CCL2) in intact and regenerating musculus longissimus thoracis from normal-muscled (NM) and double-muscled (DM) cattle. These chemokines were expressed in regenerating muscle, and their expression was always lower in DM than in NM cattle. Immunohistochemistry revealed that CXCL1 and CXCL6 were detected in the regenerating areas of myoblasts and myotubes in both NM and DM cattle. In cultures of myoblasts isolated from the regenerating muscles, significantly less CXCL1, CXCL2 and CCL2 mRNA was expressed in DM myoblasts than in NM myoblasts during the proliferating stage (P-stage). The expression of CXCL1, CXCL2 and CCL2 mRNAs in NM myoblasts and CXCL1, CXCL2 and CXCL6 mRNAs in DM myoblasts decreased upon switching from P-stage to fusion stage (F-stage). Also, the expression of CXCL1, CXCL2 and CXCL6 mRNAs was significantly lower in DM than in NM myoblasts during the F-stage. The addition of 100 ng/ml myostatin during the F-stage attenuated the expression of CXCL1 and CXCL2 mRNAs and augmented that of CCL2. These results show for the first time that myostatin regulates the differential expression of chemokines in skeletal muscle cells. (Keyword) Animals / Cattle / Cell Proliferation / Cells, Cultured / Chemokines / Gene Expression Regulation, Developmental / Muscle Development / Muscle, Skeletal / Myoblasts / Myostatin / RNA, Messenger / Regeneration (Link to Publication Site) ● Publication site (DOI): 10.1159/000351462 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23838214 ● Search Scopus @ Elsevier (PMID): 23838214 ● Search Scopus @ Elsevier (DOI): 10.1159/000351462 (DOI: 10.1159/000351462, PubMed: 23838214)
18.	Shunsuke Iwasaki, Masato Miyake, Hitoshi Watanabe, Eri Kitagawa, Kouichi Watanabe, Shyuichi Ohwada, Haruki Kitazawa, Michael T. Rose and Hisashi Aso : Expression of myostatin in neural cells of the olfactory system., Molecular Neurobiology, Vol.47, No.1, 1-8, 2012. (Summary) Recent studies show that myostatin mRNA expression is found in some regions of the brain. However, the functional significance of this is currently unknown. We therefore investigated myostatin expression and function in the brain. In this study, we used immunohistochemistry, in situ hybridization, and RT-PCR analysis to reveal that myostatin is expressed in the mitral cells in the olfactory bulb (OB) and in neurons in the olfactory cortex (OC). Using 3D reconstruction, mitral cells positive for myostatin were positioned in the lateral and ventral regions of the OB. In contrast, myostatin-positive mitral cells were detected in mice at 2 weeks of age, but not on days 0 and 7 after birth. Activin receptor IIB, a myostatin receptor, was expressed in the OB, OC, hippocampus, and paraventricular thalamic nucleus. Moreover, c-Fos immunostaining in granule cells in the OB was augmented after intracerebroventricular injection of myostatin. These findings suggest that myostatin is localized in specific cells associated with the olfactory system of the brain and may act as a key inhibitor in cell and/or signal development of the olfactory system. (Keyword) Activin Receptors, Type II / Activins / Animals / Base Sequence / Gene Expression Regulation / Injections, Intraventricular / Mice / Mice, Inbred C57BL / Molecular Sequence Data / Myostatin / Neurons / Olfactory Bulb / Olfactory Pathways / Protein Transport / Proto-Oncogene Proteins c-fos / RNA, Messenger / Reproducibility of Results (Link to Publication Site) ● Publication site (DOI): 10.1007/s12035-012-8342-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22941030 ● Search Scopus @ Elsevier (PMID): 22941030 ● Search Scopus @ Elsevier (DOI): 10.1007/s12035-012-8342-1 (DOI: 10.1007/s12035-012-8342-1, PubMed: 22941030)
19.	Masato Miyake, Hideyuki Takahashi, Eri Kitagawa, Hitoshi Watanabe, Takahiro Sakurada, Hisashi Aso and Takahiro Yamaguchi : AMPK activation by AICAR inhibits myogenic differentiation and myostatin expression in cattle., Cell and Tissue Research, Vol.349, No.2, 615-623, 2012. (Summary) AMP-activated protein kinase (AMPK) regulates metabolism in skeletal muscle, and myostatin (MSTN) negatively regulates skeletal muscle development and growth. In the present study, AMPK activation and the relationship between AMPK and MSTN during myogenic differentiation were investigated in cultures derived from bovine skeletal muscle. Myoblasts capable of forming myotubes were obtained from bovine skeletal muscle and treated with AICAR to activate AMPK, resulting in suppressed myotube formation. AICAR treatment significantly reduced the expression of MSTN mRNA during myogenic differentiation. Combined treatment with AICAR and MSTN suppressed myotube formation to a greater extent than AICAR alone. SB431542, an inhibitor of MSTN signaling, promoted myotube formation during myogenic differentiation. However, simultaneous treatment with AICAR blocked this effect of SB431542. Therefore, AMPK activation inhibits myogenic differentiation but may suppress MSTN expression to balance muscle development. (Keyword) AMP-Activated Protein Kinases / Aminoimidazole Carboxamide / Animals / Cattle / Cell Culture Techniques / Cell Differentiation / Down-Regulation / Enzyme Activation / Male / Muscle Fibers, Skeletal / Myoblasts / Myostatin / RNA, Messenger / Ribonucleotides (Link to Publication Site) ● Publication site (DOI): 10.1007/s00441-012-1422-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22622802 ● Search Scopus @ Elsevier (PMID): 22622802 ● Search Scopus @ Elsevier (DOI): 10.1007/s00441-012-1422-8 (DOI: 10.1007/s00441-012-1422-8, PubMed: 22622802)
20.	Masato Miyake, Shinichiro Hayashi, Shunsuke Iwasaki, Takafumi Uchida, Kouichi Watanabe, Shyuichi Ohwada, Hisashi Aso and Takahiro Yamaguchi : TIEG1 negatively controls the myoblast pool indispensable for fusion during myogenic differentiation of C2C12 cells., Journal of Cellular Physiology, Vol.226, No.4, 1128-1136, 2011. (Summary) The transforming growth factor (TGF)-β inducible early gene (TIEG)-1 is implicated in the control of cell proliferation, differentiation, and apoptosis in some cell types. Since TIEG1 functioning may be associated with TGF-β, a suppressor of myogenesis, TIEG1 is also likely to be involved in myogenesis. Therefore, we investigated the function of TIEG1 during myogenic differentiation in vitro using the murine myoblasts cell line, C2C12. TIEG1 expression increased during differentiation of C2C12 cells. Constitutive expression of TIEG1 reduced survival and decreased myotube formation. Conversely, knocking down TIEG1 expression increased the number of viable cells during differentiation, and accelerated myoblast fusion into multinucleated myotubes. However, expression of the myogenic differentiation marker, myogenin, remained unaffected by TIEG1 knockdown. The mechanism underlying these events was investigated by focusing on the regulation of myoblast numbers after induction of differentiation. The knockdown of TIEG1 led to changes in cell cycle status and inhibition of apoptosis during the initial stages of differentiation. Microarray and real-time PCR analyses showed that the regulators of cell cycle progression were highly expressed in TIEG1 knockdown cells. Therefore, TIEG1 is a negative regulator of the myoblast pool that causes inhibition of myotube formation during myogenic differentiation. (Keyword) Animals / Apoptosis / Cell Count / Cell Cycle / Cell Cycle Proteins / Cell Differentiation / Cell Fusion / Cell Line / DNA-Binding Proteins / Gene Knockdown Techniques / Mice / Muscle Development / Muscle Fibers, Skeletal / Myoblasts / Myogenin / Transcription Factors / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1002/jcp.22434 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20945337 ● Search Scopus @ Elsevier (PMID): 20945337 ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.22434 (DOI: 10.1002/jcp.22434, PubMed: 20945337)
21.	Hitoshi Watanabe, Daisuke Akasaka, Hideki Ogasawara, Kan Sato, Masato Miyake, Kazuki Saito, Yu Takahashi, Takashi Kanaya, Ikuro Takakura, Tetsuya Hondo, Guozheng Chao, T Michael Rose, Shyuichi Ohwada, Kouichi Watanabe, Takahiro Yamaguchi and Hisashi Aso : Peripheral serotonin enhances lipid metabolism by accelerating bile acid turnover., Endocrinology, Vol.151, No.10, 4776-4786, 2010. (Summary) Serotonin is synthesized by two distinct tryptophan hydroxylases, one in the brain and one in the periphery. The latter is known to be unable to cross the blood-brain barrier. These two serotonin systems have apparently independent functions, although the functions of peripheral serotonin have yet to be fully elucidated. In this study, we have investigated the physiological effect of peripheral serotonin on the concentrations of metabolites in the circulation and in the liver. After fasting, mice were ip injected with 1 mg serotonin. The plasma glucose concentration was significantly elevated between 60 and 270 min after the injection. In contrast, plasma triglyceride, cholesterol, and nonesterified fatty acid concentrations were decreased. The hepatic glycogen synthesis and concentrations were significantly higher at 240 min. At the same time, the hepatic triglyceride content was significantly lower than the basal levels noted before the serotonin injection, whereas the hepatic cholesterol content was significantly higher by 60 min after the injection. Furthermore, serotonin stimulated the contraction of the gallbladder and the excretion of bile. After the serotonin injection, there was a significant induction of apical sodium-dependent bile acid transporter expression, resulting in a decrease in the concentration of bile acids in the feces. Additionally, data are presented to show that the functions of serotonin are mediated through diverse serotonin receptor subtypes. These data indicate that peripheral serotonin accelerates the metabolism of lipid by increasing the concentration of bile acids in circulation. (Keyword) Animals / Bile Acids and Salts / Dose-Response Relationship, Drug / Fasting / Gallbladder / Glucose / Glycogen / Ileum / Injections, Intraperitoneal / Insulin / Lipid Metabolism / Liver / Male / Mice / Mice, Inbred C57BL / Serotonin (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2009-1349 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20685881 ● Search Scopus @ Elsevier (PMID): 20685881 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2009-1349 (DOI: 10.1210/en.2009-1349, PubMed: 20685881)
22.	Masato Miyake, Shinichiro Hayashi, Yoshikazu Taketa, Shunsuke Iwasaki, Kouichi Watanabe, Shyuich Ohwada, Hisashi Aso and Takahiro Yamaguchi : Myostatin down-regulates the IGF-2 expression via ALK-Smad signaling during myogenesis in cattle., Animal Science Journal, Vol.81, No.2, 223-229, 2010. (Summary) Myostatin (MSTN) is a negative regulator during muscle differentiation, whereas insulin-like growth factors (IGFs) are essential for muscle development. MSTN and IGFs act oppositely during myogenesis, but there is little information on the mutual relationship of MSTN and IGFs. The present study was conducted to examine whether MSTN affects IGF expression during early myogenesis in cattle. IGF-1 mRNA was similarly expressed in M. longissimus thoracis of double-muscled (DM) and normal (NM) Japanese shorthorn cattle. IGF-2 mRNA expression was consistently higher in the normal and regenerating muscle of DM cattle than those of NM cattle. When myoblasts were isolated from regenerating M. longissimus thoracis, IGF-2 mRNA expression showed a significant increase in differentiating DM derived myoblasts (DM-myoblasts) as compared with differentiating NM derived myoblasts (NM-myoblasts). An addition of recombinant mouse myostatin (rMSTN) to myoblast cultures attenuated IGF-2 mRNA expression and decreased myotube formation, but did not effect IGF-1 mRNA expression. An activin-like kinase (ALK) inhibitor, SB431542, mediates MSTN action, suppressed the translocation of Smad2/3 into the nucleus in DM-myoblasts, and restored the attenuated IGF-2 mRNA expression and the decreased myotube formation induced by rMSTN in myoblast cultures. The findings indicate that MSTN may negatively regulate myoblast differentiation by suppressing IGF-2 expression via ALK-Smad signaling. (Keyword) Activin Receptors / Animals / Cattle / Down-Regulation / Insulin-Like Growth Factor II / Muscle Development / Myostatin / Signal Transduction / Smad Proteins (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1740-0929.2009.00725.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20438504 ● Search Scopus @ Elsevier (PMID): 20438504 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1740-0929.2009.00725.x (DOI: 10.1111/j.1740-0929.2009.00725.x, PubMed: 20438504)
23.	Masato Miyake, Shinichiro Hayashi, Shunsuke Iwasaki, Guozheng Chao, Hideyuki Takahashi, Kouichi Watanabe, Shyuichi Ohwada, Hisashi Aso and Takahiro Yamaguchi : Possible role of TIEG1 as a feedback regulator of myostatin and TGF-beta in myoblasts., Biochemical and Biophysical Research Communications, Vol.393, No.4, 762-766, 2010. (Summary) Myostatin and TGF-beta negatively regulate skeletal muscle development and growth. Both factors signal through the Smad2/3 pathway. However, the regulatory mechanism of myostatin and TGF-beta signaling remains unclear. TGF-beta inducible early gene (TIEG) 1 is highly expressed in skeletal muscle and has been implicated in the modulation of TGF-beta signaling. These findings prompted us to investigate the effect of TIEG1 on myostatin and TGF-beta signaling using C2C12 myoblasts. Myostatin and TGF-beta induced the expression of TIEG1 and Smad7 mRNAs, but not TIEG2 mRNA, in proliferating C2C12 cells. When differentiating C2C12 myoblasts were stimulated by myostatin, TIEG1 mRNA was up-regulated at a late stage of differentiation. In contrast, TGF-beta enhanced TIEG1 expression at an early stage. Overexpression of TIEG1 prevented the transcriptional activation of Smad by myostatin and TGF-beta in both proliferating or differentiating C2C12 cells, but the expression of Smad2 and Smad7 mRNAs was not affected. Forced expression of TIEG1 inhibited myogenic differentiation but did not cause more inhibition than the empty vector in the presence of myostatin or TGF-beta. These results demonstrate that TIEG1 is one possible feedback regulator of myostatin and TGF-beta that prevents excess action in myoblasts. (Keyword) Animals / Cell Line / DNA-Binding Proteins / Feedback, Physiological / Mice / Muscle Development / Myoblasts / Myostatin / Signal Transduction / Smad Proteins / Transcription Factors / Transforming Growth Factor beta (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2010.02.077 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20171187 ● Search Scopus @ Elsevier (PMID): 20171187 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2010.02.077 (DOI: 10.1016/j.bbrc.2010.02.077, PubMed: 20171187)
24.	Susumu Muroya, Kouichi Watanabe, Shinichiro Hayashi, Masato Miyake, Shigeru Konashi, Youichi Sato, Manabu Takahashi, Shigeki Kawahata, Yoshisato Yoshikawa, Hisashi Aso, Koichi Chikuni and Takahiro Yamaguchi : Muscle type-specific effect of myostatin deficiency on myogenic regulatory factor expression in adult double-muscled Japanese Shorthorn cattle., Animal Science Journal, Vol.80, No.6, 678-685, 2009. (Summary) To clarify muscle type-specific effect of myostatin on myogenic regulatory factors (MRFs), we examined mRNA expression of MRFs in five skeletal muscles of normal (NM) and myostatin-deficient double-muscled (DM) adult Japanese Shorthorn cattle by quantitative reverse-transcribed PCR. Among the four MRFs, namely, Myf5, MyoD, myogenin, and MRF4, MyoD expression was different among the muscles of the DM cattle (P < 0.01) but not of the NM cattle. Meanwhile, MyoD expression was significantly elevated only in masseter (MS) muscle in the DM cattle due to the myostatin deficiency (P < 0.05). Myf5 and MRF4 expression in semitendinosus (ST) was higher in the DM than in the NM cattle (P < 0.05). According to analysis of myosin heavy chain (MyHC) isoform expression, more MyHC-2x and -2a and less -slow isoforms were expressed in the longissimus and ST muscles compared to the MS muscle in both cattle (P < 0.05), but no significant difference in MyHC expression was observed between the NM and DM cattle. Taken together, myostatin has influences on Myf5 and MRF4 expression in faster-type muscles and on MyoD expression in slower-type muscles, suggesting a possible muscle type-specific effect of myostatin in skeletal muscle growth and maintenance. (Keyword) Animals / Cattle / Muscle, Skeletal / Myogenic Regulatory Factors / Myostatin (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1740-0929.2009.00684.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20163658 ● Search Scopus @ Elsevier (PMID): 20163658 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1740-0929.2009.00684.x (DOI: 10.1111/j.1740-0929.2009.00684.x, PubMed: 20163658)
25.	Yasuhiro Nagai, Hideki Ogasawara, Yoshikazu Taketa, Hisashi Aso, Takashi Kanaya, Masato Miyake, Kouichi Watanabe, Shyuichi Ohwada, Yoshihiro Muneta and Takahiro Yamaguchi : Expression of inflammatory-related factors in porcine anterior pituitary-derived cell line., Veterinary Immunology and Immunopathology, Vol.124, No.3-4, 201-208, 2008. (Summary) Recent studies have shown that undifferentiated stem cells act as immunomodulators. To investigate the immunomodulatory function of the progenitor cells of the anterior pituitary gland, we attempted to establish a stem/progenitor cell line from the porcine anterior pituitary gland, and to detail its inflammatory cytokine expression. A cloned cell line from the porcine anterior pituitary gland was established and was designated as the porcine anterior pituitary-derived cell line (PAPC). PAPC expressed the mRNA of Nanog and Oct-4, and showed positive immunoreactivity for beta-catenin and Hes1 in its nucleus. PAPC grew stably by repeated passage and rapidly in the EGF and bFGF containing medium. RT-PCR showed that PAPC expressed mRNA of IL-1alpha, IL-6, IL-12, IL-15, IL-18 and TLR4. PAPC expressed S100alpha and IL-18 protein, which was localized in the marginal epithelial cells of Rathke's pouch. These results suggest that PAPC is a stem/progenitor cell and may regulate anterior pituitary cell function through an immuno-endocrine pathway. (Keyword) Animals / Cytokines / Female / Immunohistochemistry / Inflammation / Pituitary Gland, Anterior / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Stem Cells / Swine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.vetimm.2008.03.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18440649 ● Search Scopus @ Elsevier (PMID): 18440649 ● Search Scopus @ Elsevier (DOI): 10.1016/j.vetimm.2008.03.007 (DOI: 10.1016/j.vetimm.2008.03.007, PubMed: 18440649)
26.	Shinichiro Hayashi, Masato Miyake, Kouichi Watanabe, Hisashi Aso, Seigo Hayashi, Shyuichi Ohwada and Takahiro Yamaguchi : Myostatin preferentially down-regulates the expression of fast 2x myosin heavy chain in cattle., Proceedings of the Japan Academy. Series B, Physical and biological sciences, Vol.84, No.8, 354-362, 2008. (Summary) Myostatin is involved in an inhibitor of muscular growth and differentiation. Myoblasts derived from double-muscled Japanese shorthorn cattle (DM myoblasts) with absence of functional myostatin had higher abilities to proliferate and differentiate than myoblasts derived from normal-muscled cattle (NM myoblasts). In DM myoblasts, mRNA expressions of fetal myosin heavy chain (MyHC) in growth medium and of fast 2a and 2x MyHC in fusion medium were significantly greater than that in NM myoblasts. No significant difference existed in expressions of embryonic and slow MyHC mRNA between DM and NM myoblasts. The expression of MyoD mRNA was suppressed in myoblasts by administration of myostatin. Two cloned DM myoblast strains (DMc) were established. Addition of myostatin for DMc resulted in less myotube formation and suppression of mRNA expression of fast 2x MyHC. These findings suggest that the endogenous myostatin preferentially down-regulates the expression of the fast 2x MyHC and participates in differentiation of myofiber types during early bovine myogenesis. (Keyword) Animals / Cattle / Cells, Cultured / Down-Regulation / Muscle, Skeletal / Myosin Heavy Chains / Myostatin / RNA, Messenger / Transforming Growth Factor beta (Link to Publication Site) ● Publication site (DOI): 10.2183/pjab.84.354 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18941308 ● Search Scopus @ Elsevier (PMID): 18941308 ● Search Scopus @ Elsevier (DOI): 10.2183/pjab.84.354 (DOI: 10.2183/pjab.84.354, PubMed: 18941308)
27.	Masato Miyake, Shinichiro Hayashi, Tomomi Sato, Yoshikazu Taketa, Kouichi Watanabe, Shinji Hayashi, Sachi Tanaka, Shyuichi Ohwada, Hisashi Aso and Takahiro Yamaguchi : Myostatin and MyoD family expression in skeletal muscle of IGF-1 knockout mice., Cell Biology International, Vol.31, No.10, 1274-1279, 2007. (Summary) Insulin-like growth factor-1 (IGF-1) is a positive regulator in proliferation and differentiation of skeletal muscle cells, while myostatin (MSTN) is a member of transforming growth factor beta superfamily that acts as a negative regulator of skeletal muscle mass. The present study was performed to detail whether a correlation exists between MSTN and IGF-1 in skeletal muscle of IGF-1 knockout mice (IGF-1(-/-)) and their wild type (WT; i.e., IGF-1(+/+)) littermates. The body weight of IGF-1(-/-) animals was 32% that of WT littermates. The fiber cross-sectional areas (CSA) and number of fibers in M. rectus femoris of IGF-1(-/-) animals were 49 and 59% those of WT animals, respectively. Thus, muscle hypoplasia of IGF-1(-/-) undoubtedly was confirmed. Myostatin mRNA levels and protein levels were similar between M. gastrocnemius of IGF-1(-/-) and WT animals. Myostatin immunoreactivity was similarly localized in muscle fibers of both IGF-1(-/-) and WT M. rectus femoris. The mRNA levels of MyoD family (Myf5, MyoD, MRF4, myogenin) were differentially expressed in IGF-1(-/-)M. gastrocnemius, in which the mRNA expression of MRF4 and myogenin was significantly lower, whereas there were no changes in the mRNA expression of Myf5 and MyoD. These findings first describe that myostatin expression is not influenced by intrinsic failure of IGF-1, although MRF4 and myogenin are downregulated. (Keyword) Animals / Insulin-Like Growth Factor I / Male / Mice / Mice, Knockout / Muscle Strength / Muscle, Skeletal / MyoD Protein / Myogenic Regulatory Factor 5 / Myogenic Regulatory Factors / Myogenin / Myostatin / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Transforming Growth Factor beta (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cellbi.2007.05.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17590360 ● Search Scopus @ Elsevier (PMID): 17590360 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cellbi.2007.05.007 (DOI: 10.1016/j.cellbi.2007.05.007, PubMed: 17590360)

Review, Commentary:

1.	Masato Miyake and Seiichi Oyadomari : 小胞体膜タンパク質PERKによるオルガネラ制御と個体機能調節, Seikagaku, Vol.95, No.6, 765-774, Dec. 2023.
2.	Masato Miyake and Seiichi Oyadomari : Inter-Organ Metabolic Communication via the Unfolded Stress Response., Clinical Calcium, Vol.28, No.11, 1548-1553, Oct. 2018. (Summary) Organs do not independently coordinate their metabolic activity:close communication between different organ systems is essential to regulate metabolism effectively. In recent years, the unfolded protein response(UPR), which is an adaptive mechanism to decrease the amount of unfolded or misfolded proteins in the ER, has been found to regulate metabolic function not only at the cellular level but also at the whole-organism level by way of inter-organ communications. This manuscript will present the most recent findings on the role of the UPR in inter-organ metabolic networks. (Keyword) endoplasmic reticulum / Humans / Metabolic Networks and Pathways / Proteins / Unfolded Protein Response (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30374012 ● Search Scopus @ Elsevier (PMID): 30374012 (PubMed: 30374012)
3.	Seiichi Oyadomari and Masato Miyake : マイオカインによる代謝調節, 日本臨牀増刊号, Vol.74, No.1, 179-183, Feb. 2016.
4.	Ryosuke Sato, Masato Miyake, Kiyoe Kurahashi, Kazuna Takahara, 野村明利, 津川和江, Atsushi Ogura, Natsuo Yasui and Seiichi Oyadomari : 小胞体ストレス伝達蛋白質ATF4βは成長軟骨細胞の機能成熟に重要である, Pharma Medica, Vol.31, No.2, 163, Feb. 2013.
5.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Atsushi Ogura, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋での小胞体ストレスなどからのeIF2αリン酸化によるエネルギー消費の制御と抗肥満作用, Pharma Medica, Vol.31, No.2, 161, Feb. 2013.

Proceeding of International Conference:

1.	北風圭介, Miho Oyadomari, 張君, 津川和江, 河野恵理, Masato Miyake, 竹之内康広, 坪井一人, 岡本安雄 and Seiichi Oyadomari : 膵β細胞における小胞体ストレス応答転写因子ATF4の機能解明, 第61回日本生化学会中国・四国支部例会, 誌上開催, Jun. 2020.
2.	Masato Miyake, Zhang Jun and Seiichi Oyadomari : Preemptive activation of integrated stress responses in adipose tissue suppresses food intake and improves obesity through growth and differentiation factor 15, EMBO workshop, Nov. 2019.
3.	Akira Izutani, Yuji Furumoto, Yoshimasa Hamada, Masato Miyake, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : The Influence of Applying High Electrical Field Pulses on Unfolded Protein Response of cells, The 2019 IEEE Pulsed Power and Plasma Science Conference, 4-pages, Orlando, Jun. 2019.
4.	Keisuke Kitakaze, Kiyoe Kurahashi, Masato Miyake, Yoshimasa Hamada, Miho Oyadomari and Seiichi Oyadomari : Targeted Deletion of ATF4 in β-cells Leads to the Vulnerability and Dedifferentiation During ER Stress, American Diabetes Association 78th scientific sessions, Jun. 2018.
5.	Yuji Furumoto, Daiki Sato, Yoshifumi Hamada, Masato Miyake, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : Activation of Endoplasmic Reticulum Stress Response by Applying of Nanosecond Pulsed Electric Fields for Medical Application, Proceedings of the 2018 IEEE International Power Modulator and High Voltage Conference, 456-460, Jackson, Jun. 2018. (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85077809992 (Elsevier: Scopus)
6.	Masatoshi Morimoto, Fumitake Tezuka, Fumio Hayashi, Kazuta Yamashita, Yoichiro Takata, Toshinori Sakai, Kousaku Higashino, Akihiro Nagamachi, Koichi Sairyo, Ryosuke Sato, Masato Miyake and Seiichi Oyadomari : ER STRESS AGGRAVATES THE HYPERTROPHY OF THE LIGAMNTUM FLAVUM, International Society for the Study of Lumbar Spine(ISSLS) 2017( May 29June 2, 2017), Athens, May 2017.
7.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : Saturated Fatty Acids Predominantly Activate PERK Pathway via Altered Composition of the Endoplasmic Reticulum Membrane, and Reduce Insulin Secretion in Pancreatic Cell by Translation Attenuation, 75th ADA scientific sessions, Jun. 2015.
8.	Hiroshi Fukuda, Masato Miyake, Hiroto Hirai, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : Effects on Endoplasmic Reticulum Stress Response of Applying Nanosecond Pulsed Electric Fields, Digest of Technical Papers-IEEE International Pulsed Power Conference, 370-373, Austin, Jun. 2015. (Link to Publication Site) ● Publication site (DOI): 10.1109/PPC.2015.7296943 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1109/PPC.2015.7296943 (DOI: 10.1109/PPC.2015.7296943)
9.	Masato Miyake, Kiyoe Kurahashi and Seiichi Oyadomari : Identification and Characterization of a Small-molecule Inducer of ATF4 for Promoting Insulin Synthesis in Pancreatic cells, 74th ADA Scientific Sessions, Jun. 2014.
10.	Hiroto Hirai, Masato Miyake, Akihiko Nagano, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : Investigation About Effects on Endoplasmic Reticulum Stress Responses by Applying Nanosecond Pulsed Electricfields, Proceedings of the 2014 IEEE International Power Modulator and High Voltage Conference, 419-422, Santa Fe, Jun. 2014. (Link to Publication Site) ● Publication site (DOI): 10.1109/IPMHVC.2014.7287300 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84947087754 (DOI: 10.1109/IPMHVC.2014.7287300, Elsevier: Scopus)
11.	Nomura Akitoshi, Masato Miyake, Atsushi Ogura, Kiyoe Kurahashi, Mori Tomoko, Tsugawa Kazue, Miyamoto Chinobu, Miho Oyadomari and Seiichi Oyadomari : Role of the PERK signaling pathway in metabolic process, International Symposium Hannover-Tokushima Research Communication, Aug. 2013.
12.	Masato Miyake, NOMURA AKITOSHI, Atsushi Ogura, Kazuna Takahara, Kiyoe Kurahashi, Ryosuke Sato, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : Phosphorylation of eIF2 in skeletal muscle increases energy expenditure and are resistant to diet induced obesity., The American Diabetes Association's 73nd Scientific Sessions, Jul. 2013.

Proceeding of Domestic Conference:

1.	Masato Miyake : 脂肪細胞のストレス応答シグナルから発する食欲制御, 第58回糖尿病学の進歩, Feb. 2024.
2.	Masato Miyake : 小胞体タンパク質恒常性を改善してインスリン合成を向上させる新規低分子化合物の同定, 第34回分子糖尿病学シンポジウム, Dec. 2023.
3.	Masato Miyake : 2型糖尿病へと至る膵β細胞の小胞体プロテオスタシス変容と創薬, 第17回日本臨床ストレス応答学会大会, Nov. 2023.
4.	北風圭介, Miho Oyadomari, 張君, 津川和江, 河野恵理, Masato Miyake, 竹之内康広, 坪井一人, 岡本安雄 and Seiichi Oyadomari : 小胞体ストレス応答転写因子ATF4の機能不全は膵β細胞の脱分化を惹起する, 第93回日本生化学会大会, Sep. 2022.
5.	Masato Miyake, Mitsuaki Sobajima, 倉橋清衛, 重永章, 傳田将也, 大髙章, 齋尾智英, 小迫英尊 and Seiichi Oyadomari : 膵β細胞において小胞体ストレスを軽減しインスリン合成を促進する新規化合物の同定, 第66回日本糖尿病学会年次学術集会, May 2022.
6.	傍島光昭, Masato Miyake, 井上亮太, 白川純, 有馬寛 and Seiichi Oyadomari : グルコース応答性インスリン分泌制御における転写因子ATF4の多面的な役割, 第32回分子糖尿病学シンポジウム, Dec. 2021.
7.	Hiroki Teraoku, Yu Saitou, Tetsuya Ikemoto, Katsuki Miyazaki, Shin-ichiro Yamada, Yuji Morine, Masato Miyake, Seiichi Oyadomari and Mitsuo Shimada : ヒト脂肪由来間葉系幹細胞を基にした機能的肝細胞様細胞の分化誘導, 第57回日本移植学会総会, Sep. 2021.
8.	Yu Saitou, Tetsuya Ikemoto, Katsuki Miyazaki, Kazunori Tokuda, Shin-ichiro Yamada, Satoru Imura, Yuji Morine, Masato Miyake, Seiichi Oyadomari and Mitsuo Shimada : ヒト脂肪由来間葉系幹細胞から肝細胞様細胞の創出-肝不全・代謝性肝疾患に対する肝移植から細胞治療へ-, 第263回徳島医学会学術集会(令和3年度夏期), Aug. 2021.
9.	Yu Saitou, Tetsuya Ikemoto, Katsuki Miyazaki, Kazunori Tokuda, Shin-ichiro Yamada, Satoru Imura, Yuji Morine, Masato Miyake, Seiichi Oyadomari and Mitsuo Shimada : ヒト脂肪由来間葉系幹細胞から肝細胞様細胞の創出, 第20回日本再生医療学会総会, Mar. 2021.
10.	Yu Saitou, Tetsuya Ikemoto, Katsuki Miyazaki, Kazunori Tokuda, Shin-ichiro Yamada, Satoru Imura, Yuji Morine, Masato Miyake, Seiichi Oyadomari and Mitsuo Shimada : ヒト脂肪由来間葉系幹細胞から肝細胞様細胞の創出- 肝不全・代謝性肝疾患に対する肝移植から細胞治療へ -, 第262回徳島医学会学術集会, Mar. 2021.
11.	Katsuki Miyazaki, Yu Saitou, 高露萍, Tetsuya Ikemoto, Shin-ichiro Yamada, Satoru Imura, Yuji Morine, Masato Miyake, Seiichi Oyadomari and Mitsuo Shimada : ヒト脂肪由来間葉系幹細胞から分化誘導した肝細胞様細胞の遺伝子発現解析, 第56回日本移植学会総会, Nov. 2020.
12.	Masato Miyake and Seiichi Oyadomari : 小胞体ストレス応答による細自立的・非自立的代謝制御, 第93 回日本生化学会大, Sep. 2020.
13.	北風圭介, 谷内秀輔, 河野恵理, Yoshimasa Hamada, Masato Miyake, Miho Oyadomari, 小島宏建, Hidetaka Kosako, 栗原ともこ, 吉田優, 細谷孝充 and Seiichi Oyadomari : 小胞体ストレス下のタンパク質凝集と細胞毒性を緩和する化学シャペロンの同定, 第93回日本薬理学会年会, Mar. 2020.
14.	谷内秀輔, Hidetaka Kosako, Masato Miyake, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスセンサーPERK による炎症性メディエーター調節機構, 第14回小胞体ストレス研究会, Sep. 2019.
15.	北風圭介, 谷内秀輔, 河野恵理, Yoshimasa Hamada, Masato Miyake, Miho Oyadomari, 小島宏達, Hidetaka Kosako, 栗原ともこ, 吉田優, 細谷孝充 and Seiichi Oyadomari : 小胞体ストレス下のタンパク質凝集を標的とする新規化学シャペロンの同定, 第92回日本生化学会大会, Sep. 2019.
16.	北風圭介, 谷内秀輔, 河野恵理, Yoshimasa Hamada, Masato Miyake, Miho Oyadomari, 小島宏達, Hidetaka Kosako, 栗原ともこ, 吉田優, 細谷孝充 and Seiichi Oyadomari : プロテオパチーの治療薬創出を目指した新規化学シャペロンの探索, 第31回創薬・薬理フォーラム岡山, Jul. 2019.
17.	北風圭介, 谷内秀輔, 河野恵理, Yoshimasa Hamada, Masato Miyake, Miho Oyadomari, 小島宏達, Hidetaka Kosako, 栗原ともこ, 吉田優, 細谷孝充 and Seiichi Oyadomari : 小胞体におけるタンパク質凝集と細胞毒性を軽減する新規化学シャペロンの同定, 第60回日本生化学中国・四国支部例会, May 2019.
18.	Masato Miyake and Seiichi Oyadomari : 脂肪細胞におけるストレス応答性転写因子ATF4の機能解明, 第30回分子糖尿病学シンポジウム, Dec. 2018.
19.	谷内秀輔, Hidetaka Kosako, Masato Miyake, Miho Oyadomari and Seiichi Oyadomari : HMGB1とHMGB2はPERKの新規リン酸化基質である, 第13回小胞体ストレス研究会, Nov. 2018.
20.	山川哲生, Masato Miyake, Masatoshi Morimoto, Satoshi Hisanaga, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : ERK経路下流因子ncRNAによる癌増殖機構の解析, 第13回小胞体ストレス研究会, Nov. 2018.
21.	張君, Masato Miyake, 津川和江, Miho Oyadomari and Seiichi Oyadomari : セリン710残基によるIRE1α-RNase 活性の制御, 第13回小胞体ストレス研究会, Nov. 2018.
22.	北風圭介, 谷内秀輔, 河野恵理, 濱田良真, Masato Miyake, Miho Oyadomari, 小島宏達, Hidetaka Kosako, 栗原ともこ, 吉田優, 細谷孝充 and Seiichi Oyadomari : 細胞ベースのハイスループットスクリーニングによる新規化学シャペロンの同定, 第13回小胞体ストレス研究会, Nov. 2018.
23.	Masato Miyake, 谷内秀輔 and Seiichi Oyadomari : CRISPRスクリーンで同定した新規PERK経路制御因子の機能解明, 第13回小胞体ストレス研究会, Nov. 2018.
24.	濱田良真, Yuji Furumoto, 泉谷亮, 北風圭介, 谷内秀輔, Masato Miyake, Miho Oyadomari, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : 薬理・物理的なeIF2αのリン酸化誘導とキナーゼの同定, 第13回小胞体ストレス研究会, Nov. 2018.
25.	Masato Miyake, 張君 and Seiichi Oyadomari : 脂肪組織での統合的ストレス応答はDdit3-Gdf15経路による摂食抑制を介して肥満を改善する, 第39回肥満学会, Oct. 2018.
26.	Masato Miyake, 張君, Satoshi Hisanaga, Miho Oyadomari and Seiichi Oyadomari : 脂肪細胞における統合的ストレス応答は GDF15 を介した摂食抑制により食事性肥満を改善する, 第61回日本糖尿病学会年次学術集会, May 2018.
27.	Masato Miyake and Seiichi Oyadomari : 小胞体ストレス応答因子PERKによる代謝調節機構, ConBio2017(第41回日本分子生物学会年会，第91回日本生化学会大会), Dec. 2017.
28.	北風圭介, Masato Miyake, 森本雅俊, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : ATF4 ノックアウトマウスの膵β細胞は小胞体ストレスに脆弱で脱分化をきたす, 第29回分子糖尿病学シンポジウム, Dec. 2017.
29.	北風圭介, Masato Miyake, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 膵β細胞特異的Atf4ノックアウトマウスは小胞体ストレスを介した糖尿病が重症化する, 第12回小胞体ストレス研究会, Oct. 2017.
30.	谷内秀輔, Masato Miyake, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : eIF2αのリン酸化はミトコンドリアの代謝機能に関与する, 第12回小胞体ストレス研究会, Oct. 2017.
31.	張君, Masato Miyake, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 高血糖に伴うIRE1のO-GlcNAc修飾は小胞体ストレス応答を減弱させる, 第12回小胞体ストレス研究会, Oct. 2017.
32.	山川哲生, Masatoshi Morimoto, 久永哲, Masato Miyake, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 新規PERK経路下流因子Snhg12ホモ欠損マウス解析, 第12回小胞体ストレス研究会, Oct. 2017.
33.	久永哲, Masato Miyake, 谷内秀輔, 森本雅俊, Miho Oyadomari and Seiichi Oyadomari : PERK経路の活性化が軟骨細胞のECM分泌に与える影響, 第12回小胞体ストレス研究会, Oct. 2017.
34.	森本雅俊, Masato Miyake, 久永哲, 谷内秀輔, 張君, Koichi Sairyo and Seiichi Oyadomari : 黄色靭帯肥厚における小胞体ストレスの役割, 第12回小胞体ストレス研究会, Oct. 2017.
35.	Masato Miyake, 谷内秀輔, 久永哲, Miho Oyadomari and Seiichi Oyadomari : CRISPRライブラリーを用いた新規小胞体ストレス応答制御因子の同定, 第12回小胞体ストレス研究会, Oct. 2017.
36.	張君, Masato Miyake, Kiyoe Kurahashi, 宮本千伸, 津川和江, 尾野雅哉, Miho Oyadomari and Seiichi Oyadomari : 高血糖に伴うIRE1のO-GlcNAc修飾は小胞体ストレス応答を減弱させる, 第60回日本糖尿病学会年次学術集会, May 2017.
37.	張君, Masato Miyake, 津川和江, 宮本千伸 and Seiichi Oyadomari : UPR欠損マウス胎児線維芽細胞は小胞体からのCa2+放出を介してアポトーシスを誘導する, 第11回臨床ストレス応答学会大会, Nov. 2016.
38.	谷内秀輔, Masato Miyake, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 哺乳類ミトコンドリアUPR は統合的ストレス応答を介さずに誘導される, 第11回小胞体ストレス研究会, Oct. 2016.
39.	山川哲生, Masato Miyake, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 腎癌の予後に関係する新規PERK 経路下流因⼦(ncRNA)について, 第11回小胞体ストレス研究会, Oct. 2016.
40.	Masato Miyake and Seiichi Oyadomari : 脂肪細胞におけるPERK 経路を起点とした細胞間相互作⽤による細胞死の誘導, 第11回小胞体ストレス研究会, Oct. 2016.
41.	張君, Masato Miyake, 津川和江, 宮本千伸 and Seiichi Oyadomari : UPR⽋損マウス胎児線維芽細胞は⼩胞体からのCa2+放出を介してアポトーシスを誘導する, 第11回小胞体ストレス研究会, Oct. 2016.
42.	Masato Miyake, 張君, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 脂肪組織での小胞体ストレスなどで活性化されるeIF2αリン酸化シグナルによる肥満抑制作用, 第89回日本生化学会大会, Sep. 2016.
43.	Kiyoe Kurahashi, 河野恵理, 宮本千伸, 津川和江, Miho Oyadomari, 木村千寿子, Satoshi Hisanaga, Masatoshi Morimoto, 山川哲生, 谷内秀輔, 張君, Masato Miyake, Masahiro Abe and Seiichi Oyadomari : ラベルフリー測定によるハイスループットスクリーニングを用いた新規インスリン分泌促進薬の探索, 第59回日本糖尿病学会年次学術集会, May 2016.
44.	Masato Miyake, Kazuna Takahara, 張君, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : ATF6βの肥満・糖尿病における役割の解明, 第59回日本糖尿病学会年次学術集会, May 2016.
45.	Masato Miyake, Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, 三浦恭子, 北原吉朗 and Seiichi Oyadomari : 小胞体ストレスを減弱させ膵β細胞でのインスリン生合成を促進する新規化合物の同定, 第27回分子糖尿病学シンポジウム, Dec. 2015.
46.	谷内秀輔, Masato Miyake, 津川和江, Miho Oyadomari and Seiichi Oyadomari : CRISPR/Cas9システムを用いた統合的ストレス応答を制御するeIF2αキナーゼの検証, 第38回分子生物学会年会・第88回生化学会年会合同大会, Dec. 2015.
47.	山川哲生, Atsushi Ogura, Masato Miyake, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : PERK経路の下流因子によって制御される癌細胞増殖機構について, 第38回分子生物学会年会・第88回生化学会年会合同大会, Dec. 2015.
48.	Masato Miyake, 張君, Tetsuya Shiuchi, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどで活性化されるeIF2αリン酸化シグナルによる摂食調節を介した肥満抑制作用, 第38回分子生物学会年会・第88回生化学会年会合同大会, Dec. 2015.
49.	張君, Masato Miyake, Kiyoe Kurahashi, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : CRISPR/Cas9 を用いた小胞体ストレス応答伝達タンパク質の検証, 第38回分子生物学会年会・第88回生化学会年会合同大会, Dec. 2015.
50.	Ryosuke Sato, Masato Miyake, 谷内秀輔, 山川哲生, 張君, Kiyoe Kurahashi, Masatoshi Morimoto, Satoshi Hisanaga, Koichi Sairyo and Seiichi Oyadomari : ATF6βは非古典的小胞体ストレス応答として軟骨細胞分化を制御する, 第38回分子生物学会年会・第88回生化学会年会合同大会, Dec. 2015.
51.	谷内秀輔, Masato Miyake, 津川和江, Miho Oyadomari and Seiichi Oyadomari : CRISPR/Cas9を用いた統合的ストレス応答に関与するeIF2αキナーゼの解析, 第10回小胞体ストレス研究会, Nov. 2015.
52.	張君, Masato Miyake, Kiyoe Kurahashi, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : CRISPR/Cas9 を用いた小胞体ストレス応答伝達タンパク質の検証, 第10回小胞体ストレス研究会, Nov. 2015.
53.	Masato Miyake, Kazuna Takahara, Masatoshi Morimoto, Kiyoe Kurahashi and Seiichi Oyadomari : ATF6βの肥満・糖尿病における役割, 第10回小胞体ストレス研究会, Nov. 2015.
54.	Masatoshi Morimoto, Satoshi Hisanaga, 張君, 谷内秀輔, 山川哲生, Masato Miyake, Koichi Sairyo and Seiichi Oyadomari : ATF6αの骨形成における役割, 第10回小胞体ストレス研究会, Nov. 2015.
55.	Masato Miyake, Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, 三浦恭子, 北原吉朗, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスを標的とした膵β細胞でのインスリン生合成を促進する新規化合物の同定, 第10回臨床ストレス応答学会大会, Nov. 2015.
56.	Masato Miyake, 張君, Kiyoe Kurahashi, 宮本千伸, 津川和江, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどで活性化されるeIF2αリン酸化シグナルによる摂食調節を介した肥満抑制作用, 第58回日本糖尿病学会年次学術集会, May 2015.
57.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 膵β細胞での脂肪毒性における小胞体ストレス応答の役割の解明, 第58回日本糖尿病学会年次学術集会, May 2015.
58.	Masato Miyake, Kiyoe Kurahashi, 張君, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 肥満に伴う脂肪組織での慢性炎症の増悪プロセスへの小胞体ストレス応答経路の関与, 第37回日本分子生物学会年会, Nov. 2014.
59.	倉橋清衛, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は膵β細胞の小胞体膜の組成を変化させ，PERK 経路の活性化による翻訳抑制を介してインスリン分泌を低下させる, 第9回臨床ストレス応答学会大会, Nov. 2014.
60.	張君, Masato Miyake, 津川和江 and Seiichi Oyadomari : CRISPR/Cas9 を用いた小胞体ストレス応答伝達タンパク質の検証, 第9回臨床ストレス応答学会大会, Nov. 2014.
61.	谷内秀輔, Masato Miyake, 津川和江 and Seiichi Oyadomari : Integrated stress response を担う第 5 の eIF2αキナーゼが存在する可能性の CRISPR/Cas9 システムを用いた検証, 第9回臨床ストレス応答学会大会, Nov. 2014.
62.	福田寛, Masato Miyake, 平井寛人, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : ナノ秒パルス電界による HeLa細胞，HEK293細胞の活性化, 平成26年度電気関係学会四国支部連合大会講演論文集, 239, Sep. 2014.
63.	Akitoshi Nomura, Masato Miyake, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどにより活性化されるeIF2αリン酸化シグナルによる脂肪細胞機能調節, 第8回小胞体ストレス研究会, Oct. 2013.
64.	長野明彦, Masato Miyake, 平井寛人, Kenji Teranishi, Naoyuki Shimomura and Seiichi Oyadomari : パルス高電界による骨格筋機能制御の基礎研究, 平成25年度電気関係学会四国支部連合大会講演論文集, 240, Sep. 2013.
65.	Akitoshi Nomura, Masato Miyake, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : ポスター発表小胞体ストレスなどにより活性化されるeIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第86回日本生化学会大会, Sep. 2013.
66.	Kiyoe Kurahashi, 森智子, 野村明利, Atsushi Ogura, 津川和江, 宮本千伸, Masato Miyake, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は小胞体膜の流動性低下によるPERK経路の活性化を介して膵β細胞におけるインスリン分泌を低下させる, 第86回日本生化学会大会, Sep. 2013.
67.	Akitoshi Nomura, Masato Miyake, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどにより活性化されるeIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第86回日本生化学会大会, Sep. 2013.
68.	Kiyoe Kurahashi, 森智子, Akitoshi Nomura, Atsushi Ogura, 津川和江, 宮本千伸, Masato Miyake, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : ポスター発表飽和脂肪酸は小胞体膜の流動性低下によるPERK経路の活性化を介して膵β細胞におけるインスリン分泌を低下させる, 第86回日本生化学会大会, Sep. 2013.
69.	Masato Miyake, Akitoshi Nomura, Atsushi Ogura, Kazuna Takahara, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋での小胞体ストレスなどからのeIF2αリン酸化はFgf21発現を誘導しエネルギー消費の増加によって食事性肥満を防ぐ, 第86回日本生化学会大会, Sep. 2013.
70.	Ryosuke Sato, Masato Miyake, Kiyoe Kurahashi, Kazuna Takahara, Akitoshi Nomura, 津川和江, Natsuo Yasui and Seiichi Oyadomari : 軟骨異形成症の原因である変異型FGFR3は小胞体ストレスを介して軟骨細胞のアポトーシスを誘導する, 第86回日本生化学会大会, Sep. 2013.
71.	Kazuna Takahara, Masato Miyake, Akitoshi Nomura, Atsushi Ogura, Miho Oyadomari, 森智子, 宮本千伸, 三浦直子, 津川和江, Eiji Tanaka, 森和俊 and Seiichi Oyadomari : 軟骨異形成症の原因である変異型FGFR3は小胞体ストレスを介して軟骨細胞のアポトーシスを誘導する, Sep. 2013.
72.	Kazuna Takahara, Masato Miyake, Akitoshi Nomura, Atsushi Ogura, Miho Oyadomari, 森智子, 宮本千伸, 三浦直子, 津川和江, Eiji Tanaka, 森和俊 and Seiichi Oyadomari : 小胞体ストレス応答伝達タンパク質ATF6-alphaとATF6-betaの代謝における役割, 第86回日本生化学会大会, Sep. 2013.
73.	野村明利, Masato Miyake, Atsushi Ogura, 森智子 and 津川和江 : 小胞体ストレスなどにより活性化されるeIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第86回日本生化学会大会, Sep. 2013.
74.	Akitoshi Nomura, Masato Miyake, Hiroshi Inoue, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどにより活性化されるPERK-eIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第54回日本生化学会中国・四国支部例会, Jun. 2013.
75.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Atsushi Ogura, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋における小胞体ストレスなどによるeIF2αリン酸化は全身のエネルギー消費を増加させて肥満を抑制する, 第56回日本糖尿病学会年次学術集会, May 2013.
76.	Kiyoe Kurahashi, 三浦直子, 宮本千伸, 津川和江, 森智子, Miho Oyadomari, Masato Miyake, Atsushi Ogura, Toshio Matsumoto and Seiichi Oyadomari : 膵β細胞における飽和脂肪酸による脂肪毒性に小胞体膜流動性の低下とPERK経路が影響する, 第56回日本糖尿病学会年次学術集会, May 2013.
77.	Akitoshi Nomura, Masato Miyake, Hiroshi Inoue, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどにより活性化されるPERK-eIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第56回日本糖尿病学会年次学術集会, May 2013.
78.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋における小胞体ストレスなどからのeIF2αリン酸化はエネルギー消費を制御して食事性肥満を防ぐ, 第85回日本生化学会大会, Dec. 2012.
79.	Kiyoe Kurahashi, 森智子, Hiroshi Inoue, Atsushi Ogura, 津川和江, Masato Miyake, Hiroshi Inoue, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸による膵β細胞のインスリン分泌低下には小胞体膜流動性の変化による小胞体ストレスが関与し，PERK経路の活性化により改善される, 第85回日本生化学会大会, Dec. 2012.
80.	Akitoshi Nomura, Masato Miyake, Hiroshi Inoue, Atsushi Ogura, 森智子, 津川和江, 宮本千伸, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレスなどにより活性化されるPERK-eIF2αリン酸化シグナルによる脂肪細胞機能調節の解明, 第85回日本生化学会大会, Dec. 2012.
81.	Ryosuke Sato, Masato Miyake, Kiyoe Kurahashi, Kazuna Takahara, Akitoshi Nomura, 津川和江, Atsushi Ogura, Hiroshi Inoue, Natsuo Yasui and Seiichi Oyadomari : FGFR3遺伝子異常による軟骨異形成症における小胞体ストレスの関与, 第85回日本生化学会大会, Dec. 2012.
82.	Kazuna Takahara, Taiji Ito, 森智子, Robert Zheng, Mari Funahashi, 宮本千伸, Seiko Kagawa, Masato Miyake, Miho Oyadomari, 津川和江, Eiji Tanaka, 森和俊 and Seiichi Oyadomari : DSS誘発性大腸炎モデルを用いたATF6αとATF6βの機能解析, 第85回日本生化学会大会, Dec. 2012.
83.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋での小胞体ストレスなどによる eIF2a リン酸化はエネルギー消費を増大させて肥満を抑制する, 第 24 回分子糖尿病学シンポジウム, Dec. 2012.
84.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋での小胞体ストレスなどによる eIF2αリン酸化はエネルギー消費を増大させて肥満を抑制する, 第7回臨床ストレス応答学会大会, Nov. 2012.
85.	Masato Miyake, Akitoshi Nomura, Kazuna Takahara, Atsushi Ogura, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋での小胞体ストレスなどによる eIF2a リン酸化はエネルギー消費を増大させて肥満を抑制する, 第7回小胞体ストレス研究会, Nov. 2012.
86.	Ryosuke Sato, Masato Miyake, Kiyoe Kurahashi, Kazuna Takahara, Akitoshi Nomura, 津川和江, Atsushi Ogura and Seiichi Oyadomari : 小胞体ストレス伝達タンパク質ATF6βは成長軟骨細胞の機能成熟に重要である, 第7回小胞体ストレス研究会, Nov. 2012.
87.	Kazuna Takahara, Taiji Ito, 森智子, Robert Zeng, Mari Funahashi, 宮本千伸, Seiko Kagawa, Masato Miyake, Miho Oyadomari, Eiji Tanaka, 森和俊 and Seiichi Oyadomari : DSS誘発性大腸炎におけるATF6αとATF6βの役割, 第84回日本生化学会大会, Sep. 2011.

Et cetera, Workshop:

1.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は膵β細胞の小胞体膜の組成を変化させ，PERK 経路の活性化による翻訳抑制を介してインスリン分泌を低下させる, 第26回分子糖尿病学シンポジウム, Dec. 2014.
2.	Masato Miyake, Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, 三浦恭子, 北原吉朗, Miho Oyadomari and Seiichi Oyadomari : 小胞体ストレス応答を制御する新規化合物によるインスリン生合成の促進, 第9回小胞体ストレス研究会, Jul. 2014.
3.	張君, Masato Miyake and Seiichi Oyadomari : ゲノム編集技術を用いた小胞体ストレス応答の解析, 第9回小胞体ストレス研究会, Jul. 2014.
4.	Ryosuke Sato, Masato Miyake, 松尾顕, 張君, 谷内秀輔, Kiyoe Kurahashi, Kazuna Takahara, Satoshi Hisanaga, Koichi Sairyo and Seiichi Oyadomari : 軟骨分化におけるATF6βの役割, 第9回小胞体ストレス研究会, Jul. 2014.
5.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸による膵β細胞の小胞体膜の組成変化は，PERK経路活性化を遷延させ翻訳抑制を介してインスリン分泌を低下させる, 第9回小胞体ストレス研究会, Jul. 2014.
6.	谷内秀輔, Masato Miyake and Seiichi Oyadomari : ゲノム編集技術を用いたIntegrated Stress Response(ISR)の解析, 第9回小胞体ストレス研究会, Jul. 2014.
7.	Masato Miyake, Akitoshi Nomura, Atsushi Ogura, Kazuna Takahara, Ryosuke Sato, Kiyoe Kurahashi, Miho Oyadomari, Hiroshi Inoue and Seiichi Oyadomari : 骨格筋における小胞体ストレスなどによるeIF2αリン酸化はFgf21を介したエネルギー消費の増加によって食事性肥満を防ぐ, 第31回内分泌代謝学サマーセミナー, Jul. 2013.

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

脂肪性肝疾患における小胞体プロテオスタシス破綻の原因と意義の解明 (Project/Area Number: 24K02882 )
The role of endoplasmic reticulum sensor ATF6beta in diabetes and obesity (Project/Area Number: 20K08909 )
Role of integrated stress response in adipocyte (Project/Area Number: 17K09862 )
Development of potential anti-sarcopenia agents targeting the integrated stress response (Project/Area Number: 16H05222 )
Role of unfolded protein response on age-related skeletal muscle atrophy (Project/Area Number: 26350893 )
Physiological and pathological role of the endoplasmic reticulum stress transducer protein ATF6beta (Project/Area Number: 25293080 )
Role of endoplasmic reticulum stress induced eIF2alpha phosphorylation in skeletal muscle after exercise (Project/Area Number: 24700698 )
Role of nutrient sensor AMPK on regulation of myogenic inhibitory factor myostatin. (Project/Area Number: 22880006 )
Glucose and lipid metabolism regulated by the endoplasmic reticulum signaling (Project/Area Number: 22390061 )
Search by Researcher Number (30588976)

Associate Professor : Miyake, Masato

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