Updated on 2025/05/30

写真a

 
Ohkubo Nobutaka
 
Organization
Graduate School of Medicine Program for Medical Sciences Senior Assistant Professor
Title
Senior Assistant Professor
Contact information
メールアドレス
External link

Degree

  • 博士（医学） ( 大阪大学大学院 )

Research Interests

  • 幹細胞

  • アポリポ蛋白E

  • Apolipoprotein E

  • Alzheimer's disease

  • 機能性食品

  • zinc finger protein 521

  • アルツハイマー病

Research Areas

  • Life Science / Neuroscience-general

  • Life Science / Clinical pharmacy

  • Life Science / Anatomy

  • Life Science / Physiology

Education

  • 大阪大学大学院   医学系研究科

    1999.4 - 2003.3

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Research History

  • Ehime University   Graduate School of Medicine

    2007.10

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  • Ehime University   Graduate School of Medicine

    2007.4 - 2007.9

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  • Ehime University   Graduate School of Medicine   Research Associate

    2006.4 - 2007.3

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  • Duke University, Medical Centre   Division of Neurology   Research Associate

    2003.8 - 2006.3

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  • 学術振興会   特別研究員（PD)

    2003.4 - 2004.3

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  • 学術振興会   特別研究員（DC2)

    2002.4 - 2003.3

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  • 財団法人遺伝学普及会   日本DNAデータバンク   研究員

    1997.4 - 1999.3

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Professional Memberships

Papers

  • Lack of zinc finger protein 521 upregulates dopamine β-hydroxylase expression in the mouse brain, leading to abnormal behavior. Reviewed

    Ohkubo N, Aoto M, Kon K, Mitsuda N

    Life sciences   231   116559   2019.8

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  • Transferrin receptor 1 is required for enucleation of mouse erythroblasts during terminal differentiation Reviewed

    Mamoru Aoto, Akiho Iwashita, Kanako Mita, Nobutaka Ohkubo, Yoshihide Tsujimoto, Noriaki Mitsuda

    FEBS Open Bio   9 ( 2 )   291 - 303   2018.12

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

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  • Research for psychiatric disorder based on the phenotype analysis of Zfp521 knockout mice. Reviewed

    Nobutaka Ohkubo, Mamoru Aoto, Etsuko Matsubara, Jun Yamanouchi, Masaki Yasukawa, Noriaki Mitsuda

    Ehime Medical Journal   35 ( 3 )   117 - 1422   2016.9

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  • Abnormal Behaviors and Developmental Disorder of Hippocampus in Zinc Finger Protein 521 (ZFP521) Mutant Mice Reviewed

    Nobutaka Ohkubo, Etsuko Matsubara, Jun Yamanouchi, Rie Akazawa, Mamoru Aoto, Yoji Suzuki, Ikuya Sakai, Takaya Abe, Hiroshi Kiyonari, Seiji Matsuda, Masaki Yasukawa, Noriaki Mitsuda

    PLOS ONE   9 ( 3 )   E92848   2014.3

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：PUBLIC LIBRARY SCIENCE  

    Zinc finger protein 521 (ZFP521) regulates a number of cellular processes in a wide range of tissues, such as osteoblast formation and adipose commitment and differentiation. In the field of neurobiology, it is reported to be an essential factor for transition of epiblast stem cells into neural progenitors in vitro. However, the role of ZFP521 in the brain in vivo still remains elusive. To elucidate the role of ZFP521 in the mouse brain, we generated mice lacking exon 4 of the ZFP521 gene. The birth ratio of our ZFP521(Delta/Delta) mice was consistent with Mendel's laws. Although ZFP521(Delta/Delta) pups had no apparent defect in the body and were indistinguishable from ZFP521(+/+) and ZFP521(+/Delta) littermates at the time of birth, ZFP521(Delta/Delta) mice displayed significant weight reduction as they grew, and most of them died before 10 weeks of age. They displayed abnormal behavior, such as hyper-locomotion, lower anxiety and impaired learning, which correspond to the symptoms of schizophrenia. The border of the granular cell layer of the dentate gyrus in the hippocampus of the mice was indistinct and granular neurons were reduced in number. Furthermore, Sox1-positive neural progenitor cells in the dentate gyrus and cerebellum were significantly reduced in number. Taken together, these findings indicate that ZFP521 directly or indirectly affects the formation of the neuronal cell layers of the dentate gyrus in the hippocampus, and thus ZFP521(Delta/Delta) mice displayed schizophrenia-relevant symptoms. ZFP521(Delta/Delta) mice may be a useful research tool as an animal model of schizophrenia.

    DOI： 10.1371/journal.pone.0092848

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  • Accelerated destruction of erythrocytes in Tie2 promoter-driven STAT3 conditional knockout mice Reviewed

    Nobutaka Ohkubo, Yoji Suzuki, Mamoru Aoto, Jun Yamanouchi, Satoshi Hirakawa, Masaki Yasukawa, Noriaki Mitsuda

    LIFE SCIENCES   93 ( 9-11 )   380 - 387   2013.9

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

    Aims: STAT3 is a key modulator of activation and differentiation of macrophages. But it is still unknown if deficiency of STAT3 activates macrophages to destroy erythrocytes by phagocytosis. We generated STAT3 conditional knockout mice by crossing foxed STAT3 mice with Tie2 promoter-driven Cre-recombinase transgenic mice and clarified that Stat3 plays a critical role in the formation and activation of macrophages.
    Main methods: Blood cell count, reticulocyte count, serum lactate dehydrogenase, erythropoietin, iron and ferritin concentration, and life span of the erythrocytes in Tie2 promoter-driven STAT3 conditional knockout mice were analyzed. To explore the erythropoietic function of the mice, we subjected them to brief hemolytic anemia by injecting them intraperitoneally with phenylhydrazine. The fragility of erythrocytes was examined by scanning electron microscopy and osmotic tolerance test.
    Key findings: The conditional knockout mice had mild normocytic anemia. They also displayed higher lactate dehydrogenase, ferritin and erythropoietin concentration, higher reticulocyte count, and a shorter lifespan of erythrocytes compared with wild-type controls. These data suggest that destruction of erythrocytes and secondary blood formation were accelerated in the STAT3 conditional knockout mice. It didn't appear due to the fragility of erythrocytes. A few of the conditional knockout mice suddenly developed acute severe anemia, high body temperature and massive splenomegaly, and died within 2 weeks after the onset of anemia.
    Significance: This study provided evidence that STAT3 have a critical role in the destruction of erythrocytes by resident macrophages in the spleen. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.

    DOI： 10.1016/j.lfs.2013.07.025

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  • Histochemical analysis of brain from neural differentiation factor Zfp521 deficient mice Reviewed

    Akazawa Rie, Ohkubo Nobutaka, Aoto Mamoru, Suzuki Yoji, Matsubara Etsuko, Yamanouchi Jun, Sakai Ikuya, Yasukawa Masaki, Mitsuda Noriaki

    JOURNAL OF PHYSIOLOGICAL SCIENCES   63   S126   2013

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  • Transferrin-Transferrin receptor 1 signaling is required for mouse erythroblast enucleation through the mechanism independent of iron uptake Reviewed

    Onji Hiroshi, Kono Ryoma, Suzuki Yoji, Ohkubo Nobutaka, Mitsuda Noriaki, Tsujimoto Yoshihide, Aoto Mamoru

    JOURNAL OF PHYSIOLOGICAL SCIENCES   63   S173   2013

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  • Study of a mechanism of protective effect with saponins from Panax Ginseng against oxidative stress in blood preservation Reviewed

    Kono Yusuke, Izumi Ryo, Kono Hiroki, Suzuki Yoji, Ohkubo Nobutaka, Samukawa Keiichi, Aoto Mamoru, Mitsuda Noriaki

    JOURNAL OF PHYSIOLOGICAL SCIENCES   63   S173   2013

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  • Preventive effect of lignan on redox status of erythrocyte membrane against oxidative stress Reviewed

    Sato Masatoshi, Okada Nanae, Suzuki Yoji, Ohkubo Nobutaka, Aoto Mamoru, Yamauchi Satoshi, Mitsuda Noriaki

    JOURNAL OF PHYSIOLOGICAL SCIENCES   63   S230   2013

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  • Apolipoprotein E and Peptide Mimetics Modulate Inflammation by Binding the SET Protein and Activating Protein Phosphatase 2A Reviewed

    Dale J. Christensen, Nobutaka Ohkubo, Jessica Oddo, Michael J. Van Kanegan, Jessica Neil, Fengqiao Li, Carol A. Colton, Michael P. Vitek

    JOURNAL OF IMMUNOLOGY   186 ( 4 )   2535 - 2542   2011.2

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER ASSOC IMMUNOLOGISTS  

    The molecular mechanism by which apolipoprotein E (apoE) suppresses inflammatory cytokine and NO production is unknown. Using an affinity purification approach, we found that peptide mimetics of apoE, derived from its receptor binding domain residues 130-150, bound to the SET protein, which is a potent physiological inhibitor of protein phosphatase 2A (PP2A). Both holo-apoE protein and apoE-mimetic peptides bound to the C-terminal region of SET, which is then associated with an increase in PP2A-mediated phosphatase activity. As physiological substrates for PP2A, the LPS-induced phosphorylation status of signaling MAPK and Akt kinase is reduced following treatment with apoE-mimetic peptides. On the basis of our previous report, in which apoE-mimetic peptides reduced I-kappa B kinase and NF-kappa B activation, we also demonstrate a mechanism for reduced production of inducible NO synthase protein and its NO product. These data provide evidence for a novel molecular mechanism by which apoE and apoE-mimetic peptides antagonize SET, thereby enhancing endogenous PP2A phosphatase activity, which reduces levels of phosphorylated kinases, signaling, and inflammatory response. The Journal of Immunology, 2011, 186: 2535-2542.

    DOI： 10.4049/jimmunol.1002847

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  • Essential role of p38 MAPK in caspase-independent, iPLA(2)-dependent cell death under hypoxia/low glucose conditions Reviewed

    Mamoru Aoto, Koei Shinzawa, Yoji Suzuki, Nobutaka Ohkubo, Noriaki Mitsuda, Yoshihide Tsujimoto

    FEBS LETTERS   583 ( 10 )   1611 - 1618   2009.5

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

    The mechanisms of cell death induced by hypoxia or ischemia are not yet fully understood. We have previously demonstrated that cell death induced by hypoxia occurs independently of caspases, and is mediated by phospholipase A(2) (PLA(2)).
    Here, we show that p38 mitogen-activated protein kinase is activated under hypoxia. A selective inhibitor of p38 or decrease in the p38alpha protein level prevents hypoxia-induced cell death. The p38 inhibitor abolishes PLA(2) activation by hypoxia, indicating that p38 acts upstream of PLA(2). The antioxidant N-acetyl-cysteine inhibits activation of p38 and cell death induced by hypoxia, indicating that reactive oxygen species (ROS) are responsible for p38 activation. These results demonstrate that the ROS/p38/PLA(2) signaling axis has a crucial role in caspase-independent cell death induced by hypoxia. Crown Copyright (C) 2009 Published by Elsevier B. V. on behalf of Federation of European Biochemical society. All rights reserved.

    DOI： 10.1016/j.febslet.2009.04.028

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  • REELIN INHIBITS P19 EMBRYONAL CELL DEATH DURING NEURONAL DIFFERENTIATION Reviewed

    Nobutaka Ohkubo, Yoji Suzuki, Noriaki Mitsuda

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   341 - 341   2009

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    Language：English   Publisher：SPRINGER TOKYO  

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  • EFFECT OF GINSENOSIDES ON RHEOLOGICAL FUNCTIONS OF ERYTHROCYTES AGAINST OXIDATIVE STRESS Reviewed

    Yoji Suzuki, Nobutaka Ohkubo, Keiichi Samukawa, Mamoru Aoto, Masahiro Sakanaka, Noriaki Mitsuda

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   500 - 500   2009

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    Language：English   Publisher：SPRINGER TOKYO  

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  • ESSENTIAL ROLE OF P38 MAPK IN CASPASE-INDEPENDENT, PHOSPHOLIPASE A2-DEPENDENT CELL DEATH UNDER HYPOXIA/LOW GLUCOSE CONDITIONS Reviewed

    Mamoru Aoto, Koei Shinzawa, Yoji Suzuki, Nobutaka Ohkubo, Noriaki Mitsuda, Yoshihide Tsujimoto

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   159 - 159   2009

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    Language：English   Publisher：SPRINGER TOKYO  

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  • Protective effect of ginsenosides Rg(2) and Rh-1 on oxidation-induced impairment of erythrocyte membrane properties Reviewed

    Keiichi Samukawa, Yoji Suzuki, Nobutaka Ohkubo, Mamoru Aoto, Masahiro Sakanaka, Noriaki Mitsuda

    BIORHEOLOGY   45 ( 6 )   689 - 700   2008

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：IOS PRESS  

    The extract from Panax ginseng has been reported to improve the microcirculation in various organs. However, the mechanisms underlying this phenomenon are still poorly understood. In the present study, using the rheological properties of erythrocytes as an index, we have screened the components of Panax ginseng extract and identified Rg(2) and Rh-1 as the active ingredients. These two ginsenosides prevented the oxidative stress-induced elevation of erythrocyte suspension viscosity and the impairment of erythrocyte elongation in response to shear stress. Rg2 and Rh1 ginsenosides did not have antioxidant activity in an aqueous phase and did not inhibit the peroxidation of membrane lipids, either. However, they inhibited the oxidation-induced decrease of SH-groups in band 3 (anion exchanger-1), one of the important structural proteins of the erythrocyte membrane, but not in other structural proteins: bands 1 and 2 (spectrins), band 4.2 or band 5 (actin). These results suggest that ginsenosides Rg2 and Rh1 protect the rheological functions of erythrocytes against oxidative stress by preventing the oxidation of SH-groups in band 3 protein.

    DOI： 10.3233/BIR-2008-0516

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  • Reelin signals survival through Src-family kinases that inactivate BAD activity Reviewed

    Nobutaka Ohkubo, Michael P. Vitek, Atsuyuki Morishima, Yoji Suzuki, Tetsuro Miki, Nobuji Maeda, Noriaki Mitsuda

    JOURNAL OF NEUROCHEMISTRY   103 ( 2 )   820 - 830   2007.10

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING  

    Reelin plays an important role in the migration of embryonic neurons, but its continuing presence suggests additional functions in the brain. We now report a novel function where reelin protects P19 embryonal cells from apoptosis during retinoic acid-induced neuronal differentiation. This increased survival is associated with reelin activation of the phosphatidyl-inositol-3-kinase (P13 K)/Akt pathway. When P13 K was inhibited with LY294002, reelin failed to protect against this retinoic acid-induced apoptosis. The protective effect of reelin includes activating the Src-family kinases/P13 K/Akt pathway which then led to selective phosphorylation of Bcl-2/Bcl-XL associated death promoter (BAD) at serine-136, while the phosphorylation-incompetent mutation of BAD (S136A) suppressed this protection. These and additional studies define a novel pathway where reelin binds apoE receptors, significantly activates the P13 K/Akt pathway causing phosphorylation of BAD which helps to protect cells from apoptosing, thus serving an important role in promoting the survival of maturing neurons in the brain.

    DOI： 10.1111/j.1471-4159.2007.04804.x

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  • Androgen-mediated immune function is altered by the apolipoprotein E gene Reviewed

    Candice M. Brown, Qing Xu, Nobutaka Okhubo, Michael P. Vitek, Carol A. Colton

    ENDOCRINOLOGY   148 ( 7 )   3383 - 3390   2007.7

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：ENDOCRINE SOC  

    Androgens, like estrogens, have been linked to neuroprotective effects in the brain and to the improvement of cognitive function. Part of this effect may be due to the action of androgens on the innate immune response. We have examined the action of dihydrotestosterone (DHT) and testosterone on immune activation in primary cultures of microglia, the central nervous system macrophage. Our data indicate that DHT acts as an antiinflammatory agent and depresses both nitric oxide and TNF alpha production in a dose-dependent fashion. However, testosterone treatment of microglia and peritoneal macrophages increased supernatant nitrite levels, indicative of a proinflammatory effect. Because the apolipoprotein E ( APOE) genotype also dramatically impacts macrophage function and has been linked to neurodegenerative disease, we compared the effects of APOE genotype on androgen-mediated regulation of inflammation using targeted replacement mice expressing only the human APOE3 or human APOE4 gene. Our data show that the antiinflammatory activity of DHT is significantly reduced in APOE4 targeted replacement mice compared to APOE3 mice. The effect was not due to an APOE isoform-specific change in androgen receptor mRNA and protein expression. Rather, innate immune signaling pathways regulated by androgens are altered in the APOE4 microglia. Compared to APOE3 microglia, DHT treatment did not reduce the phosphorylation of p38 MAPK or p54/p56 Janus kinase in APOE4 mice. Thus, our data suggest that DHT modulation of kinase activity is altered in microglia from mice expressing an APOE4 genotype and may impact androgen treatment therapies in individuals with an APOE4 genotype.

    DOI： 10.1210/en.2006-1200

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  • Participation of caspase-3-like protease in oxidation-induced impairment of erythrocyte membrane properties Reviewed

    Yoji Suzuki, Nobutaka Ohkubo, Mamoru Aoto, Nobuji Maeda, Iwona Cicha, Tetsuro Miki, Noriaki Mitsuda

    BIORHEOLOGY   44 ( 3 )   179 - 190   2007

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：IOS PRESS  

    Erythrocytes are very susceptible to oxidative stress, having a high content of intracellular oxygen and hemoglobin. In the present study, exposure to oxidative stress resulted in a significant impairment of erythrocyte membrane functions, such as deformability and anion exchange. Band 3 protein, also known as anion exchanger-1, plays an important role in these two functions. We show that oxidative stress activated caspase-3 inside the erythrocytes, which resulted in band 3 protein cleavage. Interestingly, inhibition of the caspase-3 with its specific inhibitor not only suppressed the digestion of band 3 protein, but also blunted the functional damage to erythrocytes, such as deformability and anion exchange, without changing the level of peroxidation of membrane lipids. These results provide experimental evidence that activation of caspase-3 plays an important role in the oxidative stress-induced impairment of membrane functions of erythrocytes.

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  • NF kappa B regulates plasma apolipoprotein A-I and high density lipoprotein cholesterol through inhibition of peroxisome proliferator-activated receptor alpha Reviewed

    A Morishima, N Ohkubo, N Maeda, T Miki, N Mitsuda

    JOURNAL OF BIOLOGICAL CHEMISTRY   278 ( 40 )   38188 - 38193   2003.10

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    The levels of plasma HDL cholesterol and apoA-I in NFkappaB p50 subunit-deficient mice were significantly higher than those in wild-type mice under regular and high fat diets, without any significant difference in the level of total cholesterol. To examine the role of NFkappaB in lipid metabolism, we studied its effect on the regulation of apoA-I secretion from human hepatoma HepG2 cells. Lipopolysaccharide-induced activation of NFkappaB reduced the expression of apoA-I mRNA and protein, whereas adenovirus-mediated expression of IkappaBalpha super-repressor ameliorated the reduction. This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. To further support this idea, the expression of IkappaBalpha increased apoA-I promoter activity, and this increase was blocked by preincubation with MK886. Mutations in the putative PPARalpha-binding site in the apoA-I promoter or lack of the site abrogated these changes. Taking these results together, inhibition of NFkappaB increases apoA-I and HDL cholesterol through activation of PPARalpha in vivo and in vitro. Our data suggest a new aspect of lipid metabolism and may lead to a new paradigm for prevention and treatment of atherosclerotic disease.

    DOI： 10.1074/jbc.M306336200

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  • Apolipoprotein E and Reelin ligands modulate tau phosphorylation through an apolipoprotein E receptor/disabled-1/glycogen synthase kinase-3beta cascade. Reviewed

    Nobutaka Ohkubo, Young-Don Lee, Atsuyuki Morishima, Toshio Terashima, Satoshi Kikkawa, Masaya Tohyama, Masahiro Sakanaka, Junya Tanaka, Nobuji Maeda, Michael P. Vitek, Noriaki Mitsuda

    FASEB Journal   17 ( 2 )   295 - 297   2003.2

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  • N141I mutant Presenilin-2 gene enhances neuronal cell death and decreases bcl-2 expression Reviewed

    M Mori, H Nakagami, R Morishita, N Mitsuda, K Yamamoto, S Yoshimura, N Ohkubo, N Sato, T Ogihara, Y Kaneda

    LIFE SCIENCES   70 ( 21 )   2567 - 2580   2002.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

    A missense mutation (N1411) in Presenilin-2 (PS-2) gene is associated with early-onset familial Alzheimer's disease. In this study, SK-N-SH human neuroblastoma cells were transfected with wildtype and mutant PS-2 gene to examine presenilin-2 effects on apoptosis. Serum deprivation resulted in enhanced apoptosis in mutant PS-2 comparing with wild-type PS-2. Similarly, mutant PS-2 induced lactate dehydrogenase release to greater extent than wild-type PS-2. Time course experiment demonstrated that the increase in caspase-3-like activity was more pronounced and accelerated in mutant PS-2, compared to wild-type PS-2. While a significant decrease in bcl-2, an anti-apoptotic molecule, occurred in the cells overexpressing mutant PS-2, no significant change was observed in bax, a pro-apoptotic molecule, as compared with the cells overexpressing wild-type PS-2. Our study demonstrated that mutant PS-2 induces apoptosis accompanied by increased caspase-3-like activity and decreased bcl-2 expression in neuronal cells after serum-deprivation. (C) 2002 Elsevier Science Inc. All rights reserved.

    DOI： 10.1016/S0024-3205(02)01514-X

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  • Transcriptional regulation of presenilin-1 gene by cAMP-response element-binding Reviewed

    Mitsuda Noriaki, Nobutaka Ohkubo, Nobuji Maeda, Masaya Tohyama, Toshio Ogihara

    38 ( 6 )   772 - 774   2001.11

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  • Activated cAMP-response element-binding protein regulates neuronal expression of presenilin-1 Reviewed

    N Mitsuda, N Ohkubo, M Tamatani, YD Lee, M Taniguchi, K Namikawa, H Kiyama, A Yamaguchi, N Sato, K Sakata, T Ogihara, MP Vitek, M Tohyama

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 13 )   9688 - 9698   2001.3

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Upon binding to the cAMP-response element of a gene's promoter, the transcription factor known as cAMP-response element-binding protein (CREB) facilitates transcription of many different neuronal genes including those involved with synaptic function. Based on our previous reports of gene structure (GenBank (TM) accession number AF029701), we now demonstrate that activated CREB binds to the proximal promoter of the human presenilin-1 (PS-1) gene to activate PS-l transcription in rat and in human neuronal cells. Specific stimulation of the N-methyl-D-aspartate subtype of neuronal glutamate receptors activates CREB and results in increased PS-l expression. Similarly, treatment with brain-derived neurotrophic factor activates CREB and increases PS-l expression in a dose-dependent fashion. By using adenovirus vectors expressing dominant negative forms of CREB, we were able to show that induction of PS-l expression requires the activation of CREB, Conversely, constitutive expression of mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) results in activation of CREB and increased PS-1 expression that can be blocked by the addition of selective MEK inhibitors. Our findings suggest a hypothesis where stimulation of N-methyl-D-aspartate receptors signals CREB activation to enhance PS-l gene product expression that contributes to normal neuronal functions.

    DOI： 10.1074/jbc.M006153200

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  • Apolipoprotein E4 stimulates cAMP response element-binding protein transcriptional activity through the extracellular signal-regulated kinase pathway Reviewed

    N Ohkubo, N Mitsuda, M Tamatani, A Yamaguchi, YD Lee, T Ogihara, MP Vitek, M Tohyama

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 5 )   3046 - 3053   2001.2

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Inheritance of the epsilon4 allele of the apolipoprotein E gene (APOE4) is a major risk factor for the development of Alzheimer's disease (AD). Although the association between APOE4 and AD is well documented, the mechanism by which apolipoprotein E exerts an isoform-specific effect on neurons in disease is unknown. In this report, we demonstrate that apoE4 stimulates the transcriptional activity of cAMP-response element-binding protein (CREB) by activating the extracellular signal-regulated kinase (ERK) cascade in rat primary hippocampal neurons. In contrast, apoE3 was unable to stimulate CREB transcriptional activity and unable to activate the ERK pathway. Elevation of intracellular Ca2+ levels are also involved because treatment with receptor-associated protein, nifedipine, MK801, removal of Ca2+ from the medium and dantrolene all served to inhibit calcium elevation and attenuate the activation of CREB, Treatment with an apoE peptide was also found to facilitate transcription of the CREB-dependent genes, c-fos and Bcl-2. In contrast to treatment with apoE3, our findings suggest apoE4 and apoE-peptide induce a novel signaling pathway.

    DOI： 10.1074/jbc.M005070200

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  • Enhanced Stress Resistance at Stationary Phase of Oligotrophic Bacteria, Chromobacterium sp. Y95 and Aeromonas sp. Z06 Reviewed

    Yoshio Kimura, Nobutaka Ookubo, Hidetoshi Ozawa, Masayuki Sato

    Microbes and Environments   12 ( 3 )   75 - 81   1997

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

    Oligotrophic bacteria, Chromobacterium sp. Y95 and Aeromonas sp. Z06, can grow in 104-diluted nutrient broth (1/104 NB). In the two oligotrophic bacteria, the stationary phase cultures showed enhanced heat, oxidation, and osmotic resistance as compared with cultures at exponential phase, although resistance was less marked than that of Escherichia coli. On Southern bloting analysis, Chromobacterium sp. Y95 and Aeromonas sp. Z06 genomic DNA hybridized with the sigma factor probes, RpoN-X and RpoD-4.2, and RpoD-4.2, respectively. © 1997, Japanese Society of Microbial Ecology – The Japanese Society of Soil Microbiology. All rights reserved.

    DOI： 10.1264/jsme2.12.75

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Presentations

  • 紅蔘由来サポニン分画の保存血における抗酸化作用の解明

    河野祐典, 和泉遼, 河野広貴, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第90回日本生理学会大会（東京）  2013.3 

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  • Transferrin-Transferrin receptor 1 signaling is required for mouse erythroblast enucleation through the mechanism independent of iron uptake

    2013.3 

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  • STAT3コンディショナルノックアウトマウスでは脾臓マクロファージの赤血球貪食亢進による貧血が見られる

    多田聡, 大久保信孝, 鈴木洋司, 青戸守, 満田憲昭

    第89回日本生理学会大会 （松本）  2012.3 

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  • 紅蔘由来サポニン分画の保存血液におけるレオロジー機能障害に及ぼす影響

    河野佑典, 河野広貴, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第89回日本生理学会大会 （松本）  2012.3 

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  • 酸化ストレスによる赤血球膜傷害に対するリグナンの保護効果

    佐藤公俊, 岡田奈々枝, 鈴木洋司, 大久保信孝, 青戸守, 山ノ内聡, 満田憲昭

    第90回日本生理学会大会（東京）  2013.3 

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  • 神経分化誘導因子Zfp521欠損マウス脳の組織化学的解析

    赤澤里瑛, 大久保信孝, 青戸守, 鈴木洋司, 松原悦子, 山ノ内純, 酒井郁也, 安川正貴, 満田憲昭

    第90回日本生理学会大会（東京）  2013.3 

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  • 神経分化誘導因子ZFP521は海馬歯状回の形成と個体の行動に関わりがある。

    大久保信孝, 赤澤里瑛, 土居千晃, 平田香穂里, 青戸守, 鈴木洋司, 松原悦子, 山之内純, 酒井郁也, 松田正司, 安川正貴, 満田憲昭

    第65回日本生理学会中四国地方会（倉敷）  2013.11 

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  • 酸化ストレスに対する赤血球の防御機構に及ぼすリグナンの効果

    佐藤公俊, 岡田奈々枝, 鈴木洋司, 大久保信孝, 青戸守, 山内聡, 満田憲昭

    第91回日本生理学会大会（鹿児島）  2014.3 

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  • 酸化ストレスによる赤血球流動機能障害に対するジヒドロエピアンドロステロンの効果

    和泉遼, 村上慶匡, 武智佳奈, 鈴木洋司, 大久保信孝, 青戸守, 満田憲昭

    第91回日本生理学会大会（鹿児島）  2014.3 

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  • マウス赤芽球表面へのホスファチジルセリンの露出

    河野竜馬, 恩地裕史, 鈴木洋司, 大久保信孝, 満田憲昭, 青戸守

    第91回日本生理学会大会（鹿児島）  2014.3 

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  • Transferrin-Transferrin receptor 1 signaling is required for mouse erythroblast enucleation through the mechanism independent of iron uptake

    2013.12 

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  • Zinc Finger Protein 521 (ZFP521) ノックアウトマウスは統合失調症様の症状を見せる。

    土居千晃, 大久保信孝, 平田香穂里, 赤澤里瑛, 青戸守, 鈴木洋司, 満田憲昭

    第１２０回日本解剖学会総会・第９２回日本生理学会大会合同大会（神戸）  2015.3 

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  • Study of protective effect against oxidative stress on rheological disorder of erythrocyte

    2015.3 

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  • デヒドロエピアンドロステロンが酸化ストレスによる赤血球レオロジー機能障害におよぼす影響

    和泉遼, 村上慶匡, 鈴木洋司, 大久保信孝, 青戸守, 満田憲昭

    第66回日本生理学会中国四国地方会（香川）  2014.11 

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  • 酸化ストレスに対する保存赤血球の抗酸化機能への紅蔘由来サポニン分画の影響

    岡田奈々枝, 河野佑介, 和泉遼, 河野広貴, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第91回日本生理学会大会（鹿児島）  2014.3 

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  • 高麗人蔘由来の成分のマウスへの経口投与が赤血球膜タンパク質の酸化傷害に与える影響

    武智佳菜, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第67回日本生理学会中国四国地方会（鳥取）  2015.10 

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  • Apolipoprotein E4はp44/p42 MAP kinaseの活性化を介しCREBのリン酸化を行う。

    大久保信孝, 満田憲昭, 玉谷実智夫, 山口淳, 李永敦, 遠山正彌

    第23回日本神経科学会 （横浜）  2000.9 

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  • Apolipoprotein E4によるCREBの活性化とそのシグナル経路

    大久保信孝, 満田憲昭, 遠山正彌, 前田信治

    第12回日本病態生理学会 （松山）  2002.1 

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  • Apolipoprotein E4 stimulates CREB'S transcriptional Activity through the ERK pathway. International conference

    Nobutaka Ohkubo, Noriaki Mitsuda, Atsushi Yamaguchi, Young-Don Lee, Toshio Ogihara, Micheal P. Vitek, Takashi Nagano, Masaya Tohyama

    2001.11 

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  • Apolipoprotein E4はERK経路の活性化によりCREBのリン酸化を行う。

    大久保信孝, 満田憲昭, 玉谷実智夫, 山口淳, 李永敦, 荻原俊男, 遠山正彌

    第106回日本解剖学会総会 （高知）  2001.4 

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  • Activated CREB regulates Neuronal Expression of Presenilin-1.

    Noriaki Mitsuda, Michio Tamatani, Nobutaka Ohkubo, Manabu Taniguchi, Kazuhiko Namikawa, Hiroshi Kiyama, Atsushi Yamaguchi, Toshio Ogihara, Micheal P. Vitek, Masaya Tohyama

    第30回米国神経科学会大会 (New Orleans, USA)  2000.11 

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  • Signaling cascade for ApoE-peptide-mediated Inhibition of inflammation. International conference

    Nobutaka Ohkubo, Kazuko Toku, Daniel T. Laskowitz, Carol A. Colton, Micheal P. Vitek

    2005.11 

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  • Lack of Apolipoprotein E promotes phosphorylation of Tau through the activation of Glycogen synthase kinase 3 beta in mouse models of hyperphosphorylation Tau. International conference

    Nobutaka Ohkubo, Young-Don Lee, Atsuyuki Morishima, Masaya Tohyama, Nobuji Maeda, Noriaki Mitsuda

    2002.11 

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  • Apolipoprotein Eﾉｯｸｱｳﾄﾏｳｽにおけるp27kip1の発現と神経細胞死

    大久保信孝, 満田憲昭, 森島淳之, 前田信治, 遠山正彌

    第107回日本解剖学会総会 （浜松）  2002.3 

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  • 赤血球の流動挙動に及ぼす酸化ストレスの影響とGinseng由来サポニン分画の保護効果

    鈴木洋司, 大久保信孝, 寒川慶一, 前田信治, 満田憲昭

    第85回日本生理学会大会 （東京）  2008.3 

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  • アンドロゲンによる炎症抑制作用はアポリポ蛋白Eの遺伝子型により変化する

    大久保信孝, 鈴木洋司, 満田憲昭

    第59回日本生理学会中四国地方会 （岡山）  2007.10 

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  • アポリポ蛋白E由来ペプチドによるマイクログリア活性化の抑制機構の解析

    大久保信孝, 鈴木洋司, 青戸守, 満田憲昭

    第58回日本生理学会中四国地方会 （岡山）  2006.10 

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  • 酸化ストレスによる赤血球の機能障害に対するサポニンの保護効果

    鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第58回日本生理学会中四国地方会 （岡山）  2006.10 

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  • Effect of Ginsenosides on rheological functions of erythrocytes against oxidative stress International conference

    2009.7 

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  • STAT3 コンディショナルノックアウトマウスにおける貧血の解析

    大久保信孝, 鈴木洋司, 青戸守, 青野賢治, 満田憲昭

    第60回日本生理学会中四国地方会 （松山）  2008.10 

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  • アポリポ蛋白E由来ペプチドによる炎症抑制シグナル伝達機構の解析

    大久保信孝, 鈴木洋司, 満田憲昭

    第85回日本生理学会大会 （東京）  2008.3 

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  • マウス赤芽球脱核におけるサイクリンD3の役割

    坪内美菜, 三田佳夏子, 河野晋太郎, 鈴木洋司, 大久保信孝, 満田憲昭, 青戸守

    第93回日本生理学会大会（札幌）  2016.3 

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  • ZFP521欠損マウス脳のモノアミン生合成の解析

    平田香穂里, 大久保信孝, 青戸守, 鈴木洋司, 満田憲昭

    第93回日本生理学会大会（札幌）  2016.3 

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  • 赤芽球脱核時における細胞周期制御機構の解析

    青戸守, 三田佳夏子, 岩下晶穂, 坪内美菜, 大久保信孝, 満田憲昭

    第68回日本生理学会中国四国地方会（岡山）  2016.11 

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  • Zinc finger protein 521欠損マウスの行動と脳モノアミンの解析

    大久保信孝, 平田香穂里, 青戸守, 安川正貴, 満田憲昭

    2016.11 

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  • 高麗人参由来サポニンの経口投与が酸化ストレスに対するマウス赤血球膜タンパク質に対する効果

    武智佳菜, 星野真子, 鈴木洋司, 大久保信孝, 青戸守, 寒川慶一, 満田憲昭

    第93回日本生理学会大会（札幌）  2016.3 

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  • 血液保存による赤血球流動機能障害に対するデヒドロエピアンドロステロンの影響

    村上慶匡, 和泉遼, 福本健, 鈴木洋司, 大久保信孝, 青戸守, 満田憲昭

    第93回日本生理学会大会（札幌）  2016.3 

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  • マウス赤芽球の脱核にはトランスフェリンートランスフェリン受容体１シグナルが必要であり、その機構は鉄の取り込みとは無関係である

    岩下晶穂, 三田佳夏子, 大久保信孝, 満田憲昭, 青戸守

    第95回日本生理学会大会 （高松）  2018.3 

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  • 紅蔘由来サポニン成分分画の血管新生に与える効果 Invited

    青戸守, 大久保信孝, 昆和典, 満田憲昭

    第17回日本紅蔘研究会研究発表会 （台北、台湾）  2018.3 

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  • Zinc finger protein 521欠損マウスで見られる行動異常はDopamine-beta-Hydroxylaseの上昇が関与する

    大久保信孝, 平田香穂里, 青戸守, 満田憲昭

    第69回日本生理学会中国四国地方会（徳島）  2017.10 

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  • 紅蔘由来サポニンの血管新生に与える影響

    青戸守, 満田憲昭, 大久保信孝, 昆和典

    第16回日本紅蔘研究会研究発表会  2017.3 

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  • マウス赤芽球の脱核過程におけるトランスフェリン受容体１の役割

    岩下晶穂, 三田佳夏子, 大久保信孝, 満田憲昭, 青戸守

    第70回日本生理学会中国四国地方会 （東温）  2018.10 

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  • 神経幹細胞分化促進因子Zinc Finger Protein 521欠損マウスの解析

    大久保 信孝

    第19回ORIGIN 神経科学研究会  2018.8 

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  • マウス赤芽球の脱核時におけるCdk4-Cyclin D3複合体の役割

    三田佳夏子, 岩下晶穂, 大久保信孝, 満田憲昭, 青戸守

    第95回日本生理学会大会 （高松）  2018.3 

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  • Zinc finger protein 521 involved in differentiation of intestinal stem cells and absorption. International conference

    Nazuna Morisada, Kotone Miyake, Mamoru Aoto, Noriaki Mitsuda, Nobutaka Ohkubo

    9th FAOPS (9th Federation of the Asian and Oceanian Physiological Societies) congress  2019.3 

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  • 紅蔘由来サポニン由来成分の血液循環網形成への効果 Invited

    青戸守, 満田憲昭, 大久保信孝, 昆和典

    第18回日本紅蔘研究会発表会  2019.3 

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  • Zinc finger protein 521欠損マウスでは経腸吸収不良による発育不良があり、腸上皮幹細胞の分化異常の関与が示唆される

    大久保信孝, 森定なずな, 三宅琴音, 青戸守, 満田憲昭

    第70回日本生理学会中国四国地方会 （東温）  2018.10 

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  • STAT3コンディショナルノックアウトマウスで見られる貧血の解析

    大久保信孝, 鈴木洋司, 青戸守, 山之内純, 平川聡, 安川正貴, 満田憲昭

    第63回日本生理学会中国四国地方会 （広島）  2011.10 

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  • 紅蔘由来サポニンの血液保存時の機能障害に対する保護効果

    河野広貴, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭

    第62回日本生理学会中国四国地方会（出雲）  2010.11 

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  • Essential role of p38 MAPK in caspase-independent, phospholipase A2-dependent, cell death under hypoxia/low glucose conditions International conference

    Mamoru Aoto, Koei Shinzawa, Yoji Suzuki, Nobutaka Ohkubo, Noriaki Mitsuda, Yoshihide Tsujimoto

    2009.7 

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  • Apolipoprotein E4はp44/p42 MAP kinase 系の活性化によりCREBのリン酸化を行う。

    大久保信孝, 満田憲昭, 玉谷実智夫, 山口淳, 李永敦, 遠山正彌

    第43回日本神経化学会 （金沢）  2000.10 

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  • Reelin inhibits P19 embryonal cell death during neuronal differentiation International conference

    Nobutaka Ohkubo, Yoji Suzuki, Mitsuda Noriaki

    2009.7 

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Research Projects

  • 杜仲葉エキスの血管新生への効果

    2019.4 - 2020.3

    日本杜仲研究会  日本杜仲研究会 第14回 研究助成 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • 紅蔘由来サポニン成分の血液循環に与える効果の解析

    2019.4 - 2020.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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    Grant type：Competitive

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  • 紅蔘由来サポニン成分の血管新生に与える効果の解析

    2018.4 - 2019.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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    Grant type：Competitive

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  • マウス行動異常に関与する新規モノアミン調節機構の解明

    2017.4 - 2018.3

    ノバルティスファーマ株式会社  ノバルティスファーマ研究助成 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • 紅蔘由来サポニンの血管新生促進作用の解析

    2017.4 - 2018.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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    Grant type：Competitive

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  • 紅蔘と血管新生 －紅蔘は血管新生に促進的か、あるいは抑制的か－

    2016.4 - 2017.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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    Grant type：Competitive

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  • 脳形成におけるZFP521の役割の解析と行動への影響の評価

    2014.4 - 2016.3

    愛媛大学  研究活性化事業 萌芽研究 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • 赤血球における抗酸化能力を増強する紅蔘由来サポニンの作用機構の研究

    2013.4 - 2014.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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  • ZFP521ノックアウトマウス造血器および脳神経系の発生、分化機構の解明

    2012.4 - 2014.3

    愛媛大学内公募資金  研究活性化事業 女性研究者支援研究 

    松原 悦子

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  • 赤血球の老化による循環機能障害に対する紅蔘由来サポニンの抑制機構の解明

    2012.4 - 2013.3

    （財）日本紅蔘研究会  日本紅蔘研究会研究助成 

    満田 憲昭

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  • 赤血球の老化による循環機能障害に対する紅蔘由来サポニンの改善効果

    2011.4 - 2012.3

    （財）日本紅蔘研究会  日本紅蔘研究会 研究助成 

    満田 憲昭

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  • 新しい血管新生制御因子としてのアポリポ蛋白Eの機能解析

    2009.4 - 2011.3

    日本学術振興会  科学研究費補助金 若手研究（B） 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • アポリポ蛋白Eのミクログリア細胞調節機構の解明とアルツハイマー病治療への応用

    2009.4 - 2011.3

    愛媛大学内公募資金  研究活性化事業 萌芽研究 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • 赤血球の微小循環動態におけるサポニンのアンチエイジング機構の研究

    2008.4 - 2011.3

    日本学術振興会  科学研究費補助金 基盤研究（C） 

    鈴木 洋司

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    Grant type：Competitive

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  • 脳におけるアポリポ蛋白Eによる自然免疫制御機構について

    2007.4 - 2009.3

    日本学術振興会  科学研究費補助金 若手研究（B) 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • アルツハイマー病発症に関与するアポリポプロテインEの分子細胞生物学的研究

    2002.4 - 2004.3

    日本学術振興会  科学研究費補助金 特別研究員奨励費 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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  • アルツハイマー病に関与するアポリポプロテインEの分子細胞生物学的研究

    2001.4 - 2003.3

    愛媛県  学生調査研究助成 

    大久保 信孝

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    Authorship：Principal investigator  Grant type：Competitive

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