Organization
Graduate School of Medicine Program for Medical Sciences Senior Assistant Professor
Title
Senior Assistant Professor
Contact information
External link
Ohkubo Nobutaka
Degree
Degree
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博士（医学） ( 大阪大学大学院 )
Research Interests
Research Interests
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幹細胞
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アポリポ蛋白E
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Apolipoprotein E
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Alzheimer's disease
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機能性食品
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zinc finger protein 521
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アルツハイマー病
Research Areas
Research Areas
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Life Science / Neuroscience-general
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Life Science / Clinical pharmacy
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Life Science / Anatomy
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Life Science / Physiology
Education
Education
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大阪大学大学院 医学系研究科
1999.4 - 2003.3
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Research History
Research History
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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
Professional Memberships
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THE JAPAN NEUROSCIENCE SOCIETY
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THE PHYSIOLOGICAL SOCIETY OF JAPAN
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THE JAPANESE SOCIETY FOR NEUROCHEMISTRY
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Papers
Papers
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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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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.
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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. -
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.
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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. -
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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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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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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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.
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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.
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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.
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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.
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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.
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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.
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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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Zinc finger protein521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
日本生理学雑誌(Web) 80 ( 3 ) 36 (WEB ONLY) 2018.8
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Zinc finger protein521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
日本生理学雑誌(Web) 79 ( 1 ) WEB ONLY 2017.2
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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
日本生理学雑誌(Web) 79 ( 1 ) WEB ONLY 2017.2
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大久保信孝, 青戸守, 松原悦子, 山之内純, 安川正貴, 満田憲昭
愛媛医学 35 ( 3 ) 117‐122 2016.9
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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
日本生理学雑誌(Web) 78 ( 1 ) WEB ONLY 2016.1
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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
日本生理学雑誌 77 ( 1 (Web) ) WEB ONLY 2015
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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
日本生理学雑誌 76 ( 4 ) 105 - 106 2014.7
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酸化ストレスに対するデヒドロエピアンドロステロンの血液レオロジーにおよぼす影響
鈴木洋司, 和泉遼, 村上慶匡, 大久保信孝, 青戸守, 満田憲昭
日本バイオレオロジー学会年会プログラム・抄録集 37th 95 2014.6
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低温保存時における赤血球の酸化傷害と紅参由来サポニン分画の抗酸化効果
河野佑典, 河野広貴, 和泉遼, 鈴木洋司, 大久保信孝, 青戸守, 寒川慶一, 満田憲昭
日本生理学雑誌 75 ( 2 ) 81 2013.3
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トランスフェリン‐トランスフェリン受容体シグナルは鉄の取り込みと無関係なメカニズムを介してマウス赤芽球の脱核に必要とされる
青戸守, 恩地裕史, 河野竜馬, 鈴木洋司, 大久保信孝, 辻本賀英, 満田憲昭
日本分子生物学会年会プログラム・要旨集(Web) 36th 1P-0623 (WEB ONLY) 2013
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血液保存による赤血球レオロジー機能障害に対する紅蔘由来サポニン分画の保護のメカニズム
鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭
日本バイオレオロジー学会年会プログラム・抄録集 35th 64 2012.5
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赤血球の酸化ストレス度と加齢との関係(抗加齢ドックのデータを用いて)
満田憲昭, 青野賢治, 青戸守, 鈴木洋司, 大久保信孝
日本生理学雑誌 74 ( 2 ) 47 - 48 2012.3
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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
日本生理学雑誌 74 ( 2 ) 49 - 49 2012.3
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紅蔘由来サポニン分画の血液保存における赤血球レオロジー機能障害に対する保護効果
鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭
日本バイオレオロジー学会年会プログラム・抄録集 34th 76 2011.6
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河野広貴, 鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭
日本生理学雑誌 73 ( 2 ) 41 2011.2
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血液保存における赤血球レオロジー機能障害と紅蓼由来サポニンの効果
鈴木洋司, 大久保信孝, 寒川慶一, 青戸守, 満田憲昭
日本バイオレオロジー学会年会プログラム・抄録集 33rd 144 2010.5
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低酸素/低グルコース刺激によって誘導される非アポトーシス型細胞死の解析
青戸守, 新沢康英, 鈴木洋司, 大久保信孝, 満田憲昭, 辻本賀英
日本生理学雑誌 72 ( 4 ) 130 2010.4
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Tie2‐Cre STAT3コンディショナルノックアウトマウスは溶血性貧血を呈する
山之内純, 藤原弘, 越智俊元, 白方俊章, 薬師神芳洋, 羽藤高明, 平川聡史, 大久保信孝, 鈴木洋司, 満田憲昭, 安川正貴
臨床血液 50 ( 9 ) 972 - 972 2009.9
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酸化ストレスによる赤血球レオロジー機能障害と紅参由来サポニンによる保護機構の解明
鈴木洋司, 大久保信孝, 満田憲昭, 寒川慶一
日本バイオレオロジー学会年会プログラム・抄録集 32nd 64 2009.5
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酸化ストレスによる赤血球膜の酸化障害とGinseng由来サポニンの保護効果
鈴木洋司, 大久保信孝, 寒川慶一, 前田信治, 満田憲昭
日本生理学雑誌 71 ( 2 ) 66 2009.2
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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
日本生理学雑誌 71 ( 2 ) 67 2009.2
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青戸守, 新沢康英, 鈴木洋司, 大久保信孝, 満田憲昭, 辻本賀英
日本生理学雑誌 71 ( 2 ) 66 - 67 2009.2
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酸化ストレスによる赤血球レオロジー機能障害および紅参由来サポニン分画の保護効果
鈴木洋司, 大久保信孝, 満田憲昭, 寒川慶一
日本バイオレオロジー学会年会プログラム・抄録集 31st 43 2008.6
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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
日本生理学雑誌 70 ( 2 ) 71 2008.2
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赤血球の酸化障害に対する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
日本生理学雑誌 70 ( 2 ) 72 - 73 2008.2
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赤血球レオロジーからみた紅参由来サポニンの酸化ストレスに対する保護効果
鈴木洋司, 大久保信孝, 満田憲昭, 寒川慶一
日本バイオレオロジー学会年会プログラム・抄録集 30th 36 2007.6
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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
日本生理学雑誌 69 ( 3 ) 124 2007.3
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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
日本生理学雑誌 69 ( 3 ) 124 2007.3
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酸化ストレスによるカスパーゼの活性化と赤血球の微小循環動態への影響
鈴木洋司, 大久保信孝, 青戸守, 満田憲昭
日本バイオレオロジー学会年会プログラム・抄録集 29th 43 2006.6
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満田憲昭, 大久保信孝, 杉山博信, 前田信治
日本生理学雑誌 66 ( 2 ) 71 - 72 2004.2
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リーラーマウスにおける中枢神経細胞内のタウ蛋白質のリン酸化機構
満田憲昭, 大久保信孝, 前田信治
日本生理学雑誌 64 ( 4 ) 89 2002.4
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Apolipoprotein E(ApoE)ノックアウトマウスにおけるp27<SUP>Kip1</SUP>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
日本解剖学会 総会・全国学術集会 抄録号 107 ( 0 ) 94 - 94 2002
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家族性アルツハイマー病の原因遺伝子プレセニリン‐1の発現調節機構の解析
満田憲昭, 大久保信孝, 里直行, 遠山正弥, 荻原俊男
日本老年医学会雑誌 38 76 2001.5
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Apolipoprotein E4はERK経路の活性化による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, 遠山正弥
解剖学雑誌 76 ( 1 ) 125 2001.2
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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, 玉谷美智夫, 山口淳, 李永敦, 遠山正弥
神経化学 39 ( 3 ) 371 2000.10
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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, 遠山正弥
日本神経科学大会プログラム・抄録集 23rd 228 2000.9
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アルツハイマー病原因遺伝プレセニリン‐1転写因子CREBにより転写調節されている
満田憲昭, 大久保信孝, 玉谷実智夫, 谷口学, 涛川一彦, 木山博資, 山口淳, 遠山正弥
日本神経科学大会プログラム・抄録集 23rd 228 2000.9
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Presentations
Presentations
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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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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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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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Research Projects
Research Projects
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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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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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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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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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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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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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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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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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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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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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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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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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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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Teaching Experience (On-campus)
Teaching Experience (On-campus)
Teaching Experience
Teaching Experience
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基礎医学展望I
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生理学実習
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医科学研究
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基礎医学展望II
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人体生理学
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解剖生理学
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生理学II
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解剖学
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