WADA Tetsuyuki

Department of PharmacyAssociate Professor

Last Updated :2024/06/18

■Researcher basic information


  • (BLANK)

Research Field

  • Life sciences / Pharmacology
  • Life sciences / Pharmaceuticals - health and biochemistry


Educational Background

  •        -   Kindai University  Faculty of Pharmacy  Department of Pharmacy
  •        -   Kindai University  Graduate School of Pharmacy  Major in Pharmaceutical Sciences
  •        -   Kinki University  Graduate School, Division of Pharmaceutical Sciences

■Research activity information


  • Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Teruki Hagiwara; Shigeru Yoshida; Shogo Tokuyama
    EUROPEAN JOURNAL OF PHARMACOLOGY ELSEVIER SCIENCE BV 799 103 - 110 0014-2999 2017/03 [Refereed]
    We recently reported that cerebral sodium-glucose transporter type 1 (SGLT-1) plays a role in exacerbation of cerebral ischemia. However, the mechanism by which cerebral SGLT-1 acts remains unclear. Here we demonstrated that sodium influx through cerebral SGLT-1 exacerbates cerebral ischemic neuronal damage. SGLT-specific sodium ion influx was induced using alpha-methyl-D-glucopyranoside (alpha-MG). Intracellular sodium concentrations in primary cortical neurons were estimated using sodium-binding benzofuran isophthalate fluorescence. SGLT-1 knockdown in primary cortical neurons and mice was achieved using SGLT-1 siRNA. The survival rates of primary cultured cortical neurons were assessed using biochemical assays 1 day after treatment. Middle cerebral artery occlusion (MCAO) was used to generate a focal cerebral ischemic model in SGLT-1 knockdown mice. The change in fasting blood glucose levels, infarction development, and behavioral abnormalities were assessed 1 day after MCAO. Treatment with 200 mM alpha-MG induced a continuous increase in the intracellular sodium concentration, and this increase was normalized after a-MG removal. Neuronal SGLT-1 knockdown had no effect on 100 mu M H2O2-induced neuronal cell death; however, the knockdown prevented the neuronal cell death induced by 17.5 mM glucose and the co-treatment of 100 mu M H2O2/8.75 mM glucose. Neuronal SGLT-1 knockdown also suppressed the cell death induced by alpha-MG alone and the co-treatment of 100 mu M H2O2/0.01 mM alpha-MG. Our in vivo results showed that the exacerbation of cerebral ischemic neuronal damage induced by the intracerebroventricular administration of 5.0 mu g alpha-MG/mouse was ameliorated in cerebral SGLT-1 knockdown mice. Thus, sodium influx through cerebral SGLT-1 may exacerbate cerebral ischemia-induced neuronal damage.
  • Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Shigeru Yoshida; Shogo Tokuyama
    JOURNAL OF PHARMACY AND PHARMACOLOGY WILEY-BLACKWELL 68 (7) 922 - 931 0022-3573 2016/07 [Refereed]
    ObjectivesWe recently demonstrated that the cerebral sodium-glucose transporter (SGLT) is involved in postischaemic hyperglycaemia-induced exacerbation of cerebral ischaemia. However, the associated SGLT-mediated mechanisms remain unclear. Thus, we examined the involvement of cerebral SGLT-induced excessive sodium ion influx in the development of cerebral ischaemic neuronal damage. Methods[Na+]i was estimated according to sodium-binding benzofuran isophthalate fluorescence. In the in vitro study, primary cortical neurons were prepared from fetuses of ddY mice. Primary cortical neurons were cultured for 5 days before each treatment with reagents, and these survival rates were assessed using biochemical assays. In in vivo study, a mouse model of focal ischaemia was generated using middle cerebral artery occlusion (MCAO). Key findingsIn these experiments, treatment with high concentrations of glucose induced increment in [Na+]i, and this phenomenon was suppressed by the SGLT-specific inhibitor phlorizin. SGLT-specific sodium ion influx was induced using a-methyl-D-glucopyranoside (a-MG) treatments, which led to significant concentration-dependent declines in neuronal survival rates and exacerbated hydrogen peroxide-induced neuronal cell death. Moreover, phlorizin ameliorated these effects. Finally, intracerebroventricular administration of a-MG exacerbated the development of neuronal damage induced by MCAO, and these effects were ameliorated by the administration of phlorizin. ConclusionsHence, excessive influx of sodium ions into neuronal cells through cerebral SGLT may exacerbate the development of cerebral ischaemic neuronal damage.
  • Masayuki Takechi; Tetsuyuki Wada; Hideki Yagi; Takashi Masuko; Atsufumi Kawabata
    JOURNAL OF PHARMACY AND PHARMACOLOGY WILEY-BLACKWELL 67 (1) 126 - 132 0022-3573 2015/01 [Refereed]
    Objectives We tested if modulation of cytosolic K+ levels by ouabain, an inhibitor of Na+/K+-ATPase, exerts cytoprotection against distinct stressful stimuli in human leukemic cells. Methods The cytosolic K+, Na+ or Ca2+ levels and the cytotoxicity were evaluated by flow cytometry. Key findings Various cytotoxic chemicals and ultraviolet irradiation induced cell death and increased intracellular concentrations of K+, Na+ or Ca2+. Ouabain reduced the cytotoxicity and the elevation of cytosolic levels of K+ but not those of Na+ or Ca2+. Conclusions Our data thus suggest that elevated cytosolic K+ levels are associated with the cytotoxicity in response to distinct stressful stimuli and that ouabain exerts cytoprotection most probably by regulating intracellular K+ levels.
  • Sakamoto Y; Nakamoto Y; Wada T Ichida; S Minami T
    Toxicological and Environmental Chemistry. 96 (6) 1 - 14 2015 [Refereed]
  • A search for the risk factors for hiccups and evaluation of antiemetic therapy in CDDP-based chemotherapy, using cluster analysis.
    Asano H; Watanabe M; Kawaguchi A; Yanae M; Funakami Y; Wada T; Matzno S; Yamazoe Y; Nishida S; Ichida S
    Gan To Kagaku Ryoho. 40 (8) 1031 - 1036 2013/08 [Refereed]
  • Hajime Asano; Akinori Miyamoto; Mariko Nakao; Chiyuki Wakaki; Takuma Iida; Yoshinori Funakami; Tetsuyuki Wada; Seiji Ichida
    NEUROCHEMICAL RESEARCH SPRINGER/PLENUM PUBLISHERS 37 (8) 1738 - 1746 0364-3190 2012/08 [Refereed]
    Previous work from this laboratory has shown that the serotonin (5-HT) induced response is significantly augmented in differentiated NG108-15 (NG) cells treated with dibutyryl cAMP (Bt(2)cAMP) due to qualitative and quantitative changes in the expression of the 5-HT3 receptor as demonstrated by specific [H-3] LY-278584 (a selective 5HT(3) receptor antagonist) binding. In this study, we investigated whether there is any change in the relative expression of the 5-HT3A and 5-HT3B subunits in NG cells differentiated following Bt(2)cAMP treatment cells. The major findings of this study were that the relative amount of 5-HT3B subunit mRNA in Bt(2)cAMP-treated NG cells 5 days following Bt(2)cAMP-treatment was greater than that in the untreated cells. In contrast, the relative expression of the 5-HT3B subunit protein in the Bt(2)cAMP-treated NG cells was much less than in the untreated cells, but the relative expression of the 5-HT3A subunit in the Bt(2)cAMP-treated NG cells was similar to the untreated cells. Therefore, no relationship between mRNA and protein expression for 5-HT3A and 5-HT3B subunits in Bt(2)cAMP treated and untreated NG cells were observed. It was also found that fluorescent intensity for the 5-HT3B subunit in the cell body of the Bt(2)cAMP treated and untreated NG cells gradually decreased from the day 1-5 after Bt(2)cAMP treatment. However, in specific areas such as the varicosity and nerve endings of the Bt(2)cAMP treated cells, staining intensity for the 5-HT3B subunits was stronger than in the untreated cells at the all time points, peaking at day 5 post-treatment. These results suggest that the augmented response induced by 5-HT acting via 5-HT3 receptors in differentiated NG cells may be due to changes in the relative amount of the 5-HT3B subunit, particularly the ratio and distribution of the 5-HT3A to (3B) subunits.
  • 船上 仁範; 伊藤 栄次; 秦 多恵子; 和田 哲幸; 市田 成志
    BioPsychoSocial Medicine BioMed Central Ltd. 4 (13) 2010/10
  • Yoshinori Funakami; Eiji Itoh; Taeko Hata; Tetsuyuki Wada; Seiji Ichida
    Stress is closely associated with the manifestation and progress of irritable bowel syndrome (IBS). For the purpose of establishing experimentally the relationship between IBS and stress, the transportation capacity of the small intestine in specific alternation of rhythm in temperature (SART)-stressed animals was studied using charcoal transportation method. The charcoal suspension was administered orally into the stomach of fasting mice. Mice were sacrificed after a certain time and %charcoal transit (%CT) of the small intestine was measured. The %CTs in SART-stressed mice were greater than those in unstressed or continuously cold-stressed mice. This increase in %CT remained for I week after discontinuation of SART stress loading. Cholinergic blockers decreased %CTs in SART-stressed mice. Increases in %CT by a cholinesterase inhibitor were less in SART-stressed mice than in unstressed mice. Increases of %CT in SART-stressed mice were suppressed by Neurotropine. These results suggested that the parasympathetic hypertonicity, not just cold, played a role in the increases in the transportation capacity in SART-stressed mice and that these animals can be a useful tool for elucidation of the mechanism of IBS.
  • Analytical study of interaction between spdider toxin and glutamate receptors.
    和田 哲幸; 森山 隆太郎; 若宮 建昭; 吉田 繁; 山口 仁宏
    Peptide Science 2009 349 - 352 2010
  • Takashi Imanishi; Kayoko Matsushima; Akinori Kawaguchi; Hajime Asano; Yoshinori Funakami; Tetsuyuki Wada; Takashi Masuko; Shigeru Yoshida; Seiji Ichida
    NEUROCHEMICAL RESEARCH SPRINGER/PLENUM PUBLISHERS 34 (5) 1011 - 1019 0364-3190 2009/05 
    Characteristics for the up-regulated response in the concentration of intracellular calcium ion ([Ca(2+)] (i) ) and in the sodium ion (Na(+)) current by serotonin (5-HT) were investigated in differentiated neuroblastoma x glioma hybrid NG108-15 (NG) cells. The results for the changes in [Ca(2+)] (i) by 5-HT were as follows, (1) The 5-HT-induced Ca(2+) response was inhibited by 3 x 10(-9) M tropisetron (a 5-HT(3) receptor blocker), but not by other types of 5-HT receptor blockers; (2) The 5-HT-induced Ca(2+) response was mainly inhibited by calciseptine (a L-type Ca(2+) blocker), but not by other types of Ca(2+) channel blockers or 10(-7) M TTX (a voltage-sensitive Na(+) channel blocker); (3) When the extracellular Na(+) was removed by exchange with choline chloride or N-methyl-d-glucamine, the 5-HT-induced Ca(2+) response was extremely inhibited. The results for the 5-HT-induced Na(+) current by the whole cell patch-clamp technique were as follows, (1) The 5-HT-induced Na(+) current in differentiated cells was significantly larger than that in undifferentiated cells; (2) The ED(50) value for 5-HT-induced Na(+) current in undifferentiated and differentiated cells was almost the same, about 4 x 10(-6) M each other; (3) The 5-HT-induced Na(+) current was completely blocked by 3 x 10(-9) M tropisetron, but not by other 5-HT receptor antagonists and 10(-7) M TTX. These results suggested that 5-HT-induced Ca(2+) response in differentiated NG cells was mainly due to L-type voltage-gated Ca(2+) channels allowing extracellular Na(+) to enter via 5-HT(3) receptors, but not through voltage-gated Na(+) channels.
  • Study directed toward the analysis of interaction between the spider toxin NPTX-594 and glutamate receptors.
    西丸 貴弘; 吉田 繁; 森山 隆太郎; 和田 哲幸
    Peptide Science 2008 401 - 404 2009
  • Study directed toward the analysis of interaction between the spider toxin NPTX-594 and glutamate receptors.
    和田 哲幸; 森山 隆太郎; 吉田 繁; 山口 仁宏; 若宮 建昭
    Peptide Science 2008 401 - 404 2008
  • Atsufumi Kawabata; Tsuyoshi Ishiki; Kelta Nagasawa; Shigeru Yoshida; Yumi Maeda; Tomoko Takahashi; Fumiko Sekiguchi; Tetsuyuki Wada; Seiji Ichida; Hiroyuki Nishikawa
    PAIN ELSEVIER SCIENCE BV 132 (1-2) 74 - 81 0304-3959 2007/11 
    Hydrogen sulfide (H2S), an endogenous gasotransmitter, modulates various biological events such as inflammation in the mammalian body. The present study investigated possible involvement of H2S in peripheral nociceptive processing. Intraplantar (i.pl.) administration of NaHS, a H2S donor, produced prompt hyperalgesia in rats, accompanied by expression of Fos in the spinal dorsal horn. The H2S-evoked hyperalgesia was blocked by 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB), an oxidizing agent, or ethosuximide and mibefradil, T-type Ca2+ channel inhibitors. L-Cysteine, an endogenous source for H2S, given i.pl., also elicited hyperalgesia, an effect being abolished by DL-propargylglycine (PPG) and beta-cyanoalanine (BCA), inhibitors of cystathionine-gamma-lyase, a H2S synthesizing enzyme. PPG and/or BCA partially inhibited the hyperalgesia induced by i.pl. lipopolysaccharide, an effect being reversed by i.pl. NaHS. In the patch-clamp study using undifferentiated NG108-15 cells that express T-type, but not other types, of Ca2+ channels, NaHS enhanced the currents through the T-type channels, an effect being blocked by DTNB. Thus, H2S appears to function as a novel nociceptive messenger through sensitization of T-type Ca2+ channels in the peripheral tissues, particularly during inflammation. (C) 2007 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
  • Akinori Kawaguchi; Hajime Asano; Kayoko Matsushima; Tetsuyuki Wada; Shigeru Yoshida; Seiji Ichida
    Neurochemical research 32 (9) 1469 - 75 0364-3190 2007/09 
    It is well known that morphological and functional changes during neural differentiation sometimes accompany the expression of various voltage-gated ion channels. In this work, we investigated whether the enhancement of sodium current in differentiated neuroblastoma x glioma NG108-15 cells treated with dibutyryl cAMP is related to the expression of voltage-gated sodium channels. The results were as follows. (1) Sodium current density on peak voltage in differentiated cells was significantly enhanced compared with that in undifferentiated cells, as detected by the whole-cell patch clamp method. The steady-state inactivation curve in differentiated cells was similar to that for undifferentiated cells, but a hyperpolarized shift in the activation curve for differentiated cells was observed. The sodium currents of differentiated and undifferentiated cells were completely inhibited by 10(-7) M tetrodotoxin (TTX). (2) The only Na(V) mRNA with an increased expression level during neuronal differentiation was that for NaV1.7, as observed by real-time PCR analysis. (3) The increase in the level of NaV1.7 alpha subunit expression during neuronal differentiation was also observed by immunocytochemistry; in particular, the localization of NaV1.7 alpha subunits on the soma, varicosities and growth cone was significant. These results suggest that the enhancement of TTX-sensitive sodium current density in differentiated NG108-15 cells is mainly due to the increase in the expression of the TTX-sensitive voltage-gated Na+ channel, NaV1.7.
  • Tadatoshi Tanino; Akihiro Nawa; Eisaku Kondo; Fumitaka Kikkawa; Tohru Daikoku; Tatsuya Tsurumi; ChenHong Luo; Yukihiro Nishiyama; Yuki Takayanagi; Katuhiko Nishimori; Seiji Ichida; Tetsuyuki Wada; Yasuyoshi Miki; Masahiro Iwaki
    Purpose: The aim of the study was to investigate whether 2'-ethylcarbonate-linked paclitaxel (TAX-2'-Et) circumvents P-glycoprotein (P-gp)-mediated cellular efflux and cytotoxicity enhanced by TAX-2'-Et activation within human culture cells transfected with a rabbit liver carboxylesterase (Ra-CES) cDNA. Materials and Methods: TAX-2'-Et transport was characterized in a human colon carcinoma cell line (Caco-2) and paclitaxel (TAX)-resistant ovarian carcinoma cells (SKOV3/TAX60). Expression of P-gp, multidrug resistance protein (MRP) 2 and Ra-CES was detected by Western blotting. Cytotoxicity against Ra-CES-expressing cells and cellular amount of TAX produced were determined by MTT assay and using HPLC, respectively. Results: Unlike rhodamine123 and TAX, TAX-2'-Et did not exhibit polarized transport in the Caco-2 cells in the absence or presence of verapamil. P-gp levels were expressed much higher in the SKOV3/TAX60 cells than in the Caco-2 cells. MRP2 protein was not detectable in the SKOV3/TAX60 cells. Uptake by the SKOV3/TAX60 cells was similar in quantity to the amount internalized by P-gp-negative SKOV3 cells. In the SKOV3/TAX60 cells, cellular uptake of TAX-2'-Et was not altered regardless of the absence or presence of verapamil. The cytotoxicity to the untransfected SKOV3 cells induced by TAX-2'-Et was significantly lower than that induced by TAX. In the Ra-CES-expressing SKOV3 line, the EC50 value of TAX (10.6 nM) was approximately four-fold higher than that of TAX-2'-Et (2.5 nM). Transfection of Ra-CES into another TAX-resistant ovarian carcinoma cells (KOC-7c) conferred a high level of TAX-2'-Et cytotoxicity via prodrug activation. The intracellular levels of TAX produced from TAX-2'-Et in the Ra-CES-positive KOC-7c cells significantly increased compared with the levels seen in exposure of the untransfected KOC-7c cells to TAX. Conclusions: TAX-2'-Et can circumvent P-gp-associated cellular efflux of TAX. TAX-2'-Et is converted into TAX by the Ra-CES, supporting its potential use as a theoretical GDEPT strategy for cancer cells expressing high levels of P-gp. The TAX-2'-Et prodrug efficiently increased the amount of intracellular TAX, which mediates tumor cell death.
  • Takashi Imanishi; Kayoko Matsushima; Akinori Kawaguchi; Tetsuyuki Wada; Shigeru Yohida; Seiji Ichida
    NEUROSCIENCE LETTERS ELSEVIER IRELAND LTD 405 (1-2) 1 - 4 0304-3940 2006/09 
    Dynamic changes in the concentration of intracellular free-calcium ion ([Ca2+](i)) by carbachol (M) and neurotransmitter candidates was investigated in undifferentiated and differentiated neuroblastoma x glioma hybrid NG108-15 (NG)cells. [Ca2+], was increased in a dose-dependent manner by bradykinin (BK) and serotonin (5-HT) in differentiated NG cells, and the response to BK and 5-HT was significantly greater than that in undifferentiated NG cells. The EC50 value of BK was approximately 1.5 x 10(-8) M in both undifferentiated and differentiated NG cells. The EC50 value of 5-HT in differentiated NG cells was about 5 x 10(-6) M. The response to BK and 5-HT was almost completely inhibited by 10 nM Hoe140 (a BK B2 receptor antagonist) and 3 nM tropisetron (a 5-HT3 receptor antagonist), respectively. These results suggest that there are some mechanisms by which the response evoked by BK and 5-HT is up-regulated in differentiated NG cells. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
  • T Imanishi; K Matsushima; A Kawaguchi; T Wada; T Masuko; S Yoshida; S Ichida
    Developmental changes in dynamics of Na+ were studied in neuroblastoma x glioma hybrid NG108-15 cells during differentiation which was induced by dibutyryl cAMP (Bt(2)cAMP). Ratiometric Na+ imaging with a Na+-sensitive fluorescent dye SBFI (sodium-binding benzofuran isophthalate) revealed that the intracellular Na+ concentration ([Na+](i),) was not affected by the application of high K+ (60 mm) solution to either control or differentiated cells. When cells were exposed to 50,mu m veratridine (Vtd), an agonist of voltage-sensitive sodium channels (VSSCs), a significant increase in [Na+](i) was observed in differentiated but not in undifferentiated cells. Calculated mean [Na+], value increased from the basal 10.4 to 44.1 mm in response to 50 mu M Vtd. This Vtd response was reversibly inhibited by tetrodotoxin (TTX), a specific blocker for VSSCs, in a dose-dependent manner (IC50=1 nm). It is suggested that VSSCs in NG108-15 cells are sensitive to TTX and Vtd and that the number of VSSCs increases during differentiation.
  • T Imanishi; K Matsushima; A Kawaguchi; T Wada; S Yoshida; S Ichida
    Characteristics of the increasing effect for the concentration of intracellular calcium ions ([Ca2+](i)) by high-KCl application were investigated in the neuroblastoma x glioma hybrid NG108-15 cell line ( NG108-15 cells). The present study confirmed that the increasing effect of [ Ca2+](i) by high-KCl application in single NG108-15 cells, differentiated with dibutyryl cAMP ( Bt(2)cAMP), was significantly enhanced, compared to undifferentiated cells. The following observations were made at first: ( 1) The response to high-KCl application, in both undifferentiated and differentiated cells, was significantly inhibited by calciseptine ( CaS), an L-type Ca2+ channel blocker, but not by N-, P- and R- type Ca2+ channel blockers. The IC50 values for CaS in both undifferentiated and differentiated cell was almost identical. ( 2) The inhibitory effect of CaS was irreversible. ( 3) The increasing effect for [ Ca2+](i) by high-KCl application was completely dependent on the presence of extracellular calcium ions. ( 4) The increased [ Ca2+](i) by high-KCl application under a plateau concentration was quickly decreased to basal levels when the high- KCl solution was exchanged for a high- KCl solution containing EGTA ( without CaCl2). Together, these results suggest that the enhancement of the response effect of [ Ca2+](i) by high-KCl application in differentiated single NG108-15 cells was mainly due to the quantitative increase of L-type voltage-sensitive calcium channels ( VSCCs), which were irreversibly inhibited by CaS.
  • N Kawao; M Nagataki; K Nagasawa; S Kubo; K Cushing; T Wada; F Sekiguchi; S Ichida; MD Hollenberg; WK MacNaughton; H Nishikawa; A Kawabata
    We investigated proteinase-activated receptor-2 (PAR(2))-triggered signal transduction pathways causing increased prostaglandin E-2 (PGE(2)) formation in human lung-derived A549 epithelial cells. The PAR(2) agonist, SLIGRL-NH2 (Ser-Leu-Ile-Gly-Arg-Leu-amide), evoked immediate cytosolic Ca2+ mobilization and delayed (0.5-3 h) PGE(2) formation. The PAR(2)-triggered PGE(2) formation was attenuated by inhibition of the following signal pathway enzymes: cyclooxygenases 1 and 2 (COX-1 and COX-2, respectively), cytosolic Ca2+-dependent phospholipase A(2) (cPLA(2)), the mitogenactivated protein kinases (MAPKs), mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) and p38 MAPK, Src family tyrosine kinase, epidermal growth factor (EGF) receptor tyrosine kinase (EGFRK), and protein kinase C (PKC), but not by inhibition of matrix metalloproteinases. SLIGRL-NH2 caused prompt ( 5 min) and transient ERK phosphorylation, blocked in part by inhibitors of PKC and tyrosine kinases but not by an EGFRK inhibitor. SLIGRL-NH2 2 also evoked a relatively delayed (15 min) and persistent (30 min) phosphorylation of p38 MAPK, blocked by inhibitors of Src and EGFRK but not by inhibitors of COX-1 or COX-2. SLIGRL-NH2 elicited a Src inhibitor-blocked prompt (5 min) and transient phosphorylation of the EGFRK. SLIGRL-NH2 up-regulated COX-2 protein and/or mRNA levels that were blocked by inhibition of p38 MAPK, EGFRK, Src, and COX-2 but not MEK-ERK. SLIGRL-NH2 also caused COX-1-dependent up-regulation of microsomal PGE synthase-1 (mPGES-1). We conclude that PAR(2)-triggered PGE(2) formation in A549 cells involves a coordinated up-regulation of COX-2 and mPGES-1 involving cPLA(2), increased cytosolic Ca2+, PKC, Src, MEK-ERK, p38 MAPK, Src-mediated EGF receptor trans-activation, and also metabolic products of both COX-1 and COX-2.
  • T Wada; T Imanishi; A Kawaguchi; MX Mori; Y Mori; K Imoto; S Ichida
    NEUROCHEMICAL RESEARCH SPRINGER/PLENUM PUBLISHERS 30 (8) 1045 - 1054 0364-3190 2005/08 
    Characteristics for the specific binding of I-125-omega-CTX GVIA and I-125-omega-CTX MVIIC to crude membranes from BHKN101 cells expressing the alpha(1B) subunits of Ca(v)2.2 channels and from mice brain lacking the alpha(1B) subunits of Ca(v)2.2 channels, particularly, the effects of CaM and various Ca2+ channel blockers on these specific bindings were investigated. Specific binding of I-125-omega-CTX GVIA to the crude membranes from BHKN101 cells was observed, but not from control BHK6 cells. omega-CTX GVIA, omega-CTX MVIIC and omega-CTX SVIB inhibited the specific binding of I-125-omega-CTX GVIA to crude membranes from BHKN101 cells, and the IC50 values for omega-CTXGVIA, omega-CTX MVIIC and omega-CTX SVIB were 0.07, 8.5 and 1.7 nM, respectively. However, omega-agatoxin IVA and calciseptine at concentrations of 10(-9)-10(-6) M did not inhibit specific binding. Specific binding was also about 80% inhibited by 20 mu g protein/ml CaM. The amount of I-125-omega-CTX GVIA (30 pM) specifically bound to membranes from brain of knockout mice lacking alpha(1B) subunits of Ca(v)2.2 channels was about 30% of that to the crude membranes from brain of wild-type. On the other hand, specific binding of I-125-omega-CTX MVIIC (200 pM) was observed on the crude membranes of both BHKN101 and control BHK6 cells. The specific binding of I-125-omega-CTX MVIIC (200 pM) was not inhibited by omega-CTX GVIA and omega-CTX SVIB, and also omega-Aga IVA and calciseptine at concentrations of 10(-9)-10(-7) M, although specific binding was almost completely dose dependently inhibited by non-radiolabeled omega-CTX MVIIC (IC50 value was about 0.1 nM). 20 mu g protein/ml CaM did not inhibit specific binding. Therefore, these results suggest that BHKN101 cells have a typical Ca(v)2.2 channels which are also inhibited by CaM and have not specific binding sites for omega-CTX MVIIC, although omega-CTX MVIIC is a blocker for both Ca(v)2.1 (alpha(1A;) P/Q-type) and Ca(v)2.2 channels.


Books and other publications

  • ミネルヴァ書房, 『ケアマネジメント用語辞典(改訂版)』
    南 武志; 吉田 繁; 巽 純子; 辻内 俊文; 和田 哲幸; 今西 孝至 (Joint work)2007
  • ミネルヴァ書房, 『ケアマネジメント用語辞典』
    南 武志; 吉田 繁; 巽 純子; 辻内 俊文; 和田 哲幸; 今西 孝至 (Joint work)2005

Lectures, oral presentations, etc.

  • 医薬品の適正使用に関わる薬剤師の責務 ~薬学部教員からの視点~
    和田哲幸; 片岡大士; 伊内秋夫; 志熊理史; 伊内 智; 秋本義雄
    第60回 日本薬学会・日本薬剤師会・日本病院薬剤師会 中国四国支部学術大会  2021/10
  • GPR120を介した性腺刺激ホルモン合成および分泌調節メカニズムについて
    森山隆太郎; 池田隼也; 原尚輝; 萩原央記; 和田哲幸
    第114回日本繁殖生物学会大会  2021/09
  • 患者のための医療サービスと薬局薬剤師業務負担に関する予備的意識調査
    和田哲幸; 片岡大士; 瀧一洋; 米島貴夢; 伊内智; 伊内秋夫
    第54回日本薬剤師会学術大会(福岡)  2021/09
  • ゴナドトロフにおけるGPR120を介した性腺刺激ホルモン分泌調節メカニズム
    森山隆太郎; 池田隼也; 原尚輝; 北爪香菜子; 萩原央記; 和田哲幸
    第35回日本下垂体研究会学術集会  2021/08
  • 医療事故裁判例に学ぶ薬剤師の職責 ~職場コミュニケーションの重要性~
    和田哲幸; 瀧 一洋; 米島貴夢; 伊内 智; 高橋桃香; 秋本義雄
    (ア) 第59回 日本薬学会・日本薬剤師会・日本病院薬剤師会 中国四国支部学術大会  2020/12
  • 1. テキストマイニングによる薬学基礎科目の理解につなげる参加型学修システムの分析
    大内 秀一; 松野 純男; 和田 哲幸; 伊藤 栄次; 前川 智弘; 多賀 淳; 細見 光一; 大鳥 徹; 仲西 功; 川﨑 直人; 岩城 正宏
    日本薬学会第140年会  2020/03
  • 来局者に対するフレイルの啓発 ~口腔・栄養の観点から~
    和田哲幸; 宇野光裕; 神森浩司; 桑島俊恵
    日本健康体力栄養学会年会  2020/02
  • 6. 薬機法第1条6(国民の義務)と患者の協力
    和田 哲幸; 片岡 大士; 瀧 一洋; 伊内 智; 秋本 義雄
    第58回日本薬学会・日本薬剤師会・日本病院薬剤師会 中国四国支部学術大会  2019/11
  • 医療用語を含む文章におけるテキストマイニングを用いた難易度判定
    小野田 美華; 筒井 凌; 大内 秀一; 中村 武夫; 伊藤 栄次; 和田 哲幸; 八軒 浩子; 大星 直樹; 松野 純男
    第13回 日本薬局学会  2019/10
  • 薬剤師養成における生命倫理教育の重要性
    伊藤栄次; 中村武夫; 松野純男; 大内秀一; 和田哲幸; 八軒浩子
    第52回 日本薬剤師会学術大会  2019/10
  • 学部新入生に対する意識調査による学生メンタル状況の解析
    永井希佳; 大内秀一; 中村武夫; 伊藤栄次; 和田哲幸; 八軒浩子; 大対香奈子; 松野純男
    日本薬学教育学会大会  2019/08
  • 2. 基礎薬学科目の知識を臨床へつなぐ新しい学修システム構築の試み〜実務実習実施前の学生に対する効果の検証〜
    大内秀一; 松野純男; 和田哲幸; 伊藤栄次; 前川智弘; 多賀淳; 細見光一; 大鳥徹; 仲西功; 川﨑直人; 岩城正宏
    日本薬学教育学会大会  2019/08
  • 低栄養防止および重症化予防を目的とした来局高齢者へのフレイルの啓発  [Not invited]
    宇野光裕和田哲幸; 中村武夫; 神森浩司; 桑島俊恵
    第26回 日本健康体力栄養学会大会  2019/03
  • 医薬品副作用データベース (JADER) を用いた機械学習による副作用の予測  [Not invited]
    小野田 良; 松井 大樹; 山下 由依亜; 中村 武夫; 伊藤 栄次; 大内 秀一; 和田 哲幸; 八軒 浩子; 大星 直樹; 松野 純男
    第28回日本医療薬学会年会  2018/11
  • テキストマイニングを用いた薬剤師国家試験出題のトレンド分析 ―1996〜2018年の年次推移および新薬の出題傾向に関する解析―  [Not invited]
    山下由依亜; 小野田良; 八軒浩子; 中村武夫; 伊藤栄次; 大内秀一; 和田哲幸; 松野純男
    第68回 日本薬学会近畿支部総会・大会  2018/10
  • アドミッションポリシーとディプロマポリシーから見える私立薬科大学の特徴  [Not invited]
    村瀬惇; 山下由依亜; 小野田良; 八軒浩子; 北小路学; 中村武夫; 伊藤栄次; 大内秀一; 和田哲幸; 松野純男
    第3回 日本薬学教育学会大会  2018/09
  • 改定コアカリキュラム」評価方法(ルーブリック評価)について  [Not invited]
    和田 哲幸
    和歌山県薬剤師会 研修会  2018/09
  • 初期救命救急講習を通しての早期体験学習参加学生の評価およびその解析  [Not invited]
    八軒 浩子; 小野田 良; 山下 由依亜; 中村 武夫; 伊藤 栄次; 松野 純男; 大内 秀一; 和田 哲幸
    日本薬学会第138年会  2018/03
  • ヒューマニズム教育としての人体臓器観察の客観的解析  [Not invited]
    大内 秀一; 山下 由依亜; 小野田 良; 中村 武夫; 伊藤 栄次; 松野 純男; 和田 哲幸; 八軒 浩子
    日本薬学会第138年会  2018/03
  • 早期体験学習における不自由体験の教育効果について  [Not invited]
    和田 哲幸; 小野田 良; 山下 由依亜; 中村 武夫; 伊藤 栄次; 松野 純男; 大内 秀一; 八軒 浩子
    日本薬学会第138年会  2018/03
  • ヒトのカラダを知る! 薬剤師教育の第一歩  [Not invited]
    和田哲幸; 中村武夫; 伊藤栄次; 松野純男; 大内秀一; 八軒浩子
    日本薬学会第137年会 ハイライト発表  2017/03
  • Utility of the human organs observation as part of the humanistic education  [Not invited]
    和田哲幸; 中村武夫; 伊藤栄次; 松野純男; 大内秀一; 八軒浩子
    日本薬学会第137年会  2017/03
  • 細胞内カルシウム濃度上昇反応のメカニズムについて  [Not invited]
    和田 哲幸; 武智 昌幸; 中野 瑞希; 春木 恵; 井田 晴久; 吉田 繁
    BMB2015  2015/12
  • 酸化ストレス/高グルコース誘導性の神経細胞死に対するsodium-glucose transporter 機構を介した細胞内カルシウムの関与  [Not invited]
    山﨑由衣; 原田慎一; 和田哲幸; 徳山尚吾
    第127回 日本薬理学会近畿支部 部会  2015/06
  • 地域薬局薬剤師による早期体験学習参加学生の評価およびその解析  [Not invited]
    八軒浩子; 伊藤栄次; 松野純男; 大内秀一; 和田哲幸; 中村武夫
    日本薬学会第136年会  2015/03
  • 人体臓器観察(早期体験学習)を通してのヒューマニズム教育の検証  [Not invited]
    和田哲幸; 中村武夫; 伊藤栄次; 松野純男; 大内秀一; 八軒浩子
    日本薬学会第136年会  2015/03
  • 基礎薬学分野の知識定着を志向した参加型学修システム構築の試み  [Not invited]
    大内秀一; 松野純男; 和田哲幸; 仲西功; 前川智弘; 多賀淳; 伊藤栄次; 大鳥徹; 川﨑直人; 西田升三
    日本薬学会第136年会  2015/03
  • MifepistoneはSARTストレスマウスにおける視床下部-脳下垂体-副腎皮質系の機能障害を改善する  [Not invited]
    船上 仁範; 宮本 朋佳; 阪井 邦正; 植芝 慧子; 西坂 香名子; 和田 哲幸; 市田 成志
    Neuroscience2014  2014/09
  • 細胞内カリウム濃度上昇は神経細胞分化を誘導する  [Not invited]
    春木恵; 和田哲幸; 藤木亮; 植芝慧子; 船上仁範; 武智昌幸; 吉田繁; 市田成志
    生体機能と創薬シンポジウム2014  2014/08
  • SARTストレス誘発肺胞マクロファージの機能異常に対する自律神経系の関与  [Not invited]
    植芝慧子; 大友栞; 杉原小雪; 山村愛美; 船上仁範; 和田哲幸; 市田成志
    生体機能と創薬シンポジウム2014  2014/08
    T. Wada; M. Takechi; K. Sakai; K. Ueshiba; Y. Funakami; S. Yoshida; S. Ichida
    Y. Funakami; T. Miyamoto; T. Iida; K. Sakai; K. Ueshiba; T. Wada
    S. Ichida; Y. Funakami; T. Miyamoto; T. Iida; K. Sakai; K. Ueshiba; T. Wada
  • 細胞ストレスとカリウムイオンチャネルの関係について  [Not invited]
    和田哲幸; 古賀雅也; 阪井邦正; 植芝慧子; 船上仁範; 吉田繁; 武智昌幸; 市田成志
    日本薬学会第134年会  2014/03
  • Chronic stress attenuates neuronal activity of the brain stress circuit and the function of the hypothalamus-pituitary-adrenal axis in mice.  [Not invited]
    Y Funakami; T Miyamoto; T Iida; K Kurokawa; K Sakai; K Ueshiba; M Nagano; T Wada; Y Shigeyoshi; S Ichida
    Pharmacology 2013 London  2013/12
  • Diazepam improves the functional disorder of the alveolar macrophage caused by chronic stress in mice.  [Not invited]
    S Ichida; Y Funakami; C Wakaki; K Ueshiba; M Nakao; K Sakai; T Wada
    Pharmacology 2013 London  2013/12
  • 非定型抗精神病薬オランザピンによる交感神経活性化作用の検討:ラット褐色細胞腫 PC12 を用いた検討  [Not invited]
    藤原恵子; 深水千智; 松野純男; 和田哲幸; 市田成志; 八木秀樹; 益子 高; 森山博由; 森山麻里子; 大鳥 徹; 松山賢治
    第63回 日本薬学会近畿支部総会・大会  2013/10
  • SART ストレスマウスから採取した肺胞マクロファージの貪食能に対するアドレナリン、ノル アドレナリンの効果  [Not invited]
    植芝慧子; 田代のぞみ; 西島知里; 大友 栞; 杉原小雪; 浅野 肇; 阪井邦正; 船上仁範; 和田哲幸; 市田成志
    第63回 日本薬学会近畿支部総会・大会  2013/09
  • Changes in intracellular concentration of potassium in the neuronal differentiation  [Not invited]
    和田 哲幸; 藤木 亮; 淺野 肇; 船上 仁範; 武智 昌幸; 吉田 繁; 市田 成志
    第86回 日本生化学会  2013/09
  • SARTストレスによる肺胞マクロファージの貪食能低下は交感神経系の活性化によって改善する  [Not invited]
    植芝慧子; 船上仁範; 田代のぞみ; 西島知里; 大友栞; 杉原小雪; 阪井邦正; 和田哲幸; 市田 成志
    日本薬学会第134年会  2013/03
  • 分野横断型講義におけるチーム基盤型学習(TBL)について  [Not invited]
    西脇敬二; 川瀬篤史; 和田哲幸; 八木秀樹; 川﨑直人; 伊藤栄次; 岩城正宏
    日本薬学会第133年会 シンポジウム  2013/03
  • SART ストレスマウスにおける血清アンチエイジングおよびストレスホルモンの変化―コルチコステロンとデヒドロエピアンドロステロン―  [Not invited]
    阪井邦正; 船上仁範; 岸本茉希; 谷口友梨; 豊田 和; 大浦沙貴子; 岡部由季; 植芝慧子; 浅野 肇; 和田哲幸; 市田成志
    日本薬学会第133年会  2013/03
  • SART ストレスにより低下した肺胞マクロファージの貪食能はアドレナリンβ2 受容体を介して改善する  [Not invited]
    植芝慧子; 船上仁範; 田代のぞみ; 西島千里; 大友 栞; 杉原 小雪; 浅野 肇; 阪井邦正; 和田哲幸; 市田成志
    日本薬学会第133年会  2013/03
  • チメロサールのイオンチャネルへの影響について  [Not invited]
    和田哲幸; 吉田泰介; 久保田大樹; 山田 愛; 浅野 肇; 阪井邦正; 植芝慧子; 船上仁範; 南 武; 吉田 繁; 市田成志
    日本薬学会第133年会  2013/03
  • ウワバインの細胞保護作用とカリウムイオン動態について  [Not invited]
    古賀雅也; 和田哲幸; 浅野 肇; 藤木 亮; 阪井邦正; 植芝慧子; 船上仁範; 武智昌幸; 市田成志
    日本薬学会第133年会  2013/03
  • Effects of Diazepam on c-Fos expression in hypothalamus of SART-stressed mice  [Not invited]
    Y Funakami; T Iida; T Miyamoto; M Kishimoto; K Toyoda; Y Taniguchi; S Ohura; Y Okabe; H; Asano,T Wada; M Nagano; Y Shigeyoshi; S Ichida
    Neuro2012 Nagoya  2012/09
  • 腫瘍細胞における細胞内Ca2+濃度上昇反応について  [Not invited]
    和田哲幸; 羽賀景子; 池原茉理; 山田愛; 吉田泰介; 豊山舞佳; 川口明範; 浅野 肇; 坂本大和; 若木千幸; 三好梨左; 飯田拓真; 船上仁範; 吉田繁; 市田成志
    日本薬学会第132年会  2012/03
  • NG108-15細胞のcoline acetyltransferase 発現に関する細胞内シグナルについて  [Not invited]
    若木千幸; 山本達也; 中尾真理子; 川口明範; 浅野肇; 宮本朋佳; 渡辺瑞貴; 三好梨左; 飯田拓真; 船上仁範; 和田哲幸; 市田成志
    日本薬学会第131年会  2011/03
  • NG108-15細胞の神経分化における、5-HT によって引き起こされた細胞内Ca2+濃度上昇反応の性質について  [Not invited]
    三好梨左; 川口明範; 浅野肇; 宮本朋佳; 中尾真理子; 渡辺瑞貴; 若木千幸; 飯田拓真; 船上仁範; 和田哲幸; 吉田繁; 市田成志
    日本薬学会第131年会  2011/03
  • 急激な環境温度変化が視床・視床下部におよぼす影響  [Not invited]
    飯田拓真; 宮本朋佳; 尾鍋明子; 谷岡紗良; 川口明範; 浅野肇; 中尾真理子; 渡辺瑞貴; 若木千幸; 三好梨左; 船上仁範; 長野護; 和田哲幸; 重吉康史; 市田成志
    日本薬学会第131年会  2011/03
  • 寒冷刺激の反復による橋・延髄領域の神経活性への影響  [Not invited]
    宮本朋佳; 飯田拓真; 岸孝之; 若木千幸; 三好梨左; 川口明範; 浅野肇; 中尾真理子; 渡辺瑞貴; 船上仁範; 長野護; 和田哲幸; 重吉康文; 市田成志
    日本薬学会第131年会  2011/03
  • Characteristics for response to serotonin and serotonin 3A/B receptor localization at nerve endings, in NG108-15 cells at the early phase after Bt2cAMP treatment  [Not invited]
    T Miyamoto; H Asano; A Kawaguchi; M Nakao; M Watanabe; R Miyoshi; T Wakaki; T Iida; Y Funakami; T Wada; S Yoshida; S Ichida
    第84回日本薬理学会年会  2011/03
  • イオンチャネルの構造と機能から疾患を読み解  [Invited]
    和田 哲幸
    第14回 南大阪薬剤師業務研究会  2010/11
  • クモ毒NPTX-594のCa2+透過性グルタミン酸受容体に対する阻害効果について  [Not invited]
    和田 哲幸; 市田 成志; 船上 仁範; 若宮 建昭; 吉田 繁; 森山 隆太郎
    日本薬学会 第130年会  2010/03  日本薬学会 第130年会
  • 学生のニーズ把握と具体的な問題解決手法の修得を目的とした学生ワークショップの試み  [Not invited]
    安原 智久; 川﨑 直人; 八木 秀樹; 川瀬 篤史; 伊藤 栄次; 大鳥 徹; 和田 哲幸; 松山 賢治; 岩城 正宏
    日本薬学会第130年会  2010  日本薬学会第130年会
  • NG108-15 細胞の神経分化過程における5-HT3 受容体を介した反応性の変化  [Not invited]
    和田 哲幸; 市田 成志; 船上 仁範; 吉田 繁
    第82回日本生化学会年会  2009/10  第82回日本生化学会年会
  • レチノイン酸により分化誘導したNG108-15 細胞における5-HT3受容体の反応性の変化について  [Not invited]
    和田 哲幸; 市田 成志; 船上 仁範
    第59回日本薬学会近畿支部総会・大会  2009/10  第59回日本薬学会近畿支部総会・大会
  • NG108-15 細胞のBt2cAMP 処理による神経突起伸長に対する各種シグナル阻害剤の効果およびERK-リン酸量の変化  [Not invited]
    市田 成志; 和田 哲幸; 船上 仁範; 吉田 繁
    第82回日本生化学会年会  2009/10  第82回日本生化学会年会
  • SARTストレスマウスの小腸輸送能亢進とセロトニン神経  [Not invited]
    船上 仁範; 伊藤 栄次; 市田 成志; 和田 哲幸
    第82回日本薬理学会年会  2009/03  第82回日本薬理学会年会
  • Change for 3A and 3B subunits of 5-HT3 receptors in differentiated NG108-15 cells  [Not invited]
    市田 成志; 和田 哲幸; 船上 仁範; 吉田 繁
    The 38th annual meeting of the Society for Neuroscience  2008/11  The 38th annual meeting of the Society for Neuroscience
  • Change for 3A and 3B subunits of 5-HT3 receptors during neural differentiation  [Not invited]
    Seiji Ichida; Hajime Asano; Yoshinori Funakami; Tetsuyuki Wada; Shigeru Yoshida
    北米神経科学会 ワシントンDC POSTER  2008/07
  • 神経分化したNG108-15細胞における5-HT3受容体サブユニットの変化について  [Not invited]
    市田 成志; 和田 哲幸; 船上 仁範
  • Zinc induces calcium uptake in rat pancreatic AR42J cells.  [Not invited]
    T. Minami; T. Wada; H. Sugito; A. Kubo; S. Ichida; S. Yoshida
    International Congress of Toxicology,Canada POSTER  2007/06
  • Characteristic of serotonin-induced Na+ current in undifferentiated and differentiated NG108-15 cells  [Not invited]
    和田 哲幸; 市田 成志; 吉田 繁
    Neuroscience2006  2006/10  Neuroscience2006
  • Enhancement of sodium current during neural differentiation is mainly attributable to increase of Nav1.7 (voltage-gated sodium channel subtype) expression  [Not invited]
    市田 成志; 和田 哲幸; 吉田 繁
    Neuroscience2006  2006/10  Neuroscience2006
  • Hydrogen sulfide sensitizes T-type calcium channels via redox modulation.  [Not invited]
    川畑 篤史; 関口 富美子; 吉田 繁; 市田 成志; 和田 哲幸; 西川 裕之
    Neuroscience 2006  2006/10  アメリカ合衆国、アトランタ  Neuroscience 2006
  • 保険薬局および病院実務実習に対する学生の意識調査  [Not invited]
    北小路 学; 石渡 俊二; 石本 真美子; 船上 仁範; 八軒 浩子; 多賀 淳; 八木秀樹; 和田 哲幸; 田邉 元三; 市田 成志; 西田 升三
    日本社会薬学会第25年会  2006/09  徳島  日本社会薬学会第25年会
  • 内因性ガス状情報伝達物質H2Sは未分化NG108-15細胞においてT型カルシウムチャネルの感受性を増大させる.  [Not invited]
    川畑 篤史; 関口 富美子; 吉田 繁; 市田 成志; 和田 哲幸; 西川 裕之
    第109回日本薬理学会近畿部会  2006/06  岡山  第109回日本薬理学会近畿部会
  • 未分化及び分化したNG108-15細胞におけるbradykinin刺激による[Ca2+]i上昇反応の性質について  [Not invited]
    市田 成志; 和田 哲幸
    日本薬学会126年会  2006/03  日本薬学会126年会
  • NG108-15細胞の分化に伴うCa2+電流の変化  [Not invited]
    和田 哲幸; 市田 成志
    日本薬学会126年会  2006/03  日本薬学会126年会
  • 分化したNG108-15細胞ではveratridineによる細胞内Na+濃度の上昇反応が認められる  [Not invited]
    市田 成志; 和田 哲幸
    日本薬学会125年会  2006/03  日本薬学会125年会
  • NG108-15細胞の神経分化過程におけるテトロドトキシン感受性ナトリウムチャネルの発  [Not invited]
    市田 成志; 和田 哲幸
    第78回日本生化学会大会  2005/10  第78回日本生化学会大会
  • 様々な生理活性物質によって生じた未分化及び分化NG108-15細胞内Ca2+濃度変化の性質について  [Not invited]
    市田 成志; 和田 哲幸
    第28回日本神経科学会  2005/07  第28回日本神経科学会
  • Decreased Intestinal Detoxification Functions in an Absorption Process in Adjuvant-Induced Arthritis Rats  [Not invited]
    岩城 正宏; 谷野 公俊; 和田 哲幸; 西田 升三; 市田 成志; S. Uno; A. Tsuji; K. Miyauchi; M. Yanae
    第20回年会 2005マウイJSSX-ISSX合同学会  2005  第20回年会 2005マウイJSSX-ISSX合同学会
  • ヒト肺胞上皮細胞におけるPAR-2活性化によるCOX-2の誘導とそれに関与するシグナルの解析  [Not invited]
    川畑 篤史; 河尾 直之; 和田 哲幸; 関口 富美子; 市田 成志; Wallace K. MacNaughton; Morley D. Hollenberg
    第106回日本薬理学会近畿部会  2004/11  京都  第106回日本薬理学会近畿部会
  • Characteristics of N-type calcium channels stably expressed in BHK N101cells.  [Not invited]
    和田 哲幸; 吉田 繁; 川口 明範; 阿部 順一; 今西 孝至; 市田 成志; 井本 敬二; 森 泰生
    2004/10  34th Annual Meeting of Neuroscience (San Diego)
  • Characteristics of calcium influx elicited by high-KCl in differentiated and undifferentiated NG108-15 cells  [Not invited]
    和田 哲幸; 市田 成志; 吉田 繁
    Neuroscience2004  2004/10  Neuroscience2004
  • N型カルシウムチャネルを強制発現させたBHK N101細胞の性質について  [Not invited]
    和田 哲幸; 市田 成志
    Neuro2004  2004/09  大阪  Neuro2004
  • 未分化及び分化したNG108-15細胞における高濃度KClによって惹起されたCa流入の性質について  [Not invited]
    市田 成志; 和田 哲幸
    Neuro2004  2004/09  大阪  Neuro2004
  • Signal transduction mechanisms for prostanoid formation caused by protease-activated receptor-2 activation in human lung epithelial cells.  [Not invited]
    川畑 篤史; 河尾 直之; 和田 哲幸; 市田 成志; 関口 富美子; Morley D. Hollenberg
    XVIIth International Congress on Fibrinolysis and Proteolysis  2004/03  Melbourne, Australia  XVIIth International Congress on Fibrinolysis and Proteolysis
  • Study for the characteristic of specific omega-conotoxin MVIIC binding on CaV2.1 and CaV2.2 channels fixed with antibodies and on membranes from N101 cells induced by CaV2.2 channel ?1 subunits  [Not invited]
    市田 成志; 和田 哲幸
    第76回日本生化学  2003/10  第76回日本生化学
  • カルモデュリンは P・N 型カルシウムチャネルブロッカーであるomega-conotoxin MVIIC の特異的結合を抑制しない  [Not invited]
    市田 成志; 和田 哲幸
    第75回日本生化学会大会  2003/10  第75回日本生化学会大会
  • 特異的ω-コノトキシンGVIA結合に対するカルモジュリンの効果に関する研究  [Not invited]
    和田 哲幸; 市田 成志
    第52回日本薬学会近畿支部総会  2002/10  第52回日本薬学会近畿支部総会
  • 架橋剤により標識した125I ω-Conotoxin GVIA結合部位の抗体による同定  [Not invited]
    和田 哲幸; 市田 成志
    日本薬学会121年会  2001/03  日本薬学会121年会

Affiliated academic society

  • Society for Neuroscience   日本神経化学会   日本生化学会   日本薬学会   

Research Themes

  • Study on characteristics of Specific 125I-ω-conotoxin GVTA binding sites
  • 漏洩カリウムチャネルを標的とするウワバインの細胞保護機構解明
    Author : 和田 哲幸