ミオイノシトール1
WordNet
- an optically inactive alcohol that is a component of the vitamin B complex
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- 『私の』 / 《親しみをこめた呼び掛けに用いて》 / 《驚きを表して》おや,まあ
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- 1. T細胞受容体シグナル伝達 t cell receptor signaling
- 2. Chapter 4C：細胞容積の維持 chapter 4c maintenance of cell volume
- 3. Chapter 6A：ホルモンの作用機序 chapter 6a mechanisms of hormone action
- 4. 神経系および行動に及ぼすステロイドの作用 glucocorticoid effects on the nervous system and behavior
- 5. 低ナトリウム血症および高ナトリウム血症の症状 manifestations of hyponatremia and hypernatremia
English Journal
- Molecular mechanism of 2-APB-induced Ca(2+) influx in external acidification in PC12.
- Takahashi K1, Yokota M1, Ohta T2.Author information 1Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, 4-101, Koyama-minami, Tottori 680-8553, Japan.2Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, 4-101, Koyama-minami, Tottori 680-8553, Japan. Electronic address: tohta@muses.tottori-u.ac.jp.Abstract2-Aminoethoxydiphenyl borate (2-APB) is used as a pharmacological tool because it antagonizes inositol 1,4,5-trisphosphate receptors and store-operated Ca(2+) (SOC) channels, and activates some TRP channels. Recently, we reported that 2-APB enhanced the increase in cytotoxic [Ca(2+)]i, resulting in cell death under external acidic conditions in rat pheochromocytoma cell line PC12. However, the molecular mechanism and functional role of the 2-APB-induced Ca(2+) influx in PC12 have not been clarified. In this study, to identify the possible target for the action of 2-APB we examined the pharmacological and molecular properties of [Ca(2+)]i and secretory responses to 2-APB under extracellular low pH conditions. 2-APB dose-dependently induced a [Ca(2+)]i increase and dopamine release, which were greatly enhanced by the external acidification (pH 6.5). [Ca(2+)]i and secretory responses to 2-APB at pH 6.5 were inhibited by the removal of extracellular Ca(2+) and SOC channel blockers such as SK&F96365, La(3+) and Gd(3+). PC12 expressed all SOC channel molecules, Orai 1, Orai 2 and Orai 3. When we used an siRNA system, downregulation of Orai 3, but not Orai 1 and Orai 2, attenuated both [Ca(2+)]i and secretory responses to 2-APB. These results suggest that 2-APB evokes external acid-dependent increases of [Ca(2+)]i and dopamine release in PC12 through the activation of Orai 3. The present results indicate that 2-APB may be a useful pharmacological tool for Orai channel-related signaling.
- Experimental cell research.Exp Cell Res.2014 May 1;323(2):337-45. doi: 10.1016/j.yexcr.2014.03.001. Epub 2014 Mar 11.
- 2-Aminoethoxydiphenyl borate (2-APB) is used as a pharmacological tool because it antagonizes inositol 1,4,5-trisphosphate receptors and store-operated Ca(2+) (SOC) channels, and activates some TRP channels. Recently, we reported that 2-APB enhanced the increase in cytotoxic [Ca(2+)]i, resulting in
- PMID 24630903
- Bradykinin regulates the expression of claudin-5 in brain microvascular endothelial cells via calcium-induced calcium release.
- Zhou L1, Yang B, Wang Y, Zhang HL, Chen RW, Wang YB.Author information 1Department of Neurosurgery, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.AbstractTo investigate the mechanism underlying the regulation of claudin-5, a tight junction protein that participates primarily in the constitution of the blood-brain barrier by bradykinin (BK), we established a primary culture of rat brain microvascular endothelial cells (BMECs). BMECs were treated with 10(-5) M BK, and changes in the intracellular Ca(2+) levels were measured by using the sensitive fluorescent dye fluo-3; the expression and distribution of claudin-5 were investigated by immunocytochemistry and Western blot analyses. We did not detect any expression of bradykinin B2 receptors in the BMECs or freshly isolated rat brain microvessels. We found that 10(-5) M BK triggered Ca(2+) transients in BMECs, and further investigations revealed that inositol 1,4,5-trisphosphate receptors (IP3 Rs) and ryanodine receptors (RyRs) on the endoplasmic reticulum (ER) were responsible for the Ca(2+) fluctuation. Consequently, these intracellular Ca(2+) changes that occur in response to BK application were identified as Ca(2+) -induced Ca(2+) release (CICR). Immunocytochemistry and Western blot results demonstrated that 10(-5) M BK could cause the internalization and a decrease in the expression of claudin-5; agonists of IP3 Rs and RyRs, such as IP3 and caffeine, enhanced the BK-induced downregulation of claudin-5, whereas antagonists of IP3 Rs and RyRs, such as 2-APB and ryanodine, abrogated BK's effect on claudin-5. In conclusion, the BK-induced CICR in primary culture BMECs might be the mechanism by which BK modulates claudin-5. © 2014 Wiley Periodicals, Inc.
- Journal of neuroscience research.J Neurosci Res.2014 May;92(5):597-606. doi: 10.1002/jnr.23350. Epub 2014 Jan 27.
- To investigate the mechanism underlying the regulation of claudin-5, a tight junction protein that participates primarily in the constitution of the blood-brain barrier by bradykinin (BK), we established a primary culture of rat brain microvascular endothelial cells (BMECs). BMECs were treated with
- PMID 24464430
- Enhanced expression and purification of inositol 1,4,5-trisphosphate 3-kinase A through use of the pCold1-GST vector and a C-terminal hexahistidine tag in Escherichia coli.
- Lee D1, Han S1, Woo S1, Lee HW1, Sun W1, Kim H2.Author information 1Department of Anatomy, College of Medicine, Korea University, Brain Korea 21, Seoul 136-705, Republic of Korea.2Department of Anatomy, College of Medicine, Korea University, Brain Korea 21, Seoul 136-705, Republic of Korea. Electronic address: kimhyun@korea.ac.kr.AbstractInositol 1,4,5-trisphosphate 3-kinase A (IP3K-A, alternative name: ITPKA) is a neuron-specific enzyme that converts 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) through its kinase domain. In addition, transient overexpression of IP3K-A induces morphological changes in dendritic spines of excitatory synapses in a kinase-independent manner, apparently by modulating the organization of the neuronal cytoskeleton. Although the procurement of a purified recombinant IP3K-A protein would be indispensable for the biochemical elucidation of its physiological roles, production of recombinant IP3K-A has proven technically challenging in conventional Escherichia coli expression systems. These difficulties stem from low enzyme solubility, as well as poor protein quality caused by the tendency of IP3K-A to split into partial fragments. In present study, we newly introduced cold-shock expression vector (pCold1) together with a C-terminal hexahistidine tag (C-HIS) to enhance the expression levels of recombinant IP3K-A in E. coli. Importantly, when compared with other commonly-employed bacterial expression systems, the pCold1 system improved the yield and the purity of full-length IP3K-A due to the exclusion of truncated enzyme forms, and also enhanced the solubility of the enzyme. Furthermore, the functional integrity of purified IP3K-A was confirmed in both kinase activity assay and microtubule binding assay. Recombinant IP3K-A acquired via this modified protocol will be expected to facilitate the exploration of the enzyme's biochemical profile, both structurally and functionally.
- Protein expression and purification.Protein Expr Purif.2014 May;97:72-80. doi: 10.1016/j.pep.2014.02.006. Epub 2014 Feb 25.
- Inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A, alternative name: ITPKA) is a neuron-specific enzyme that converts 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) through its kinase domain. In addition, transient overexpression of IP3K-A induces morphological changes in dend
- PMID 24576661
Japanese Journal
- Intercellular Ca2+ Response Triggered by IP3 among Endothelial Cells in Shear Stress Flow
- 工藤 奨,細渕 誠人,紅床 省吾,隅井 干城,島田 知弥,寺田 麻理枝,谷下 一夫
- 日本機械学会論文集Ｂ編 77(784), 2431-2441, 2011
- … effects on Ca2+ wave among cultured bovine aorta endothelial cells (BAECs) upon inhibiting the main intercellular signaling pathways, such as gap junction and paracrine pathways by inducing Ca2+ wave using D-myo-inositol 1,4,5-trisphosphate, P4(5)-(1-(2-nitrophenyl)ethyl) ester trisodium salt (Caged IP3) due to an intracellular IP3 …
- NAID 130002050625
- 環変換に基づく糖関連生物活性物質の合成研究
- 高橋 秀依
- 藥學雜誌 122(10), 755-771, 2002-10-01
- … The first is an efficient conversion of 5-enopyranosides and 6-O-acetyl-5-enopyranosides to the corresponding substituted cyclohexanones mediated by a catalytic amount of palladium dichloride. … Furthermore, novel synthesis of all enantiomerically pure diastereoisomers of inositol starting with 6-O-acetyl-5-enopyranosides was investigated. …
- NAID 110003614821
- Pd(II)を用いた触媒的Ferrier環化反応の開発とその生物活性物質合成への応用
- 高橋 秀依,橘高 寿枝,池上 四郎
- 有機合成化学協会誌 58(2), 120-128, 2000-02-01
- … This article summarizes our recent works concerning the development of the catalytic Ferrier (II) carbocyclization mediated by Pd (II) salts and the application of this reaction to the total syntheses : i) β-glucosidase inhibitor, cyclophellitol, ii) all diastereoisomers of inositol and D-<I>myo</I>-inositol phosphates. …
- NAID 10008819058
Related Links
- A collection of model organism databases of metabolic pathways, including reactions, enzymes, genes and substrate compounds ... Summary: D-myo-inositol (1,4,5)-trisphosphate is a secondary messenger molecule used in ...
- View and buy high purity D-myo-Inositol 1,4,5-trisphosphate, hexapotassium salt from Tocris Bioscience, the leading worldwide supplier of high performance life science reagents ... References Joseph et al (1984) myo-Inositol 1,4,5 ...
Related Pictures
★リンクテーブル★
| リンク元 | 「イノシトール1,4,5-トリスリン酸」「inositol 1,4,5-triphosphate」「ミオイノシトール1,4,5-三リン酸」 |
| 関連記事 | 「my」「trisphosphate」「inositol」 |
「イノシトール1,4,5-トリスリン酸」
- 英
- inositol 1,4,5-trisphosphate
- 同
- イノシトール三リン酸 inositol trisphosphate、IP3
- 関
- イノシトール、myo-inositol 1,4,5-trisphosphate
- 細胞内二次メッセンジャー;カルシウム遊離
- シグナル伝達に関わる。
「inositol 1,4,5-triphosphate」
;関:inositol 1
「ミオイノシトール1,4,5-三リン酸」
- 英
- myo-inositol 1
「my」
- comb form.
- 関
- muscle, muscular, muscularis, musculus
「trisphosphate」
「inositol」