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Cyclic ADP-ribose as a universal calcium signal molecule in the nervous system
http://hdl.handle.net/2297/6932
http://hdl.handle.net/2297/69324b7847aa-e042-4370-ac3e-ee439321ade5
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-HIGASHIDA-H-192.pdf (184.7 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-05 | |||||
| タイトル | ||||||
| タイトル | Cyclic ADP-ribose as a universal calcium signal molecule in the nervous system | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Higashida, Haruhiro
× Higashida, Haruhiro× Salmina, Alla B.× Olovyannikova, Raissa Ya× Hashii, Minako× Yokoyama, Shigeru× Koizumi, Keita× Jin, Duo× Liu, Hong-Xiang× Lopatina, Olga× Amina, Sarwat× Mohammad, Saharul Islam× Huang, Jian-Jun× Noda, Mami |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学大学院医学系研究科脳細胞分子学 | |||||
| 書誌情報 |
Neurochemistry International 巻 51, 号 2-4 SPEC. ISS., p. 192-199, 発行日 2007-07-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0197-0186 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.neuint.2007.06.023 | |||||
| 出版者 | ||||||
| 出版者 | Elsevier | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | β-NAD+ is as abundant as ATP in neuronal cells. β-NAD+ functions not only as a coenzyme but also as a substrate. β-NAD+-utilizing enzymes are involved in signal transduction. We focus on ADP-ribosyl cyclase/CD38 which synthesizes cyclic ADP-ribose (cADPR), a universal Ca2+ mobilizer from intracellular stores, from β-NAD+. cADPR acts through activation/modulation of ryanodine receptor Ca2+ releasing Ca2+ channels. cADPR synthesis in neuronal cells is stimulated or modulated via different pathways and various factors. Subtype-specific coupling of various neurotransmitter receptors with ADP-ribosyl cyclase confirms the involvement of the enzyme in signal transduction in neurons and glial cells. Moreover, cADPR/CD38 is critical in oxytocin release from the hypothalamic cell dendrites and nerve terminals in the posterior pituitary. Therefore, it is possible that pharmacological manipulation of intracellular cADPR levels through ADP-ribosyl cyclase activity or synthetic cADPR analogues may provide new therapeutic opportunities for treatment of neurodevelopmental disorders. © 2007. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.elsevier.com/locate/issn/01970186 | |||||
