Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells

Haruhiro Higashida, Sarah E.H. Bowden, Shigeru Yokoyama, Alla Salmina, Minako Hashii, Naoto Hoshi, Jia Sheng Zhang, Rimma Knijnik, Mami Noda, Zen Guo Zhong, Duo Jin, Kazuhiro Higashida, Hisashi Takeda, Tenpei Akita, Kenji Kuba, Sayaka Yamagishi, Noriaki Shimizu, Shin Takasawa, Hiroshi Okamoto, Jon Robbins

研究成果: ジャーナルへの寄稿学術誌査読

14 被引用数 (Scopus)

抄録

The role of cyclic ADP-ribose (cADPR) and its synthetic enzyme, CD38, as a downstream signal of muscarinic acetylcholine receptors (mAChRs) was examined in neuroblastoma cells expressing M1 mAChRs (NGM1). NGM1 cells were further transformed with both wild-type and mutant (C119K/C201E) human CD38. The dual transformed cells exhibited higher cADPR formation than ADPR production and elevated intracellular free Ca2+ concentrations ([Ca2+]i) in response to ACh. These phenotypes were analyzed in detail in a representative CD38 clone. The intracellular cADPR concentration by ACh application was significantly increased by CD38 overexpression. Digital image analysis by a confocal microscopy revealed that topographical distribution of the sites of Ca2+ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca2+ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.

本文言語英語
ページ(範囲)339-346
ページ数8
ジャーナルNeuroscience Research
57
3
DOI
出版ステータス出版済み - 3月 2007
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 神経科学一般

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