| Autor: |
Higashida H; Department of Biophysical Genetics, Kanazawa University Graduate School of Medicine, Kanazawa, Japan. haruhiro@med.kanazawa-u.ac.jp, Bowden SE, Yokoyama S, Salmina A, Hashii M, Hoshi N, Zhang JS, Knijnik R, Noda M, Zhong ZG, Jin D, Higashida K, Takeda H, Akita T, Kuba K, Yamagishi S, Shimizu N, Takasawa S, Okamoto H, Robbins J |
| Jazyk: |
angličtina |
| Zdroj: |
Neuroscience research [Neurosci Res] 2007 Mar; Vol. 57 (3), pp. 339-46. Date of Electronic Publication: 2006 Dec 14. |
| DOI: |
10.1016/j.neures.2006.11.008 |
| Abstrakt: |
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 Ca(2+) concentrations ([Ca(2+)](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 Ca(2+) release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca(2+) signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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