Abstract
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.
Original language | English |
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Pages (from-to) | 339-346 |
Number of pages | 8 |
Journal | Neuroscience Research |
Volume | 57 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2007 Mar |
Keywords
- ADP-ribosyl cyclase
- CD38
- Ca
- Cyclic ADP-ribose
- Muscarinic acetylcholine receptor
ASJC Scopus subject areas
- Neuroscience(all)