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

H Higashida; S E H Bowden; S Yokoyama; A Salmina; M Hashii; N Hoshi; J S Zhang; R Knijnik; M Noda; Z G Zhong; D Jin; K Higashida; H Takeda; T Akita; K Kuba; S Yamagishi; N Shimizu; S Takasawa; H Okamoto; J Robbins

doi:10.1016/j.neures.2006.11.008

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

H Higashida, S E H Bowden, S Yokoyama, A Salmina, M Hashii, N Hoshi, J S Zhang, R Knijnik, M Noda, Z G Zhong, D Jin, K Higashida, H Takeda, T Akita, K Kuba, S Yamagishi, N Shimizu, S Takasawa, H Okamoto, J Robbins

Wolfson SPaRC

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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 rnAChR-cADPR signalling. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved

Original language	English
Pages (from-to)	339 - 346
Number of pages	8
Journal	Neuroscience Research Supplement
Volume	57
Issue number	3
DOIs	https://doi.org/10.1016/j.neures.2006.11.008
Publication status	Published - Mar 2007

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Higashida, H., Bowden, S. E. H., Yokoyama, S., Salmina, A., Hashii, M., Hoshi, N., Zhang, J. S., Knijnik, R., Noda, M., Zhong, Z. G., Jin, D., Higashida, K., Takeda, H., Akita, T., Kuba, K., Yamagishi, S., Shimizu, N., Takasawa, S., Okamoto, H., & Robbins, J. (2007). Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells. Neuroscience Research Supplement, 57(3), 339 - 346. https://doi.org/10.1016/j.neures.2006.11.008

@article{e81a8a1f636142aea7491b66e8dd1d6c,

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

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 rnAChR-cADPR signalling. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved",

author = "H Higashida and Bowden, {S E H} and S Yokoyama and A Salmina and M Hashii and N Hoshi and Zhang, {J S} and R Knijnik and M Noda and Zhong, {Z G} and D Jin and K Higashida and H Takeda and T Akita and K Kuba and S Yamagishi and N Shimizu and S Takasawa and H Okamoto and J Robbins",

year = "2007",

month = mar,

doi = "10.1016/j.neures.2006.11.008",

language = "English",

volume = "57",

pages = "339 -- 346",

journal = "Neuroscience Research Supplement",

publisher = "Elsevier Scientific Publishers Ireland",

number = "3",

}

Higashida, H, Bowden, SEH, 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 2007, 'Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells', Neuroscience Research Supplement, vol. 57, no. 3, pp. 339 - 346. https://doi.org/10.1016/j.neures.2006.11.008

TY - JOUR

T1 - Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells

AU - Higashida, H

AU - Bowden, S E H

AU - Yokoyama, S

AU - Salmina, A

AU - Hashii, M

AU - Hoshi, N

AU - Zhang, J S

AU - Knijnik, R

AU - Noda, M

AU - Zhong, Z G

AU - Jin, D

AU - Higashida, K

AU - Takeda, H

AU - Akita, T

AU - Kuba, K

AU - Yamagishi, S

AU - Shimizu, N

AU - Takasawa, S

AU - Okamoto, H

AU - Robbins, J

PY - 2007/3

Y1 - 2007/3

N2 - 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 rnAChR-cADPR signalling. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved

AB - 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 rnAChR-cADPR signalling. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved

U2 - 10.1016/j.neures.2006.11.008

DO - 10.1016/j.neures.2006.11.008

M3 - Article

VL - 57

SP - 339

EP - 346

JO - Neuroscience Research Supplement

JF - Neuroscience Research Supplement

IS - 3

ER -

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

Abstract

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