http://www.cnr.it/ontology/cnr/individuo/prodotto/ID9659
NAADP(+) is an agonist of the human P2Y(11) purinergic receptor. (Articolo in rivista)
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- NAADP(+) is an agonist of the human P2Y(11) purinergic receptor. (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
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Moreschi I, Bruzzone S, Bodrato N, Usai C, Guida L, Nicholas RA, Kassack MU, Zocchi E, De Flora A. (2008)
NAADP(+) is an agonist of the human P2Y(11) purinergic receptor.
in Cell calcium (Edinburgh)
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- Moreschi I, Bruzzone S, Bodrato N, Usai C, Guida L, Nicholas RA, Kassack MU, Zocchi E, De Flora A. (literal)
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- Titolo
- NAADP(+) is an agonist of the human P2Y(11) purinergic receptor. (literal)
- Abstract
- Nicotinic acid adenine dinucleotide phosphate (NAADP+) is an intracellular second messenger releasing Ca2+ from intracellular stores in different cell types. In addition, it is also active in triggering [Ca2+](i) increase when applied extracellularly and various underlying mechanisms have been proposed. Here, we used hP2Y(11)-transfected 1321N1 astrocytoma cells to unequivocally establish whether extracellular NAADP+ is an agonist of the P2Y(11) receptor, as previously reported for beta-NAD+ [I. Moreschi, S. Bruzzone, R.A. Nicholas, et al., Extracellular NAD+ is an agonist of the human P2Y11 purinergic receptor in human granulocytes, J. Biol. Chem. 281 (2006) 31419-31429]. Extracellular NAADP+ triggered a concentration-dependent two-step elevation of [Ca2+](i) in 1321N1-hP2Y(11) cells, but not in wild-type 1321N1 cells, secondary to the intracellular production of IP(3), cAMP and cyclic ADP-ribose (cADPR). Specifically, the transient [Ca2+](i) rise proved to be related to IP(3) overproduction and to consequent Ca2+ mobilization, while the sustained [Ca2+](i) elevation was caused by the cAMP/ADP-ribosyl cyclase (ADPRC)/cADPR signalling cascade and by influx of extracellular Ca2+. In human granulocytes, endogenous P2Y(11) proved to be responsible for the NAADP+-induced cell activation (as demonstrated by the use of NF157, a selective and potent inhibitor of P2Y(11)), unveiling a role of NAADP+ as a pro-inflammatory cytokine. In conclusion, we provide unequivocal evidence for the activation of a member of the P2Y receptor subfamily by NAADP+. (literal)
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