β-Adrenergic receptor signaling increases NAADP and cADPR levels in the heart.
Alexander M Lewis, Parvinder K Aley, Ali Roomi, Justyn M Thomas, Roser Masgrau, Clive Garnham, Katherine Shipman, Claire Paramore, Duncan Bloor-Young, Luke E L Sanders, Derek A Terrar, Antony Galione, Grant C Churchill
文献索引:Biochem. Biophys. Res. Commun. 427(2) , 326-9, (2012)
全文:HTML全文
摘要
Evidence suggests that β-Adrenergic receptor signaling increases heart rate and force through not just cyclic AMP but also the Ca(2+)-releasing second messengers NAADP (nicotinic acid adenine dinucleotide phosphate) and cADPR (cyclic ADP-ribose). Nevertheless, proof of the physiological relevance of these messengers requires direct measurements of their levels in response to receptor stimulation. Here we report that in intact Langendorff-perfused hearts β-adrenergic stimulation increased both messengers, with NAADP being transient and cADPR being sustained. Both NAADP and cADPR have physiological and therefore pathological relevance by providing alternative drug targets in the β-adrenergic receptor signaling pathway.Copyright © 2012 Elsevier Inc. All rights reserved.
相关化合物
相关文献:
2012-01-01
[Islets 4(2) , 145-51, (2012)]
2013-07-01
[Biochem. J. 453(1) , 147-51, (2013)]
2013-05-31
[J. Biol. Chem. 288(22) , 16017-30, (2013)]
2014-12-01
[Development 141(23) , 4598-609, (2014)]
2013-07-01
[Biochem. J. 453(1) , e1-2, (2013)]