Guanylyl cyclase stimulatory coupling to K(Ca) channels

M. Nara, P. D.K. Dhulipala, G. J. Ji, U. R. Kamasani, Y. X. Wang, S. Matalon, M. I. Kotlikoff

研究成果: Article査読

46 被引用数 (Scopus)


We coexpressed the human large-conductance, calcium-activated K (K(Ca)) channel (α- and β-subunits) and rat atrial natriuretic peptide (ANP) receptor genes in Xenopus oocytes to examine the mechanism of guanylyl cyclase stimulatory coupling to the channel. Exposure of oocytes to ANP stimulated whole cell K(Ca) currents by 21 ± 3% (at 60 mV), without altering current kinetics. Similarly, spermine NONOate, a nitric oxide donor, increased K(Ca) currents (20 ± 4% at 60 mV) in oocytes expressing the channel subunits alone. Stimulation of K(Ca) currents by ANP was inhibited in a concentration-dependent manner by a peptide inhibitor of cGMP-dependent protein kinase (PKG). Receptor/channel stimulatory coupling was not completely abolished by mutating the cAMP-dependent protein kinase phosphorylation site on the α-subunit (S869; Nars M, Dhulipals PD, Wang YX, and Kotlikoff MI. J Biol Chem 273: 14920-14924, 1998) or by mutating a neighboring consensus PKG site (S855), but mutation of both residues virtually abolished coupling. Spermine NONOate also failed to stimulate channels expressed from the double mutant cRNAs. These data indicate that nitric oxide donors stimulate K(Ca) channels through cGMP-dependent phosphorylation and that two serine residues (855 and 869) underlie this stimulatory coupling.

ジャーナルAmerican Journal of Physiology - Cell Physiology
6 48-6
出版ステータスPublished - 2000

ASJC Scopus subject areas

  • 生理学
  • 細胞生物学


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