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. 2014 Jan 17;306(6):H856–H866. doi: 10.1152/ajpheart.00353.2013

Fig. 2.

Fig. 2.

Pharmacological manipulation of UcnII-induced NFATc1 redistribution via phosphatidylinositol-3 kinase (PI3K)/Akt kinase (Akt)/endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway. A: confocal images of subcellular NFATc1-GFP distribution in control (a), after UcnII treatment (b), and UcnII treatment in combination with blockers antisauvagine-30 (ASV; c), wortmannin (Wort; d), N5-(1-iminoethyl)-l-ornithine (l-NIO; e), and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; f). B: average data of RNFATc1 normalized to control (left ordinate) and expressed as %change relative to UcnII (right ordinate). *P < 0.001 vs. UcnII. Scale bar = 20 μm.