Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells
J. Clin. Invest. Kip A. West, et al. 111:81 doi:10.1172/JCI16147 [Go to this article.]

Figure 3
Effect of nAchR antagonists on nicotinic activation of Akt in NHBEs and SAECs. (a) Nicotine. Only LY294002 or the α₃/α₄ antagonist DHβE inhibited nicotine-induced Akt phosphorylation in NHBEs (upper left panels) and SAECs (lower panels). To confirm the role of α₃ nAchRs in activating Akt in NHBEs, α-ATX (an α₃ agonist) was added to NHBEs with or without DHβE (upper right panels). (b) NNK. In contrast to nicotine-mediated Akt phosphorylation, NNK-induced phosphorylation in NHBEs was inhibited by LY294002, the α₇ antagonists α-BTX and MLA, and the nonspecific inhibitor MCA. DHβE was ineffective.