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 [
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Figure 2Akt kinase activity and effect on downstream substrates. (
a) We measured Akt kinase activity in NHBEs by immunoprecipitating active Akt and assessing phosphorylation of an exogenous peptide, GSK-3α/β, after administration of nicotine (left panels) or NNK (right panels). LY294002, DHβE (an α
3/α
4 nAchR antagonist), or α-BTX (an α
7 nAchR antagonist) inhibited nicotinic induction of Akt kinase activity. (
b) Phosphorylation of substrates downstream of Akt in NHBEs was increased after administration of nicotine (Nic; middle lane) or NNK (right lane), compared with that in untreated cells (Con), as assessed by immunoblotting with the indicated phosphospecific antibodies.
