Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells

Keyphrases

• Normal Human 100%
• Nicotine 100%
• Akt Activation 100%
• Airway Epithelial Cells 100%
• Tobacco Carcinogens 100%
• Tobacco 40%
• Smokers 40%
• Contact Loss 40%
• Phosphorylation 20%
• Lung Cancer 20%
• Growth Factors 20%
• Signaling Pathway 20%
• Hydrogen Peroxide 20%
• Apoptosis 20%
• Human Lung Cancer 20%
• Etoposide 20%
• Cell Tumor 20%
• Oncogenesis 20%
• Cell Growth 20%
• Tumorigenesis 20%
• Cigarette Smoking 20%
• Nicotinic Acetylcholine Receptor (nAChR) 20%
• Lung Tumor 20%
• Cell Apoptosis 20%
• Tobacco-related 20%
• Glycogen Synthase Kinase 3 (GSK3) 20%
• Carcinogen 20%
• 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone 20%
• Cancer Causes 20%
• P70S6K 20%
• Serine-threonine Kinase 20%
• Two-component 20%
• Ultraviolet Irradiation 20%
• Transformed Phenotype 20%
• Tobacco-related Disease 20%
• 4E-BP1 20%
• Contact Inhibition 20%
• Genotoxic Effect 20%
• Exogenous Growth 20%

Pharmacology, Toxicology and Pharmaceutical Science

• Normal Human 100%
• Carcinogen 100%
• Nicotine-Derived Nitrosamine Ketone 100%
• Lung Cancer 40%
• Carcinogenesis 40%
• Disease 20%
• A J Mouse 20%
• Etoposide 20%
• Hydrogen Peroxide 20%
• Cigarette Smoke 20%
• Lung Tumor 20%
• Nicotinic Receptor 20%
• 4 (Methylnitrosamino) 1 (3 Pyridyl) 1 Butanone 20%
• Growth Factor 20%
• Ultraviolet Irradiation 20%
• Glycogen Synthase Kinase 20%
• Protein Serine Threonine Kinase 20%