Suppressing the activation of protein kinase A as a DNA damage-independent mechanistic lead for dihydromethysticin prophylaxis of NNK-induced lung carcinogenesis

Keyphrases

• Protein Kinase 100%
• Nitrosamines 100%
• Dihydromethysticin 100%
• Ketones 100%
• Lung Carcinogenesis 100%
• DNA Damage 100%
• Lung Tissue 20%
• DNA Adducts 20%
• Protein Kinase A Pathway 20%
• In Vivo Data 20%
• Acute Phase 10%
• Active Metabolite 10%
• Lung Cancer 10%
• Signaling Pathway 10%
• Tobacco Carcinogens 10%
• Stress Response 10%
• Cell Culture Model 10%
• Cancer Chemoprevention 10%
• Phytochemicals 10%
• Knowledge Gaps 10%
• Transcriptomic Profiling 10%
• 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone 10%
• Mouse Lung 10%
• Tissue Damage 10%
• Gavage 10%
• Insults 10%
• Adrenergic Receptors 10%
• Snapping 10%
• Damage Response 10%
• Drive Mechanism 10%
• Lung Cancer Cells 10%
• Kava 10%
• Cancer Cell Culture 10%
• Tissue Stress 10%
• Restraining Effect 10%
• Nicotine-derived Nitrosamine Ketone 10%
• RNA-seq Transcriptomics 10%
• Systems Biology Approach 10%

Pharmacology, Toxicology and Pharmaceutical Science

• Nitrosamine 100%
• Lung Carcinogenesis 100%
• Cyclic AMP Dependent Protein Kinase 100%
• Dihydromethysticin 100%
• Lung Cancer 20%
• Carcinogen 10%
• NNK 10%
• Cell Culture 10%
• Active Metabolite 10%
• Adrenergic Receptor 10%
• 4 (Methylnitrosamino) 1 (3 Pyridyl) 1 Butanol 10%
• Tissue Injury 10%
• Phytochemical 10%
• Kava 10%