Genetic disruption of the Nrf2 compromises cell-cycle progression by impairing GSH-induced redox signaling

Keyphrases

• Cell Cycle Progression 100%
• Nuclear Factor Erythroid 2-related Factor 2 (Nrf2) 100%
• Redox Signaling 100%
• Colocalization 20%
• Oxidative Stress 20%
• Cell Proliferation 20%
• AKT Pathway 20%
• Mitosis 20%
• Promoting Factors 20%
• DNA Lesions 20%
• GSH Supplementation 20%
• Transcription Factor 10%
• Akt Activation 10%
• Human Disorders 10%
• M Phase Arrest 10%
• Glutathione 10%
• Growth Arrest 10%
• Cell Cycle Arrest 10%
• GSH Depletion 10%
• N-acetylcysteine 10%
• Carcinogen-induced 10%
• Stress-induced 10%
• DNA Damage Response Pathway 10%
• G2-M Checkpoint 10%
• Pro-oxidant 10%
• Novel Functions 10%
• Oxidative DNA 10%
• Checkpoint Arrest 10%
• Epithelial Cultures 10%

Biochemistry, Genetics and Molecular Biology

• Genetics 100%
• Cell Cycle Progression 100%
• Transcription Factor Nrf2 100%
• Cell Proliferation 20%
• Oxidative Stress 20%
• Akt Signaling 20%
• DNA Damage 20%
• Transcription Factors 10%
• Glutathione 10%
• Wild Type 10%
• Cell Cycle M Phase 10%
• Experimental Model 10%
• Cell Cycle Arrest 10%
• DNA Damage Response 10%
• Acetylcysteine 10%

Immunology and Microbiology

• Transcription Factor Nrf2 100%
• Cell Cycle Progression 100%
• Cell Proliferation 20%
• Oxidative Stress 20%
• DNA Damage 20%
• Akt Signaling 20%
• Wild Type 10%
• Transcription Factors 10%
• Experimental Model 10%
• Cell Cycle Arrest 10%
• DNA Damage Response 10%
• Cell Cycle M Phase 10%