Specific inhibition of NEIL-initiated repair of oxidized base damage in human genome by copper and iron: Potential etiological linkage to neurodegenerative diseases

Keyphrases

• 5-hydroxymethyluracil 33%
• Alzheimer's Disease 33%
• AP Lyase 33%
• Base Damage 100%
• Base Excision 33%
• Base Excision Repair 33%
• Base Excision Repair Pathway 33%
• Cell-free Extract 33%
• Chelator 33%
• Chemopreventive 33%
• Copper Inhibition 33%
• Copper Overload 33%
• Copper-iron 100%
• Cu(II) 33%
• Curcumin 33%
• Cytosine 33%
• DNA Glycosylase 33%
• DNA Polymerase 33%
• Double-edged Sword 33%
• Dyshomeostasis 33%
• Fe(II) 66%
• Flap Endonuclease 1 (FEN1) 33%
• Human Genome 100%
• Human Neurodegenerative Diseases 33%
• Mammalian Genome 33%
• Metal Binding 33%
• Metal Iron 33%
• Metallic Copper 33%
• NEIL1 100%
• NEIL2 66%
• Neuroblastoma SH-SY5Y Cells 33%
• Neurodegenerative Diseases 100%
• NTH1 33%
• OGG1 100%
• Oxidation Products 33%
• Oxidative DNA Damage 66%
• Oxidized Bases 100%
• Parkinson's Disease 33%
• Physiological Level 33%
• Protein-DNA Complex 33%
• Reactive Oxygen Species 33%
• Repair Proteins 33%
• Secondary Structure 33%
• Specific Inhibition 100%
• Surface Plasmon Resonance 33%
• Therapeutic Potential 33%

Biochemistry, Genetics and Molecular Biology

• Base Excision Repair 66%
• Cell Extract 33%
• Cytosine 33%
• Deoxyribonuclease I 33%
• DNA Damage 33%
• DNA Glycosylase 33%
• DNA Polymerase 33%
• Enzyme 33%
• Flap Endonuclease 33%
• Gene Linkage 100%
• Human Genome 100%
• Lyase 33%
• Metal Binding 33%
• NEIL1 100%
• Protein Secondary Structure 33%
• Surface Plasmon Resonance 33%