Cell functions impaired by frataxin deficiency are restored by drug-mediated iron relocation

Keyphrases

• Cell Function 100%
• Frataxin 100%
• Deferiprone 60%
• Friedreich Ataxia 60%
• Siderophore 40%
• Chelator 40%
• Attenuation 20%
• Metabolic 20%
• Cell Properties 20%
• Mitochondria 20%
• Oxidative Stress 20%
• Adenosine 20%
• Mitochondrial Membrane Potential 20%
• Oxygen Consumption 20%
• HEK293 Cells 20%
• Induced Apoptosis 20%
• Redox Potential 20%
• High Affinity 20%
• Iron Toxicity 20%
• Iron Chelation 20%
• Bioavailable 20%
• Staurosporine 20%
• Permeant 20%
• Mitochondrial Iron 20%
• Aconitase 20%
• Production versus Consumption 20%
• Anemia of Chronic Disease 20%
• Ataxia 20%
• Labile Iron 20%
• Chelation 20%
• Human Disorders 20%
• Chelated Iron 20%
• Mitochondrial Redox State 20%
• Sideroblastic Anemia 20%
• Iron-depleted 20%
• Rational Basis 20%
• Triphos 20%
• Mitochondrial DNA Damage 20%
• Iron Chaperone 20%

Biochemistry, Genetics and Molecular Biology

• Cell Function 100%
• Frataxin 100%
• Friedreich's Ataxia 60%
• Siderophore 40%
• DNA Damage 20%
• Mitochondrion 20%
• Mitochondrial Membrane Potential 20%
• Oxygen Consumption 20%
• Oxidative Stress 20%
• Iron Poisoning 20%
• Iron Overload 20%
• Chelation 20%
• HEK 293 Cells 20%
• Erethism 20%
• Aconitase 20%
• Iron Chelation 20%
• Staurosporine 20%
• Mitochondrial DNA 20%
• Adenosine 20%
• Programmed Cell Death 20%