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Impaired nuclear Nrf2 translocation undermines the oxidative stress response in friedreich ataxia.

BACKGROUND:

Friedreich ataxia originates from a decrease in mitochondrial frataxin, which causes the death of a subset of neurons. The biochemical hallmarks of the disease include low activity of the iron sulfur cluster-containing proteins (ISP) and impairment of antioxidant defense mechanisms that may play a major role in disease progression.

Read More: Impaired nuclear Nrf2 translocation undermines the oxidative stress response in friedreich ataxia.

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