""In this paper, instead of trying to pursue hypoxia to slow or postpone the disease as a therapy, we simply used it as a trick. We used it as a laboratory tool with which to discover genetic suppressors,""
""The reason this is exciting is because the suppressor that we've identified, FDX2, is now a protein that can be targeted using more conventional medicines.""
Friedreich's ataxia is an inherited condition that typically begins in childhood or adolescence and often shortens life expectancy into the 30s or 40s. The disease is caused by loss of frataxin, a mitochondrial protein required for assembly of iron-sulfur clusters that support essential cellular energy processes. Exposure to low oxygen (hypoxia) can partially compensate for frataxin deficiency in human cells, worms, and mice. Hypoxia was used as an experimental tool to uncover genetic suppressors of frataxin loss. Reduced activity of FDX2 was identified as a suppressor that helps cells overcome damage from frataxin deficiency and represents a druggable protein target.
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