Mechanism of frataxin “bypass” in human iron-sulfur cluster biosynthesis with implications for Friedreich’s ataxia

Deepika Das, Shachin Patra, Jennifer Bridwell-Rabb, and David P. Barondeau; J. Biol. Chem. jbc.RA119.007716. doi:10.1074/jbc.RA119.007716

These results reveal an unexpected mechanism that replaces FXN-based stimulation of the Fe-S cluster biosynthetic pathway and suggest new strategies to overcome the loss of cellular FXN that may be relevant to the development of therapeutics for Friedreich’s ataxia.



Mechanism of frataxin “bypass” in human iron-sulfur cluster biosynthesis with implications for Friedreich’s ataxia