Frataxin
 Fedreich’s ataxia (FRDA) is an autosomal recessive neuro- and cardiodegenerative disorder for which there are no proven effective treatments. FRDA is caused by decreased expression and/or function of the mitochondrial protein frataxin. Its function is not entirely clear, but it seems to be involved in assembly of iron-sulfur clusters. Frataxin is degraded via the ubiquitin−proteasomal pathway. Thus, small-molecule inhibitors that promote frataxin stabilization are desirable and could potentially have therapeutic value. We aim to identify novel small molecules targeting the frataxin/ubiquitin interaction through structure based virtual screening. Recent Publications |
