Yogesh K. Chutake, Christina C. Lam, Whitney N. Costello, Michael P. Anderson and Sanjay I. Bidichandani; Nucl. Acids Res. (2016) doi: 10.1093/nar/gkw107 First published online: February 20, 2016
OPEN
We conclude that repeat-mediated epigenetic promoter silencing in FRDA is mediated by class I HDACs, and it is reversible via treatment with specific inhibitors. It is noteworthy that the correction of both the structural and functional defects of the FXN promoter in FRDA, albeit partial, occurs in its natural genomic context, i.e. while in continued physical proximity to the cis-acting expanded GAA-TR sequence. These features bode well for the development of class I HDAC inhibitors as a rational therapeutic modality for FRDA.
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