1. Epigenetic therapy reprograms hereditary disease
by José M. Bautista
Blood
Volume 124(1):7-8
July 3, 2014
©2014 by American Society of Hematology

2. Model for transcription activation of G6PD by HDACi according to the data obtained by Makarona and colleagues.1 Components shown are those that have been analyzed by the authors.
Model for transcription activation of G6PD by HDACi according to the data obtained by Makarona and colleagues.1 Components shown are those that have been analyzed by the authors. Schematic representations of the steady-state (A) and the HDACi (B) treatment are shown. Different families and classes of HATs and HDACs are depicted in green and orange, respectively. In a steady state, transcription levels obey the extant equilibrium between HAT and HDAC that participates with multiprotein transcriptional complexes, including transcription factors and RNA polymerases. The treatment with HDACis (shown in red: sodium butyrate [NaBu]) modifies the acetylation level in histones and changes residential HAT and HDAC components by increasing accessibility to the G6PD promoter. Transcription factor Sp1 specifically binds to several motifs within the G6PD promoter and attracts RNA polymerase II to activate transcription.
José M. Bautista Blood 2014;124:7-8
©2014 by American Society of Hematology