EZ Switch From EZH2 to EZH1
Histone Methylation Opens a Window of Cardiac Regeneration
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An important area of research is the functional significance of posttranslational modifications of histone proteins. The modification of histones is maintained by a balance of enzymes which place specific modifications (writers), factors which read modifications (readers), and enzymes which remove modifications (erasers). Histone methylation is regulated by histone methyltransferases (writers) and demethylases (lysine demethylases; erasers).1 Lysine residues can be mono- (me1), di- (me2), or tri- (me3) methylated with different resultant functions (Figure A). A connection between histone methylation and Polycomb group–mediated gene silencing was established by purification and characterization of the Polycomb repressive complex 2 (PRC2).2 PRC2 is essential for maintenance of histone H3K27me3 in embryonic stem cells,3 and enhancer of zeste 1 (EZH1) and EZH2, SUZ12, and EED are the key components of the PRC2 complex. EZH2, a histone methyltransferase, catalyzes H3K27me3, and it has been shown to be dysregulated in various cancers. EZH1 is an alternative core subunit to EZH2 in PRC2 complexes. Increasing evidence indicates that EZH2 is highly expressed in cancer stem cells and mediates cancer stem cell expansion and maintenance.