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Fig. 2 | Molecular Medicine

Fig. 2

From: Histone Acetylation Modifiers in the Pathogenesis of Malignant Disease

Fig. 2

Histone acetylation levels in cells result from a dynamic equilibrium between the competing enzymatic activities of HATs and HDACs. Changes in histone acetylation levels have been reported to affect transcriptional regulation, signal transduction cascades, cell survival, differentiation, and the activities of target proteins (e.g., transcription factors, cell-cycle regulators, etc.). While HDACs, which may be recruited to specific promotors by transcription factor-bound multisubunit repressor complexes (e.g., N-COR/SMRT-SIN3A) have mainly been associated with transcriptional repression (16,74,75,80–83,158,193,194,234), HATs may be part of enhancer complexes and have predominantly been associated with transcriptional activation (19,41,151,235,236). In addition, HAT modifiers have been implicated in the regulation of diverse signaling cascades (122,237,238), in the alteration of protein conformation and protein activities (e.g., hormone receptors, transcription factors, DNA-associated regulators) (20,239–241), and in the regulation of cell-cycle events, whereas HDAC has been observed to result in a lengthening of G2 and M phases (20,242). Inhibition of HDAC arrested the cell cycle in Gl and G2 (20,212). HATs, on the other hand, have been connected mainly with cell-cycle progression (235,243–246).

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