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. 2009 Sep 10;2(5):325–332. doi: 10.1111/j.1752-8062.2009.00141.x

Figure 1.

Figure 1

MEF2‐HDAC model, schematic representation of class II HDAC repression of MEF2 transcriptional activation. In the stressed or damaged heart multiple receptor‐activated pathways increase intracellular calcium, which among other processes, activates calcium dependent CaMKII. Downstream from CaMK, another kinase activated by hypertrophic signals, PKD1, phosphorylates class II HDACs, leading to a conformational change and dissociation from MEF2. The class II HDACs then bind to the chaperone 14–3‐3 and are exported to the cytosol.