Figure 8. MP interacts with Nkx2.5 and controls its subcellular localization downstream of ROCK/Wnt3a.
Under cardiomyogenic conditions, Nkx2.5 resides in the nucleus and activates cardiac gene expression. In response to Wnt3a signalling, Mypt1 is phosphorylated at Thr853 by ROCK, causing MP to translocate into the nucleus, where it can engage Nkx2.5 and form a complex, which is then exported from the nucleus in a Crm1-dependent pathway.