CEBPD and cardiac hypertrophy: We previously demonstrated that targeted repression of CELF activity in the postnatal mouse heart by expression of a nuclear dominant negative CELF protein (NLSCELFΔ) under the control of the cardiac muscle-specific α-myosin heavy chain promoter (MHC-CELFΔ) leads to not only changes in alternative splicing of target transcripts, but also cardiac hypertrophy, chamber dilation, severe cardiac dysfunction, and premature death [21], [22].