MAPK1 and cardiac hypertrophy: Experimental data using a phosphorylation-deficient mutant (ERK2T188A), that is dominant-negative for ERK1 and ERK2 autophosphorylation at threonine 18810 suggested that interference with ERKT188-phosphorylation may offer a possibility to selectively target pathological cardiac hypertrophy without affecting anti-apoptotic signaling of ERK1/210.