To validate the functional importance of AP-1 and ETS binding motifs for the induction of IREs upon injury, we chose mouse cardiomyocyte cell line HL-1 as a model system for its capacity of maintaining cardiac-specific phenotype [42], and simulated myocardial infarction that results from LAD in vivo by treating HL-1 cells with hypoxia [43]. Here, JUNB is linked to myocardial infarction.