encodes myosin light chain 3, an alkali light chain also referred to in the literature as both the ventricular isoform and the slow skeletal muscle isoform. Mutations in MYL3 have been identified as a cause of mid-left ventricular chamber type hypertrophic cardiomyopathy.
Adenoviral gene transfer of p35 in vivo prevented caspase-3 activation and MYL3 cleavage, with positive impact on contractility. These data suggested that direct cleavage of the myosin light chain by activated caspase-3 may contribute to depression of myocyte function by altering crossbridge interaction between myosin and actin molecules. Therefore, activation of apoptotic pathways in the heart may lead to contractile dysfunction before cell death.