Required for precocious cardiac adaptation to stress through integrated regulation of the AKT/mTOR pathways and FOXO1. Regulates cardiac homeostasis and plays an important role in protection against cardiac hypertrophy (PubMed:26359501, PubMed:22343712, PubMed:26436652). Acts as a transcriptional cofactor, represses transactivator activity of ISL1 and MYOCD (PubMed:22343712). Interacts with LMNA (PubMed:21498514, PubMed:26436652). Interacts with ISL1 (via N-terminal domain); the interaction represses ISL1 transactivator activity (PubMed:22343712). Additional isoforms seem to exist. PubMed:21498514 identified at least seven MLIP proteins ranging from 23 to 57 kDa, differentially expressed in tissues which are probably alternative splicing products. Ubiquitous but more abundantly expressed in heart, skeletal and smooth muscle (at protein level). In brain, expressed by a subpopulation of cells within the hippocampus and cortex. In heart, expressed by ventricular cardiomyocytes. Expression is highly reduced in hypertrophic hearts (PubMed:26359501, PubMed:22343712, PubMed:26436652). First detected in heart at 8.5 dpc and restricted to heart from 9.5 dpc to 15.5 dpc. At 9.5 dpc, transiently detected in the truck. From 11.5 dpc to 15.5 dpc, expression is higher in the ventricles of embryonic hearts. During embryogenesis, specifically expressed in cardiomyocytes. Myocardial expression continue in the adult heart. Mutants are viable and exhibit normal cardiac function despite myocardial metabolic abnormalities and cardiac-specific overactivation of AKT/mTOR pathways (PubMed:26359501, PubMed:26436652). In aged mutants, cardiac function is depressed with increased left ventricular dimension (PubMed:26436652). They show an impaired capacity to adapt to stress such as hypertrophy induced by isoproterenol (ISO). After 9 days of continuous ISO treatment, they display an increase in heart to body weight ratio, thickened interventricular septum nad blunted contractile response compared to their wild type littermates (PubMed:26359501). Upon transverse aortic constriction (TAC), animals develop a dramatic cardiac dilation with a significant increase in left ventricular internal dimension and decreased in left ventricular wall thickness. While control mice exhibit a trend toward decreased cardiac contraction, the cardiac function in knockout animals is dramatically impaired after TAC. TAC induces a greater increase in the size of cardiomyocytes and more extensive fibrosis in hearts compared to the control ones (PubMed:26436652). Double knockouts for MLIP and LMNA die sooner than single LMNA knockout. They develop much more severe ventricular dilation and cardiac dysfunction (PubMed:26436652).