Required for maintaining the proliferative activity of embryonic cardiomyocytes by preventing premature activation of the negative cell cycle regulator CDKN1C/p57KIP and maintaining the required expression levels of cardiogenic factors such as MEF2C and NKX2-5. Acts as a ligand for ACVRL1/ALK1, BMPR1A/ALK3 and BMPR1B/ALK6, leading to activation of SMAD1, SMAD5 and SMAD8 transcription factors. Inhibits endothelial cell migration and growth. May reduce cell migration and cell matrix adhesion in breast cancer cell lines (By similarity). Homodimer; disulfide-linked (By similarity). Interacts with FBN1 (via N-terminal domain) and FBN2 (By similarity). Interacts with ENG (PubMed:21737454). In the embryo, expressed exclusively in the ventricular trabecular myocardium of the developing heart from 9.0 dpc-13.5 dpc. By 16.5 dpc-18.5 dpc, only detectable in atria. Highly expressed in the adult heart where it is found in the right atrium but not in the left atrium. Lower levels in adult liver and lung. Down-regulation after 14.5 dpc is critical for cardiomyocytes to undergo normal developmental hypertrophic growth in early postnatal life. Mice die in utero between 9.5 dpc and 10.5 dpc. They appear normal at 8.5 dpc-8.75 dpc but display cardiac dysgenesis at 9.0 dpc-9.5 dpc with profound hypoplastic ventricular walls and absence of ventricular trabeculae and have a significantly lower heart rate than wild type embryos. Mutants show up-regulation of Cdkn1c/p57KIP throughout the ventricular wall while levels of Mef2c and Nkx2-5 are normal at 8.5 dpc-8.75 dpc but are down-regulated at 9.25 dpc-9.5 dpc. Belongs to the TGF-beta family.