Precursor of the Latency-associated peptide (LAP) and Transforming growth factor beta-2 (TGF-beta-2) chains, which constitute the regulatory and active subunit of TGF-beta-2, respectively. Required to maintain the Transforming growth factor beta-2 (TGF-beta-2) chain in a latent state during storage in extracellular matrix. Associates non-covalently with TGF-beta-2 and regulates its activation via interaction with 'milieu molecules', such as LTBP1 and LRRC32/GARP, that control activation of TGF-beta-2. Multifunctional protein that regulates various processes such as angiogenesis and heart development (By similarity). Activation into mature form follows different steps: following cleavage of the proprotein in the Golgi apparatus, Latency-associated peptide (LAP) and Transforming growth factor beta-2 (TGF-beta-2) chains remain non-covalently linked rendering TGF-beta-2 inactive during storage in extracellular matrix (By similarity). At the same time, LAP chain interacts with 'milieu molecules', such as LTBP1 and LRRC32/GARP, that control activation of TGF-beta-2 and maintain it in a latent state during storage in extracellular milieus (By similarity). Once activated following release of LAP, TGF-beta-2 acts by binding to TGF-beta receptors (TGFBR1 and TGFBR2), which transduce signal (By similarity). Interacts with the serine proteases, HTRA1 and HTRA3 (By similarity). Interacts with ASPN (By similarity). Interacts with MFAP5 (By similarity). Interacts with Transforming growth factor beta-2 (TGF-beta-2) chain; interaction is non-covalent and maintains (TGF-beta-2) in a latent state (By similarity). Interacts with LRRC32/GARP; leading to regulate activation of TGF-beta-2 (By similarity). Interacts with NREP; the interaction results in a decrease in TGFB2 autoinduction (By similarity). Transforming growth factor beta-2: Homodimer; disulfide-linked (By similarity). Transforming growth factor beta-2: Interacts with TGF-beta receptors (TGFBR1 and TGFBR2), leading to signal transduction (By similarity). Expressed in the aorta, primary bronchus, uterus, heart, skeletal muscle, sciatic nerve and spinal cord but not in the intestine. High expression at E14. Sharp decline in expression between E16 and E18. Absent in adulthood. Both isoforms down-regulated during muscle development. Up-regulated after denervation. The precursor proprotein is cleaved in the Golgi apparatus to form Transforming growth factor beta-2 (TGF-beta-2) and Latency-associated peptide (LAP) chains, which remain non-covalently linked, rendering TGF-beta-2 inactive. Belongs to the TGF-beta family.