TGF beta 3 Antibody (YA6797)

TGF-β3 (transforming growth factor-β3) is a member of a TGF­beta superfamily subgroup that performs many cellular functions. TGF-β3 has a role in embryogenesis and cell differentiation. TGF-β3 also plays a critical role in palatogenesis, the wound healing process. TGF-β3 is capable of binding directly to the type II receptor (TβRII). Three TGF-β isoforms have been found in mammals: TGF-β1, 2, and 3, which are structurally and functionally similar. TGF-β3 is important in embryonic development, scarless repair of injury in the embryo, adult wound healing and tissue homeostasis. It has an important role in regulating cell migration, angiogenesis, epithelial-mesenchymal transition, apoptosis, modulation of immune function, extracellular matrix (ECM) production and the regulation of ECM remodelling; biological processes that are often required for tumour growth and maintenance^[1][2].
As with all members of the family, TGF-β3 is highly conserved across species, with mouse, rat and human TGF-β3 demonstrating >97% sequence homology.
TGF-β3 is released from LAP by integrins: integrin-binding results in distortion of the LAP chain and subsequent release of the active TGF-β3. TGF-β3 expression increases in fetal wound healing and reduces fibronectin and collagen I and III deposition, and also improves the architecture of the neodermis. Fibroblasts are key cells in the wound healing process. In addition, TGF-β3 may actually play a protective role against tumourigenesis in a range of tissues including the skin, breast, oral and gastric mucosa. TGF-β3 is a more potent inhibitor of DNA synthesis in human keratinocytes compared to TGF-β1 and TGF-β2. TGF-β3 mRNA is expressed in lymphocytes such as CD4⁺ T cells, CD8⁺ T cells, γδT cells, and B cells. TGF-β3 has the potential to regulate systemic autoimmune diseases by inhibiting B cells. Moreover, during palatogenesis, TGF-β3 is supposed to transduce signals via both canonical Smad-dependent and non-canonical Smad-independent signaling. In human B cells, TGF-β3 induces phosphorylation of Smad1/5 along with Smad2 and Smad3^[1][2][3].