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A DNA sequence encoding the human stem cell factor (VEGF-C) protein sequence (containing the signal peptide sequence, pro-peptides and the mature VEGF-C sequence) was expressed in modified human 293 cells.

Vascular endothelial growth factor C (VEGF-C), also known as Flt4 ligand (Flt4-L), vascular endothelial growth factor-related protein (VRP) and VEGF-2, is a member of the cysteine-knot growth factor superfamily and exhibits homology with VEGF-121 (32%) and PDGF (27%). However VEGF-C also possesses a 180 amino acid C-terminal cysteine-rich domain absent in other VEGFs. The major secreted form of VEGF-C is a disulfide linked antiparallel homodimeric protein containing 5 potential N-linked glycosylation sites and has a theoretical molecular weight of 44 kDa. Synthesis and secretion of VEGF-C from the cell involves a series of cleavage steps to produce the mature protein. The first step is antiparallel precursor homodimerization followed by proteolytic cleavage between Arg-227 and Ser-228 dividing the VEGF-C precursor into 2 nearly equal parts. This is followed by slow proteolytic cleavage to remove the N-terminal propeptide, with most of the VEGF-C secreted by different cell types being found as the disulfide linked antiparallel homodimeric precusor, rather than as the mature protein. The actions of VEGF-C are exerted through VEGF Receptor-2 (VEGFR-2) and VEGF Receptor-3 (VEGFR-3) however only the fully cleaved VEGF-C can activate VEGF2 receptor. Thus it is hypothesized that the complex proteolytic processing pathway of VEGF-C is used to prevent unnecessary angiogenic effects, elicited via VEGFR-2 which is present in many types of endothelia, and allows VEGF-C to signal preferentially via VEGFR-3, which has restricted expression. Please see Joukov et al., (1997) EMBO J 16:3898-3911 for further information. VEGF-C is predominantly involved in angiogenesis, vasculogenesis, lymphangiogenesis as well as an inhibitor of dendritic cell maturation. VEGF-C also possesses both mitogenic and chemotactic activity w.r.t. endothelial cells and monocytes. VEGF-C is over-expressed in a number of carcinomas such as breast and colorectal carcinoma and has been shown to enhance metastasis to regional lymph nodes and to the lungs. For a review on the biology of VEGFs, including VEGF-C, please refer to Ferrara N et al., (2003) Nat Med. 9(6): 669-76 and Carmeliet (2005) Nature 438: 932-936.