Human VEGF-C
25 ug recombinant
By
SABio is an official distributor of Vegenics products in Singapore.
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Catalogue Number: VC_025
Amount: 25 ug Details • This superior product is expressed as a dimer. (Expressed in Human HEK 293 cells to yield biologically active disulphide-linked homodimer) • Typically 10ng/mL exceeds the ED50 as measured in VEGFR-2 or VEGFR-3 BaF cell proliferation assays • Measured by surface plasmon resonance recombinant human VEGF-C binds to immobilised VEGF-R2 receptor Fc with an apparent KD of 1.1nM which agrees well with the figure obtained by Joukov et.al. using porcine aortic endothelial (PAE) cells expressing the full-length VEGF-R2 receptor (0.41 nM). • The corresponding KD for VEGF-C dimer binding to VEGF-R3 Fc was 9.43 pM, a > 10-fold increase in affinity to the value obtained by Joukov et.al. who used the cell-surface form of VEGF-R3 (0.135 nM). • Reproducible • Extended stability data • Research use only Material safety data sheet (MSDS) Size: (108.75 KB) Product Data Sheet Size: (136.99 KB) |
About VEGF-C
VEGF-C is a member of the VEGF family of secreted glycoprotein that are critical mediators of angiogenesis and lymphangiogenesis1,2. The VEGFs bind to VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1) and VEGFR-3 (Flt-4), a family of structurally related receptor tyrosine kinases that are predominantly expressed on the endothelial cells of blood and/or lymphatic vessels1. The VEGFs have distinct receptor binding specificities which contribute to their diversity of function. VEGF-C was first described in 1996 by Vegenics collaborators in the Laboratory of Prof. Kari Alitalo3. VEGF-C is synthesised as an immature protein consisting of the receptor binding domain (VEGF homology domain, VHD) flanked by amino and carboxyl-terminal propetides3. During secretion, the immature protein undergoes proteolytic processing to remove the propeptides, yielding the mature form of the protein, a VHD homodimer4. As a consequence of processing the affinity of the mature form of VEGF-C for its receptors is substantially increased4. VEGF-C induces angiogenesis via the activation of both VEGFR-2 and VEGFR-3, and lymphangiogenesis via activation of VEGFR-3. VEGF-C stimulates proliferation of endothelial cells in vitro4 and induces angiogenesis in several in vivo models5-7. VEGF-C is essential during embryonic formation of the lymphatic system8, whereas in the adult its expression is down regulated in normal tissues and up regulated in pathological states that require the formation of vascular and/or lymphatatic network, including wound healing and tumor growth9,10. Indeed high expression levels of VEGF-C in human colorectal11,12, lung13, breast14, gastric15 and pancreatic16 cancers indicates that increased expression of VEGF-C correlates with greater tumour aggression and a poorer prognosis.
References
VEGF-C is a member of the VEGF family of secreted glycoprotein that are critical mediators of angiogenesis and lymphangiogenesis1,2. The VEGFs bind to VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1) and VEGFR-3 (Flt-4), a family of structurally related receptor tyrosine kinases that are predominantly expressed on the endothelial cells of blood and/or lymphatic vessels1. The VEGFs have distinct receptor binding specificities which contribute to their diversity of function. VEGF-C was first described in 1996 by Vegenics collaborators in the Laboratory of Prof. Kari Alitalo3. VEGF-C is synthesised as an immature protein consisting of the receptor binding domain (VEGF homology domain, VHD) flanked by amino and carboxyl-terminal propetides3. During secretion, the immature protein undergoes proteolytic processing to remove the propeptides, yielding the mature form of the protein, a VHD homodimer4. As a consequence of processing the affinity of the mature form of VEGF-C for its receptors is substantially increased4. VEGF-C induces angiogenesis via the activation of both VEGFR-2 and VEGFR-3, and lymphangiogenesis via activation of VEGFR-3. VEGF-C stimulates proliferation of endothelial cells in vitro4 and induces angiogenesis in several in vivo models5-7. VEGF-C is essential during embryonic formation of the lymphatic system8, whereas in the adult its expression is down regulated in normal tissues and up regulated in pathological states that require the formation of vascular and/or lymphatatic network, including wound healing and tumor growth9,10. Indeed high expression levels of VEGF-C in human colorectal11,12, lung13, breast14, gastric15 and pancreatic16 cancers indicates that increased expression of VEGF-C correlates with greater tumour aggression and a poorer prognosis.
References
- Tammela, T., et al., The biology of vascular endothelial growth factors. Cardiovasc Res, 2005. 65(3): p. 550-63.
- Adams, R.H. and K. Alitalo, Molecular regulation of angiogenesis and lymphangiogenesis. Nat Rev Mol Cell Biol, 2007. 8(6): p. 464-78.
- Joukov, V., et al., A novel vascular endothelial growth factor, VEGF-C, is a ligand for the Flt4 (VEGFR-3) and KDR (VEGFR-2) receptor tyrosine kinases. EMBO J, 1996. 15(2): p. 290-98.
- Joukov, V., et al., Proteolytic processing regulates receptor specificity and activity of VEGF-C. EMBO J, 1997. 16(13): p. 3898-911.
- Cao, Y., et al., Vascular endothelial growth factor C induces angiogenesis in vivo. Proc Natl Acad Sci U S A, 1998. 95(24): p. 14389-94.
- Witzenbichler, B., et al., Vascular endothelial growth factor-C (VEGF-C/VEGF-2) promotes angiogenesis in the setting of tissue ischemia. Am J Pathol, 1998. 153(2): p. 381-94.
- Chung, E.S., et al., Contribution of macrophages to angiogenesis induced by vascular endothelial growth factor receptor-3-specific ligands. Am J Pathol, 2009. 175(5): p. 1984-92.
- Karkkainen, M.J., et al., Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic veins. Nat Immunol, 2004. 5(1): p. 74-80.
- Witmer, A.N., et al., VEGFR-3 in adult angiogenesis. J Pathol, 2001. 195(4): p. 490-7.
- Tammela, T., et al., Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation. Nature, 2008. 454(7204): p. 656-60.
- Akagi, K., et al., Vascular endothelial growth factor-C (VEGF-C) expression in human colorectal cancer tissues. Br J Cancer, 2000. 83(7): p. 887-91.
- Onogawa, S., et al., Expression of VEGF-C and VEGF-D at the invasive edge correlates with lymph node metastasis and prognosis of patients with colorectal carcinoma. Cancer Sci, 2004. 95(1): p. 32-9.
- Takizawa, H., et al., The balance of VEGF-C and VEGFR-3 mRNA is a predictor of lymph node metastasis in non-small cell lung cancer. Br J Cancer, 2006. 95(1): p. 75-9.
- Mohammed, R.A., et al., Prognostic significance of vascular endothelial cell growth factors -A, -C and -D in breast cancer and their relationship with angio- and lymphangiogenesis. Br J Cancer, 2007. 96(7): p. 1092-100.
- Morita, H., et al., Histopathological predictor for regional lymph node metastasis in gastric cancer. Virchows Arch, 2009. 454(2): p. 143-51.
- Kurahara, H., et al., Impact of vascular endothelial growth factor-C and -D expression in human pancreatic cancer: its relationship to lymph node metastasis. Clin Cancer Res, 2004. 10(24): p. 8413-20.
