Anti-Mouse CD309 (VEGFR2) – DyLight® 488
Anti-Mouse CD309 (VEGFR2) – DyLight® 488
Product No.: V181
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Clone DC101 Target VEGFR2 Formats AvailableView All Product Type Hybridoma Monoclonal Antibody Alternate Names CD309, KDR, FLK-1, vascular endothelial growth factor receptor 2 Isotype Rat IgG1 κ Applications FC |
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Antibody DetailsProduct DetailsReactive Species Mouse Host Species Rat Immunogen Recombinant full-length Mouse VEGFR2 protein Product Concentration 0.2 mg/ml Formulation This DyLight® 488 conjugate is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative. State of Matter Liquid Storage and Handling This DyLight® 488 conjugate is stable when stored at 2-8°C. Do not freeze. Regulatory Status Research Use Only Country of Origin USA Shipping 2 - 8°C Wet Ice Additional Applications Reported In Literature ? FC Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change. DescriptionDescriptionSpecificity DC101 activity is directed against VEGFR-2. Background Vascular endothelial growth factors (VEGF) and VEGF receptors (VEGFR) play an essential role in angiogenesis1. There are three VEGFRs: VEGFR-1, VEGFR-2, and VEGFR-3. VEGFR-1 and VEGFR-2 are responsible for angiogenesis, and VEGFR-3 affects lymphogenesis. In the pathogenesis of diseases including diabetes mellitus, rheumatoid arthritis, and cancer, new blood vessel formation is highjacked. Changes at the VEGF/VEGFR-2 axis are particularly potent at allowing VEGF-induced proliferation, migration, and vascular endothelial cell differentiation during tumor angiogenesis. Additionally, VEGFR-2 is upregulated in tumor vascular endothelial cells, and VEGF levels are associated with poor prognosis and resistance to chemotherapy. Consequently, the VEGF/VEGFR axis is a prime anti-cancer target. DC101 greatly reduces melanoma tumor growth and cell proliferation in murine mouse models without adverse effects as well as promotes tumor vessel normalization2. Additionally, DC101 therapy enhances immune cell penetration of melanoma cells by increasing the proportion of CD19+ B cells, CD11c+ dendritic cells, and CD3+ and CD8+ T cells. DC101 treatment also increases expression of PD-1 and PD-L1 in CD45+ immune cells and tumors. Additionally, DC101 directly inhibits angiogenesis in vivo, and, in tumors, reduces xenograft tumor growth, decreases endothelial cells and microvessel density, and increases tumor cell apoptosis3. DC101 binds to an extracellular, ligand-binding domain on the amino-terminal of VEGFR-2, thereby blocking ligand binding and preventing VEGF165-induced receptor phosphorylation4. DC101 has been used in Cy5.5-, FITC, and HYNIC-labeled chitosan conjugates to study VEGFR-2 expression in ischemia5. Antigen Distribution VEGFR-2 is widely expressed by vascular endothelial cells, some vascular tumors, carcinomas, malignant melanomas, and lymphomas. Certain leukemia cells express functional VEGFR on the cell surface. Ligand/Receptor VEGF-A, VEGF-C, and VEGF-D splice isoforms NCBI Gene Bank ID UniProt.org Research Area Cell Biology . Immunology References & Citations1. Spratlin J. Curr Oncol Rep. 13(2):97-102. 2011. 2. Wang Z, Shi X, Zhao Y, et al. Biochem Biophys Res Commun. 661:10-20. 2023. 3. Prewett M, Huber J, Li Y, et al. Cancer Res. 59(20):5209-5218. 1999. 4. Patent EP1602668A1: https://patentimages.storage.googleapis.com/10/da/cb/f945064c422659/EP1602668A1.pdf 5. Lee CM, Kim EM, Cheong SJ, et al. J Biomed Mater Res A. 92(4):1510-1517. 2010. 6. Rockwell P, Neufeld G, Glassman A, et al. Mol Cell Differ. 3(1): 91–109. 1995. Technical ProtocolsCertificate of Analysis |
Formats Available
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Prod No. | Description |
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V176 | |
V179 | |
V173 | |
V181 | |
V182 | |
V183 | |
V184 | |
V177 | |
V178 | |
V273 |
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