Technical Data

V2110-18M
Clone Type
Monoclonal
Host
Rabbit
Source
Human
Isotype
IgG
Clone Number
4i6(55B11)
Grade
Purified
Applications
E FC IC IF IHC IP WB
Crossreactivity
Hu Mo
Gene ID
3791
Shipping Temp
Blue Ice
Storage Temp
-20°C
Rabbit Anti-VEGF Receptor 2 (CD309 antigen, Fetal liver kinase 1, FLK1, KDR, Kinase insert domain receptor, KRD1, Ly73, Protein tyrosine kinase receptor FLK1, Vascular endothelial growth factor receptor 2, VEGFR, VEGFR2)

Vascular endothelial growth factor receptor 2 (VEGFR-2, KDR, Flk-1) is a major receptor transducing VEGF-induced signaling in endothelial cells. Upon ligand binding, VEGFR-2 undergoes autophosphorylation and becomes activated (1). Major autophosphorylation sites of VEGFR-2 are located in the kinase insert domain (Tyr951/996) and in the tyrosine kinase catalytic domain (Tyr1054/1059) (2). Activation of the receptor leads to rapid recruitment of adaptor proteins, including Shc, GRB2, PI-3 kinase, Nck and the protein tyrosine phosphatases SHP-1 and SHP-2 (3). The phosphorylation of Tyr1212 provides a docking site for GRB2 binding, and phospho-Tyr1175 binds with the p85 subunit of PI-3 kinase and PLCg, as well as Shb (5, 6). The signaling of VEGFR-2 is necessary for the execution of VEGF-stimulated proliferation, chemotaxis and sprouting, as well as survival of cultured endothelial cells in vitro and angiogenesis in vivo (4).

Applications
Suitable for use in Western Blot, Immunoprecipitation, Immonofluorescence, Flow Cytometry, Immunohistochemistry, ELISA and Immunocytochemistry. Other applications not tested.
Recommended Dilution
Western Blot: 1:1000 Incubate membrane with diluted antibody in 5% BSA, 1X TBS, 0.1% Tween-20 at 4°C with gentle shaking, overnight. Immunohistochemistry (Paraffin): 1:300 Immunoprecipitation: 1:100 Immunofluorescence (IF-IC): 1:100 Immunofluorescence (IF-F): 1:100 Flow Cytometry: 1:200 Optimal dilutions to be determined by the researcher.
Storage and Stability
May be stored at 4°C for short-term only. For long-term storage, store at -20°C. Aliquots are stable for 12 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.
Immunogen
GST-fusion protein containing the C-terminal 150aa residues of human VEGF receptor 2.
Form
Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, 0.1mg/ml BSA, <0.02% sodium azide, 50% glycerol.
Purity
Purified
Specificity
Recognizes endogenous levels of human VEGF receptor 2 protein at 210, 230kD. Does not crossreact with other family members. Species Crossreactivity: Mouse

Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.

References
(1) Meyer, M. et al. (1999) EMBO J. 18, 363–374. (2) Dougher-Vermazen, M. et al. (1994) Biochem. Biophys. Res. Commun. 205, 728–738. (3) Kroll, J. and Waltenberger, J. (1997) J. Biol. Chem. 272, 32521–32527. (4) Karkkainen, M.J. and Petrova, T. (2000) Oncogene 19, 5598–5605. (5) Rahimi, N. et al. (2000) J. Biol. Chem. 275, 16986–16992. (6) Claesson-Welsh, L. (2003) Biochem. Soc. Transact. 31, 20–24. General References: 1. Spieker-Polet H, et al. Proc Natl Acad Sci. 1995 Sep 26;92(20):9348-52. 2. Liguori MJ, et al. Hybridoma. 2001 Jun; 20(3):189-98. 3. G.Cano1, F. Milanezi2, D. Leitao2,3, S. Ricardo2, M.J. Brito1, F. C. Schmitt2-3 1Garcia da Orta Hospital, Almada, Portugal,2 Inst. Molec. Pathology and Immunology of Porto University, Portugal,3 Medical Faculty of Porto university, Portugal Diagn Cytopathol, 2003 Oct; 29(4): 207 -11. 4. L.K. Diaz* and N.Sneige *Department of Pathology,Northwestern University, Chicago,+ Department of Pathology, University of Texas, Huston, Adv Anat Pathol,2005; 12(1), 10-19. 5. Z. Huang1, W. Zhu2, G. Szekeres3, H. Xia1 1Spring Bioscience Corp, Fremont,CA, 2 Epitomics Inc, Burlingame,CA, , 4Histopathology Ltd, Hungary, Appl Immunohistochem Mol Morphol. 2005; 13 (1): 91-95 6. S. Rossi1, E. Orvieto1, S.Chinellato1, A. Furlanetto1, L.Laurino1, F. Facchetti2, AP Dei Tos 2 1Department of Pathology, 2Treviso, Italy; *Brescia, University School of Medicine, Brescia, Italy., Abstract presented at USCAP 2004. Modern Pathology 2004; 17 (suppl 1): 361A 7. M. Blechner, E. Ballesteros, D. Mandich, D. Stevens, R. Cartun, Hartford Hospital, Hartford, CT. Abstract presented at USCAP 2004. Modern Pathology 2004; 17 (suppl 1): 241A 8. W. Cheuk, K.O.Y. Wong, C.S.C. Wong and J.K.C. Chan, Department of Pathology, Queen Elizabeth Hospital, Hong Kong, Am J Surg Path, 2004; 28 (6): 801-807. 9. G.B. Budd, E. Tso, B. Yoder, T. Choueiri, P. Elson, S. Tarr, M. Skacel, R. Tubbs, A. Dawson, D. Hicks, Cleveland Clinic Foundation, Cleveland, OH, Abstract presented at ASCO Annual meeting, June 2004, New Orleans 10. S. M. Tarr, S. Short, K. Hansen, T. Morken, H. Xia, E. Downs-Kelly, R. R. Tubbs, D. G. Hicks, Department of Pathology and Laboratory Medicine. The Cleveland Clinic Foundation, Cleveland, Ohio. Lab Vision Corp., Fremont, Ca., Spring Bioscience Corp, Fremont ,CA, Abstract presented at Association for Molecular Pathology meeting, Los Angeles, 2004 11. A.M. Gown, T.S. Barry, P. Kandalaft, L.C. Goldstein, C.C. Tse and D.O. Treaba, Clinical Research Division , PhenoPath Laboratories and IMPRIS, Seattle, WA, Abstract presented at USCAP 2005. Modern Pathology 2005; 18, suppl.1,pag 35A 12. D.O. Treaba, A.W. Hing, L.C. Goldstein, T.S. Barry, P. Kandalaft, C.B. Gilks, T.O. Nielsen and A.M. Gown, Clinical Research Division , PhenoPath Laboratories and IMPRIS, Seattle, WA, USA Genetic Pathology Evaluation Centre, University of British Columbia, Vancouver, BC, Canada, Abstract presented at USCAP 2005. Modern Pathology 2005; 18, suppl.1,pag 53A 13. S. Rossi1, L. Laurino1, A. Furlanetto1, S.Chinellato1, E. Orvieto1, F. Canal1, F. Facchetti2, A.P. Dei Tos1 1 Depart. Pathology, Hospital of Treviso, Italy, 2 Brescia University School of Medicine, Brescia, Italy, Am J Clin Pathol, 2005, Aug;124(2):295-302
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