Vascular Endothelial Growth Factor Receptor 2, phosphorylated (Tyr951) (VEGF R2, Flk1, KDR, Receptor Tyrosine Kinase) | US Biological V2110-19 product information

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product summary

company name :

US Biological

product type :

antibody

product name :

Vascular Endothelial Growth Factor Receptor 2, phosphorylated (Tyr951) (VEGF R2, Flk1, KDR, Receptor Tyrosine Kinase)

catalog :

V2110-19

quantity :

100 ul

clonality :

monoclonal

host :

domestic rabbit

conjugate :

nonconjugated

antigen modification :

phosphorylated

clone name :

5i133(15D2)

reactivity :

human

product information

Catalog Number :

V2110-19

Product wo Prefix :

Vascular Endothelial Growth Factor Receptor 2, phosphorylated (Tyr951) (VEGF R2, Flk1, KDR, Receptor Tyrosine Kinase)

Host :

rabbit

Product Type :

Mab

Antigen Modification :

Phosphorylated

Category :

Antibodies

Size1 :

100 ul

Clone # USB :

5i133(15D2)

Isotype :

IgG

Desc1 :

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. Major autophosphorylation sites of VEGFR-2 are located in the kinase insert domain (Tyr951/996) and in the tyrosine kinase catalytic domain (Tyr1054/1059). 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. 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. Signaling from 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. Applications: Suitable for use in ELISA, Western Blot and Immunohistochemistry. Other applications not tested. Recommended Dilutions: Western Blot: 1:1000. Incubate membrane with diluted antibody in 1X TBS, 5% BSA, 0.1% Tween-20 at 4°C with gentle shaking, overnight. Immunohistochemistry (Paraffin): 1:125 Use citrate as the unmasking buffer and TBST-5%NGS as antibody diluent. Optimal dilutions to be determined by the researcher. Storage and Stability: May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 12 months after receipt. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Calc Crossreactivity :

Hu Mo

Immunogen :

Synthetic phosphopeptide corresponding to residues surrounding Tyr951 of human VEGF receptor 2.

Specificity :

Recognizes endogenous levels of human VEGF receptor 2 only when phosphorylated at Tyr951 at ~230kD. May crossreact with activated VEGF receptor 1, but does not react with other related tyrosine phosphorylated tyrosine kinases. Species Crossreactivity: mouse

Purity :

Purified

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.

Concentration :

Not Determined

Desc2 :

Product Type: Mab Isotype: IgG Clone No: 5i133(15D2) Host: rabbit Source: human Concentration: Not Determined 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 Immunogen: Synthetic phosphopeptide corresponding to residues surrounding Tyr951 of human VEGF receptor 2. Specificity: Recognizes endogenous levels of human VEGF receptor 2 only when phosphorylated at Tyr951 at ~230kD. May crossreact with activated VEGF receptor 1, but does not react with other related tyrosine phosphorylated tyrosine kinases. Species Crossreactivity: mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.

Calc Applications Abbrev :

E IHC WB

Storage Temperature :

-20°C

Reference :

(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

Picture 1 File Name :

https://usbio-images.r.worldssl.net/prodimages/38/V2110-19_1.jpg