Lycopersicon esculentum Lectin (LEL, Tomato Lectin, TL) (FITC)

Tomato lectin is a very stable glycoprotein containing about 50 percent arabinose and galactose. This lectin is composed of a single polypeptide of about 100,000D that may form aggregates in solution. Like other lectins that bind N-acetylglucosamine oligomers, tomato lectin prefers trimers and tetramers of this sugar. Tomato lectin, although sharing some specificities with potato, Datura lectin and wheat germ agglutinin, has been reported to be dissimilar in many respects. Tomato lectin binds well to such glycoproteins as glycophorin and Tamm-Horsfall glycoprotein. Tomato lectin (from Lycopersicon esculentum) is an effective marker of blood vessels and microglial cells in rodents. Conjugation of the lectin with a fluorophore facilitates fast, one-step detection and visualization using intravascular perfusion methods or direct application to tissue sections. The tomato lectin complements our existing range of lectin reagents and should be a valuable tool in examining rodent tumor angiogenesis, tracing neovascular development in xenograft models and brain research. Fluorescein labeled Lycopersicon Esculentum (Tomato) Lectin is produced by using the highest quality fluorescein isothiocyanate, our affinity-purified lectin, and special conjugation procedures. Fluorescein labeled Lycopersicon Esculentum (Tomato) Lectin has an appropriate number of fluorochromes bound which provide the maximum fluorescence and optimum staining characteristics for this particular lectin. This lectin is supplied essentially free of unconjugated fluorochromes and inactive lectin. Accompanying each fluorescent lectin is an analysis data sheet summarizing the results of our quality control tests and providing pertinent information on the product. All of these reagents are supplied as solutions perserved with sodium azide.\n\nApplications: \nSuitable for use in ELISA. Other applications not tested.\n\nRecommended Dilution:\nOptimal dilutions to be determined by the researcher.\n\nInhibiting/Eluting Sugar: \nChitin Hydrolysate \n\nExcitation:\n495nm \n\nEmission:\n515nm\n\nF/P (molar):\n2.7\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Aliquots are stable for 6 months at -20 degrees 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.

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SPECIFICATIONS

Catalog Number

L7785-25C

Size

1mg

Form

Supplied as a liquid in 10mM HEPES, 0.15M sodium chloride, pH 7.5, 0.08% sodium azide,\n0.1mM Ca++, 5mg/ml B cyclodextrin. Labeled with Fluorescein.

References

1. Debbage, P.L., et al., Lectin intravital perfusion studies in tumor-bearing mice: Micrometer-resolution, wide-area mapping of microvascular labeling, distinguishing efficiently and inefficiently perfused microregions in the tumor. J. Histochem Cytochem, 1998. 46(5):p.627-639. (General lectin perfusion reference). 2. Thurston, G., et al., Cationic liposomes target angiogenic endothelial cells in tumors and chronic inflammation in mice. J. Clin Invest, 1998. 101(7):p.1401-1413. 3. Hashizume, H., et al., Openings between defective endothelial cells explain tumor vessel leakiness. Amer J Pathol, 2000. 156(4): p. 1363-1380. 4. Debbage, P.L., et al., Intravital lectin perfusion analysis of vascular permeability in human micro- and macro- blood vessels. Histochemistry Cell Biol, 2001. 116(4):p.349-359. 5. Lee, J.C., et al., Interleukin-12 inhibits angiogenesis and growth of transplanted but not in situ mouse mammary tumor virus-induced mammary carcinomas. Cancer Res, 2002. 62(3):p.747-755. 6. Akerman, M.E., et al., Nanocrystal targeting in vivo. Proc Nat Acad Sci Usa, 2002. 99(20): p.12617-12621. 9. Gee, M.S., et al., Tumor vessel development and maturation impose limits on the effectiveness of anti-vascular therapy. Amer J Pathol, 2003. 162(1): p. 183-193. 11. Jilani, S.M., et al., Selective binding of lectins to embryonic chicken vasculature. J Histochem Cytochem, 2003. 51(5): p. 597-604. 12. Krasnici, S., et al., Effect of the surface charge of liposomes on their uptake by angiogenic tumor vessels. Int J Cancer, 2003. 105(4):p.561-567. 13. Huang, J.Z. et al., Regression of established tumors and metastases by potent vascular endothelial growth factor blockade. Proc Nat Acad Sci Usa, 2003. 100(13):p.7785-7790. 14. Inai, T., et al., Inhibition of vascular endothelial growth factor (VEGF) signaling in cancer causes loss of endothelial fenestrations, regression of tumor vessels, and appearance of basement membrane ghosts. Amer J Pathol, 2004. 165(1):p.35-52.