Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, Po||FC||M||FITC||Monoclonal Antibody|
|Description||Anti-E-Selectin Antibody, clone 1.2B6, FITC conjugated|
|Presentation||The conjugate is supplied as a 100 test vial in phosphate buffered saline containing 10mM sodium azide and 1mg/ml bovine serum albumin. For flow cytometry we recommend using 10μL of conjugate per test.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Store at +4°C protected from light. DO NOT FREEZE. For long term use and storage aliquot conjugate into small volumes and store at +4°C.|
|Material Size||100 assays|
|Reference overview||Pub Med ID|
|Identification of uPAR-positive chemoresistant cells in small cell lung cancer.|
Gutova, M; Najbauer, J; Gevorgyan, A; Metz, MZ; Weng, Y; Shih, CC; Aboody, KS
PloS one 2 e243 2007
The urokinase plasminogen activator (uPA) and its receptor (uPAR/CD87) are major regulators of extracellular matrix degradation and are involved in cell migration and invasion under physiological and pathological conditions. The uPA/uPAR system has been of great interest in cancer research because it is involved in the development of most invasive cancer phenotypes and is a strong predictor of poor patient survival. However, little is known about the role of uPA/uPAR in small cell lung cancer (SCLC), the most aggressive type of lung cancer. We therefore determined whether uPA and uPAR are involved in generation of drug resistant SCLC cell phenotype.We screened six human SCLC cell lines for surface markers for putative stem and cancer cells. We used fluorescence-activated cell sorting (FACS), fluorescence microscopy and clonogenic assays to demonstrate uPAR expression in a subpopulation of cells derived from primary and metastatic SCLC cell lines. Cytotoxic assays were used to determine the sensitivity of uPAR-positive and uPAR-negative cells to chemotherapeutic agents. The uPAR-positive cells in all SCLC lines demonstrated multi-drug resistance, high clonogenic activity and co-expression of CD44 and MDR1, putative cancer stem cell markers.These data suggest that uPAR-positive cells may define a functionally important population of cancer cells in SCLC, which are resistant to traditional chemotherapies, and could serve as critical targets for more effective therapeutic interventions in SCLC.
Bevilacqua, M P and Nelson, R M
J. Clin. Invest., 91: 379-87 (1993) 1993
|Endothelial leucocyte adhesion molecule-1 (ELAM-1) expression in cutaneous inflammation.|
Groves, R W, et al.
Br. J. Dermatol., 124: 117-23 (1991) 1991
Endothelial leucocyte adhesion molecule-1 (ELAM-1) is a recently described endothelial surface glycoprotein which is inducible by interleukin 1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) or bacterial lipopolysaccharide (LPS). Using an immunohistochemical technique and a monoclonal antibody (1.2B6) specific for ELAM-1 we have found marked vascular endothelial expression of ELAM-1 in many cutaneous inflammatory disorders, including allergic contact dermatitis, atopic dermatitis and psoriasis, and in dermal infiltrates associated with benign, premalignant and malignant keratinocyte proliferation. In normal skin, minimal levels of ELAM-1 expression were detected. In psoriasis, double-immunoenzyme staining studies revealed a close spatial relationship between ELAM-1 expression and neutrophil margination, suggesting a functional link. Recombinant human interferon-gamma (30 micrograms) injected intradermally in normal adult human volunteers did not substantially upregulate ELAM-1 in contrast to its marked effect on intercellular adhesion molecule-1 (ICAM-1) expression, indicating that this cytokine is probably not involved in ELAM-1 induction in vivo. These results indicate that ELAM-1 is widely induced in cutaneous inflammation with a time course of expression that is longer than that observed in vitro. As ELAM-1 acts as an adhesion ligand for neutrophils, and perhaps monocytes, the expression of this molecule in cutaneous lesions is likely to be an indication of the ability of vascular endothelium to recruit these cells from the circulation. Furthermore, the cytokine inducibility of ELAM-1 is indirect evidence for functional interactions between perivascular mononuclear cells, other resident cells and the blood vessel wall.
|Anti-E-selectin, Clone 1.2B6, FITC Conjugated - Data Sheet|