Recombinant Human ALCAM Fc Chimera Protein, CF Summary
Additional Information
A New and Improved rh ALCAM is Available! ~2 fold better activity; HEK293 expressed; no His tag!
Details of Functionality
Measured by its ability to block adhesion of HuT 78 human cutaneous T cell lymphoma cells to immobilized Recombinant Human CD6 Fc Chimera (Catalog # 627-CD). The ED50 for this effect is 0.3-1.5 μg/mL. Optimal dilutions should be determined by each laboratory for each application.
Source
Mouse myeloma cell line, NS0-derived human ALCAM/CD166 protein
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Theoretical MW
83.5 kDa (monomer). Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
120 kDa, reducing conditions
Publications
Read Publications using 656-AL in the following applications:
ALCAM (activated leukocyte cell adhesion molecule), designated CD166 and also called MEMD and SC‑1/DM‑GRASP/BEN in the chicken, is a 100‑110 kDa type I transmembrane glycoprotein and a member of the Ig CAM family within the immunoglobulin superfamily (1). ALCAM is expressed on thymic epithelium, microvascular endothelium, activated lymphocytes and monocytes, and monocyte‑derived dendritic cells (1, 2). Human ALCAM cDNA encodes 583 amino acid (aa), including signal peptide (27 aa), extracellular domain (ECD, 500 aa) with two V‑type and three C2‑type Ig‑like domains, transmembrane (22 aa) and cytoplasmic (34 aa) domains (1). Human ALCAM ECD shares 93%, 95% and 96% aa sequence identity with mouse/rat, bovine and porcine/equine ALCAM, respectively. A 570 aa isoform lacks aa 503‑515, while a 555 aa form lacks most of the cytoplasmic domain. A secreted isoform in endothelial cells that is truncated at aa 133 (sALCAM) antagonizes full‑length ALCAM (3, 4). ALCAM mediates low‑affinity adhesion with itself or the cysteine‑rich scavenger receptor CD6 to regulate T cell development, immunological synapses (IS), and cell migration through endothelial junctions (1‑11). ALCAM on thymic epithelia mediates adhesion to CD6 on CD4+CD8+ T cells (6). Adhesion of ALCAM‑expressing antigen presenting cells and CD6‑expressing T cells stabilizes the early IS, while later it enhances CD3 effects on T cell proliferation, CD25 expression, and Th1 commitment (2, 7, 8). High ALCAM expression at the blood‑brain barrier in active multiple sclerosis, and its mouse model (EAE), promotes leukocyte migration to the brain (8, 9). High ALCAM expression on melanoma cell lines appears to be pro‑metastatic, but anti‑metastatic activity has been reported in breast cancer (3, 10, 11). ALCAM may influence expression or adhesion of the neuronal adhesion molecule NCAM‑L1, both in the developing retina and invasive melanoma (3, 12).
Bowen, M.A. et al. (1995) J. Exp. Med. 181:2213.
Zimmerman, A.W. et al. (2006) Blood 107:3212.
van Kilsdonk, J.W.J. et al. (2008) Cancer Res. 68:3671.
Ikeda, K. and T. Quertermous (2004) J. Biol. Chem. 279:55315.
van Kempen, L.C. et al. (2001) J. Biol. Chem. 276:25783.
Castro, M.A.A. et al. (2007) J. Immunol. 178:4351.
Nair, P. et al. (2010) Clin. Exp. Immunol. 162:116.
Masedunskas, A. et al. (2006) FEBS Lett. 580:2637.
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Diseases for ALCAM/CD166 (656-AL)
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