Recombinant Cynomolgus Monkey ALCAM His-tag Protein, CF Summary
Trp28-Ala526, with a C-terminal 6-His tag
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.|
|Reconstitution||Reconstitute at 1 mg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||
When Recombinant Cynomolgus Monkey ALCAM (Catalog # 10027-AL) is coated onto amicroplate at 1 µg/mL, Biotinylated Recombinant Human CD6 Fc Chimera binds withan ED50 of 10-50 ng/mL.
2 μg/lane of Recombinant Cynomolgus Monkey ALCAM/CD166 was resolved with SDS-PAGE underreducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Bluestaining, showing bands at 67-89 kDa.
ALCAM (activated leukocyte cell adhesion molecule), designated CD166, is a 100‑110 kDa type I transmembrane glycoprotein and a member of the Ig CAM family within the immunoglobulin superfamily (1). The cynomologous ALCAM amino acid (aa) sequence includes a signal peptide, an extracellular domain (ECD) with two V‑type and three C2‑type Ig‑like domains, a transmembrane domain and a short cytoplasmic domain (1). Human ALCAM has several isoforms, including an isoform lacking most of the cytoplasmic domain and a secreted isoform (sALCAM) which antagonizes full‑length ALCAM (2, 3). Mature cynomologous ALCAM ECD shares 93% and 96% aa sequence identity with human and mouse/rat ALCAM, respectively. ALCAM is expressed on multiple cell types including thymic epithelium, microvascular endothelium, activated lymphocytes and monocytes, and monocyte‑derived dendritic cells (1, 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 (4, 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 (2, 12).
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