Recombinant Cynomolgus CD200 R1 His-tag Protein, CF Summary
Ala27-Leu267, with a C-terminal 6-His tag
When Recombinant Cynomolgus Monkey CD200 R1 (Catalog # 10055-CD) is coated at 0.5 μg/mL, 100 μL/well, Recombinant Human CD200 Fc Chimera (Catalog # 2724-CD) binds with an ED50 of 0.02‑0.12 μg/mL.
2 μg/lane of Recombinant Cynomolgus Monkey CD200 R1 was resolved with SDS-PAGE underreducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Bluestaining, showing bands at 60-67 kDa.
Background: CD200 R1
CD200 R1, also known as OX-2 receptor, is a 90 kDa transmembrane protein in the immunoglobulin superfamily and is important in the regulation of myeloid cell activity (1-3). The cynomolgus CD200 R1 cDNA encodes a 241 amino acid (aa) extracellular domain (ECD) and 61 aa cytoplasmic tail. The ECD is composed of one Ig-like V‑type domain and one Ig-like C2-type domain (4). Within the ECD, cynomolgus CD200 R1 shares 91%, 54%, and 57% aa sequence identity with human, mouse, and rat CD200 R1, respectively. Alternate splicing of the human CD200 R1 mRNA generates four isoforms, two of which are truncated in the Ig-C2 domain and are likely secreted (5). CD200 R1 expression is restricted primarily to mast cells, basophils, macrophages, and dendritic cells (6-8), while its ligand, CD200, is widely distributed (9). Disruption of this receptor-ligand system by knockout of the CD200 gene in mice leads to increased macrophage number and activation and predisposition to autoimmune disorders (10). Association of CD200 with CD200 R1 takes place between their respective N-terminal Ig-like domains (11). CD200 R1 propagates inhibitory signals despite lacking a cytoplasmic ITIM (immunoreceptor tyrosine-based inhibitory motif) (7, 8, 12, 13). CD200R1 signaling inhibits the expression of proinflammatory molecules including TNFs, IFNs, and inducible nitric oxide synthase in response to selected stimuli, which implicate that CD200/CD200R1 inhibitory signaling pathway plays a prominent role in limiting inflammation in a wide range of inflammatory diseases (14). Furthermore, the CD200/CD200R inhibitory signaling constitutes one of the most suitable endogenous immunoregulatory molecule candidate to restore the immune suppressive status of the CNS altered in chronic neuroinflammatory situations (15).
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