Biotinylated Human CD200 R1 / CRTR2 Protein, Fc,Avitag™

Source : 

Biotinylated Human CD200 R1, Fc,Avitag (CR2-H82F4) is expressed from human 293 cells (HEK293). It contains AA Ala 27 - Leu 266 (Accession # AAQ19772.1).

 

Molecule : CD200 R1

 

Synonyms : CD200R,CRTR2,MOX2R,OX2R

 

Format : Powder

 

Category : MABSol® Biotin Labeled Proteins

 

Accession : AAQ19772.1

 

Storage : -20℃

 

Shipping condition : Powder,RT

 

Molecular Weight : 55.8 kDa

 

Characteristics :

This protein carries a human IgG1 Fc tag at the C-terminus, followed by a Avi tag (Avitag™). The protein has a calculated MW of 55.8 kDa. The protein migrates as 70-115 KDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.

 

Buffer : Tris with Glycine, Arginine and NaCl, pH7.5

 

Description :

Cell surface glycoprotein CD200 receptor 1 is a protein that in humans is encoded by the CD200R1 gene.
This gene encodes a receptor for the OX-2 membrane glycoprotein. Both the receptor and substrate are cell surface glycoproteins containing two immunoglobulin-like domains. This receptor is restricted to the surfaces of myeloid lineage cells and the receptor-substrate interaction may function as a myeloid downregulatory signal.
CD200 and its receptor CD200R are both type-1 membrane glycoproteins, which are members of the immunoglobulin superfamily (IgSF). Besides the inhibitory effect on macrophages, CD200/CD200R also play an important role in regulating the regulatory T cells, allergicreaction, autoimmune diseases, allograft, neurological diseases and other autoimmune-related diseases.
The interaction between CD200, which is mainly present in neurons but also in astrocytes, and CD200R1, which is mainly present in microglia, is one of the mechanisms involved in keeping the microglial proinflammatory phenotype under control in physiological conditions. Alterations in the expression of CD200 and CD200R1 have been described in neurodegenerative diseases, but little is known about the mechanism of regulation of these proteins under physiological or pathological conditions.

 

References :

(1) Elshal MF., et al., 2016, Clin Lab 62(8):1521-1529
(2) Valente T., et al., 2017, Front Cell Neurosci 11:129
(3) Dentesano G., et al., 2014, Glia 62(6):982-98