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Sino Biological Inc. liefert Rat DCIR / CLEC4A2 Protein (His Tag) mit höherer Qualität und günstiger Kosten im Vergleich mit anderen globalen Lieferanten.
Weitere Informationen über Rat DCIR / CLEC4A2 Protein (His Tag) lesen Sie bitte: http://www.sinobiological.com/DCIR-CLEC4A2-Protein-g-10564.html
| Synonym | CLEC4A2, Dcir2 |
| Protein Construction | A DNA sequence encoding the rat CLEC4A2 (Q5YIS1) (Gln70-Ser235) was expressed with a polyhistidine tag at the N-terminus. |
| Source | Rat |
| Expression Host | Human Cells |
| Purity | > 95 % as determined by SDS-PAGE | SDS-PAGE:![]() DCIR protein |
| Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method | |
| Stability | Samples are stable for up to twelve months from date of receipt at -70℃ | |
| Predicted N terminal | His | |
| Molecular Mass | The recombinant rat CLEC4A2 comprises 186 amino acids and has a predicted molecular mass of 21.8 kDa. The apparent molecular mass of the protein is approximately 32-36 kDa in SDS-PAGE under reducing conditions. | |
| Formulation | Lyophilized from sterile PBS, pH 7.4.
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| Storage | Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles. |
| Reconstitution | A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information. |
DCIR, also known as CLEC4A2, is a member of the subfamily of cell surface C-type lectin receptors (CLR), whose multifunctional capacities range from classical Ag uptake and immunoregulatory mechanisms to the involvement in dendritic cell (DC) ontogeny. DCIR acts as an inhibitory receptor depending on its immunoreceptor tyrosine-based inhibitory motif. Expression of mouse DCIR mRNA was observed specifically in spleen and lymph node, slightly increased with dendritic cell maturation during in vitro culture of bone marrow cells, and was not detected in cultured natural killer cells. DCIR deficiency causes development of autoimmune diseases in mice due to excess expansion of dendritic cells.