|Datasheet||Specific References||Reviews||Related Products||Protocols|
|A DNA sequence encoding the cynomolgus CD40 [(Identical to the rhesus CD40 (NP_001252791.1)] (Met1-Arg193) was expressed with the Fc region of human IgG1 at the C-terminus.|
|In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.|
Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
|> 90 % as determined by SDS-PAGE|
|< 1.0 EU per μg of the protein as determined by the LAL method|
|Samples are stable for up to twelve months from date of receipt at -70℃|
|The recombinant cynomolgus CD40 is a disulfide-linked homodimer. The reduced monomer comprises 414 amino acids and has a calculated molecular mass of 46.2 KDa.The apparent molecular mass of the protein is approximately 56 KDa respectively in SDS-PAGE.|
|Lyophilized from sterile PBS, pH 7.4|
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
|Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.|
|A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.|
CD40, also known as TNFRSF5, is a member of the TNF receptor superfamily which are single transmembrane-spanning glycoproteins. CD40 protein plays an essential role in mediating a broad variety of immune and inflammatory responses including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation. CD40 protein is expressed in B cells, dendritic cells, macrophages, endothelial cells, and several tumor cell lines. Defects in CD40 result in hyper-IgM immunodeficiency type 3 (HIGM3). In addition, CD40/CD40L interaction is found to be necessary for amyloid-beta-induced microglial activation, and thus is thought to be an early event in Alzheimer disease pathogenesis.