This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 26.0 kDa. The protein migrates as 35-45 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>95% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
Contact us for customized product form or formulation.
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
-20°C to -70°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.
Human TNFR2, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
Immobilized ActiveMax® Human TNF-alpha, Tag Free, low endotoxin (HPLC-verified) (Cat. No. TNA-H4211) at 5 μg/mL (100 μL/well) can bind Human TNFR2, His Tag (Cat. No. TN2-H5227) with a linear range of 5-39 ng/mL (QC tested).
TNF RI is also known as the p60 or p55 TNFR) and TNF RII (the p75 or p80 TNFR) are two distinct type I transmembrane glycoproteins that bind TNF with highaffinity.Both RI and RII are prototypic members of the TNF receptor superfamily and have been designated TNFRSF1A and TNFRSF1B, respectively. Human TNF RII cDNA encodes a 461 amino acid (aa) residue precursor protein with a 22 aa putative signal peptide, a 235 aa extracellular domain, a 20 aa transmembrane domain and a 174 aa cytoplasmic domain. TNFRII is expressed in fetal brain. The protein is produced naturally as a soluble form (sTNFRII). The soluble receptor inhibits TNFα action by competing with cell surface receptors in binding TNFα, thereby blocking its biologic effects. TNFRII is strongly expressed at the cartilage–pannus junction, and plays a major role in a subset of families with multiple cases of rheumatoid arthritis (RA). Further, high plasma levels of sTNFRII were significantly associated with increased incidence of coronary heart disease, independent of established cardiovascular risk factors, and seems to be useful for monitoring the inflammatory activity of sarcoidosis.