Recombinant Human TNF RII/TNFRSF1B Fc Chimera Protein, CF

Recombinant Human TNF RII/TNFRSF1B Fc Chimera Protein, CF Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: TNF RII/TNFRSF1B

Tumor Necrosis Factor Receptor II (TNF RII), also known as TNFRSF1B, p75/p80, and CD120b, is a type I transmembrane protein that belongs to the TNF receptor superfamily. It has a molecular weight of approximately 75 kDa (1-4). The TNF receptor superfamily is comprised of structurally related receptors that bind to TNF-related ligands and regulate numerous processes such as immune cell activation and apoptosis. Receptors in this superfamily are characterized by the presence of a cysteine-rich region in their extracellular domain (ECD) (1-3, 5). Human TNF RII contains four cysteine-rich repeats in its ECD, which shares 58% and 56% amino acid sequence identity with the mouse and rat orthologs, respectively. Several receptors in the TNF superfamily also contain intracellular death domains (DDs) that recruit caspase-interacting proteins to initiate apoptosis upon ligand binding. Those receptors that lack DDs, like TNF RII, bind TNF Receptor-associated Factors, which transduce signals generated by activation of these receptors (6, 7).

TNF RII is expressed predominantly on cells of the hematopoietic lineage, such as T and natural killer cells, as well as on endothelial cells, microglia, astrocytes, neurons, oligodendrocytes, cardiac myocytes, thymocytes, and mesenchymal stem cells (6, 8-10). TNF RII binds to the membrane-bound forms of TNF-alpha and Lymphotoxin-alpha /TNF-beta ; soluble TNF is thought to signal predominately through TNF RI (7, 11). TNF RII activation primarily initiates pro-inflammatory and pro-survival responses via NF kappa B-dependent signaling pathways (6, 7, 12-15). However, under certain conditions, TNF RII signaling can induce apoptosis (6). TNF RII also exists as a soluble receptor, which can be generated by proteolytic cleavage of its ECD from the cell surface or by alternative splicing (2, 16). Soluble TNF RII is believed to inhibit TNF biological activity by binding TNF thereby preventing it from activating membrane TNF receptors (17). Polymorphisms of the human TNFR2 gene, which result in increased expression of both membrane-bound and soluble TNF RII, have been associated with several autoimmune diseases including Crohn’s disease, systemic lupus erythematosus, and familial rheumatoid arthritis (6, 17).

Related Research Areas

• Adipocytokines
• Cell Structure and Signaling Molecules
• Co-stimulatory and Co-inhibitory Molecules
• Cytokines and Receptors in Allergy and Asthma
• Cytokines and Receptors in Angiogenesis
• Cytokines in Lipid/Cholesterol Metabolism
• Diabetes
• Diabetic Peripheral Neuropathy
• Endothelial Cell Markers
• Neuroinflammation
• Obesity
• Regulation of Apoptosis by TNF Superfamily Members
• Regulation of Natural Killer Cell Co-stimulation by TNF Superfamily Members
• Regulation of T Cell Co-stimulation by TNF Superfamily Members
• Regulatory T Cells (Tregs)
• T Cell Cytokine Signaling
• TNF Superfamily
• TNF Superfamily Receptors