LTβR (human):Fc (human) (rec.) (non-lytic)
|Synonyms||Lymphotoxin-beta Receptor; Tumor Necrosis Factor Receptor 2 Related Protein; Tumor Necrosis Factor C Receptor; Tumor Necrosis Factor Receptor Superfamily Member 3; TNFRSF3|
The extracellular domain of human LTβR (aa 31-225) is fused to the N-terminus of the Fc region of a mutant human IgG1.
Shows the biological function of the LTβR moiety and exerts a prolonged circulating half-life caused by the modified Fc domain.
|Endotoxin Content||<0.06EU/μg protein (LAL test; Lonza).|
|Reconstitution||Reconstitute at 100μg/ml in sterile PBS.|
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Protein Negative Control|
|Other Product Data||
Non-lytic: Acts as a long lasting fusion protein which only binds to the receptor. Mutations to the complement (C1q) and FcgR I binding sites of the IgGs Fc fragment render the fusion proteins incapable of antibody directed cytotoxicity (ADCC) and complement directed cytotoxicity (CDC).
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
The LTβR activates two different NF-κB pathways that lead to distinct patterns of gene induction, including selected chemokines, and the cytokine BAFF, which is essential for the survival of mature B lymphocytes. LTβR activates the classical NF-κB (relA/p50) pathway, like the type 1 TNF receptor (TNFR1), that regulates proinflammatory genes, like the chemokine MIP1β. However, LTβR, unlike TNFR1, also activates the processing of p100 to form RelB/p52 complexes, which activate genes involved in lymphoid organ formation and lymphocyte survival.