Recombinant Human LT beta R/TNFRSF3 Fc Chimera (CHO), CF Summary
|Human Lymphotoxin beta R
Accession # NP_002333
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.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 100 μg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
Background: Lymphotoxin beta R/TNFRSF3
Lymphotoxin beta receptor (LT beta R), previously called TNF RIII or TNF R-related protein (TNF Rrp), is a type I transmembrane glycoprotein member of the TNF receptor superfamily, designated TNFRSF3 (1-3). Human LT beta R cDNA encodes 435 amino acids (aa) including a 30 aa signal peptide, a 197 aa extracellular domain (ECD), a 21 aa transmembrane domain, and a 187 aa cytoplasmic domain. The ECD contains four cysteine-rich motifs characteristic of the TNF receptor superfamily (1, 2). Within the ECD, human LT beta R shares 67‑74% aa sequence identity with mouse, rat, canine, porcine, equine and bovine LT beta R. Soluble LT beta R can be formed by proteolytic cleavage of the ECD, and is an inhibitor of transmembrane LT beta R. This natural cleavage product, as well as a recombinant LT beta R-Fc construct, has been found to block the onset of collagen (type II)-induced arthritis, an experimental model for rheumatoid arthritis (3-6). Potential human isoforms include a 416 aa form with an alternative N-terminal signal sequence, and a 328 aa form that begins at Met108 (7). LT beta R is expressed by visceral, lymphoid, and other stroma, epithelia and myeloid cells, but not lymphocytes (2, 4). LT beta R ligands include homotrimers of LIGHT (TNFSF14; also a ligand for HVEM) and the heterotrimeric lymphotoxin LT alpha 1/ beta 2 (3, 4, 6). Depending on the cell type and expression of TRAF3, activation of LT beta R has been shown to induce canonical (IKK/RelA; pro‑inflammatory) or alternative (NIK/RelB; lymphoid organogenic) NF kappa B activation (6, 8). LT beta R is expressed on mesenchymal stromal organizing cells that give rise to stroma of primary (thymus), secondary (tonsils, lymph nodes and Peyers patches) and tertiary (ectopic inflammatory) lymphoid structures (3‑5, 9‑11). Secondary immune tissues are absent in LT beta R-deficient mice (3-5). LT beta R engagement induces production of IL-7, RANK, TRANCE/RANK L, VEGF-C, adhesion molecules such as VCAM-1, ICAM-1 and MAdCAM, and chemokines such as CXCL13, CCL19 and CCL21 (3, 9‑11). LT beta R is expressed by hepatocytes, is up‑regulated in regeneration, hepatitis and hepatocellular carcinoma, and influences lipid metabolism and atherosclerosis (4, 6, 12). It regulates cell growth and can initiate inflammation-related carcinogenesis (6, 12).
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- Entrez Accession # BAH11468 and BAG53051.
- Bista, P. et al. (2010) J. Biol. Chem. 285:12971.
- van de Pavert, S.A. et al. (2010) Nat. Rev. Immunol. 10:664.
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- Vondenhoff, M.F. et al. (2009) J. Immunol. 182:5439.
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