Recombinant Cynomolgus Lymphotoxin beta R/TNFRSF3 Fc, CF Summary
| Details of Functionality |
Measured by its ability to inhibit Lymphotoxin alpha 1/ beta 2-induced IL-8 secretion in A375 human melanoma cells. Degli-Esposti, M. et al. (1997) J. Immunol. 158:1756. The ED 50 for this effect is 30.0-180 ng/mL in the presence of 100 ng/mL Recombinant Human Lymphotoxin alpha 1/ beta 2 (Catalog # 8884-LY). |
| Source |
Chinese Hamster Ovary cell line, CHO-derived cynomolgus monkey Lymphotoxin beta R/TNFRSF3 protein | Cynomolgus Monkey Lymphotoxin beta R/TNFRSF3 (Ser28-Met227) Accession # XP_005569951.1 | IEGRMD | Human IgG 1 (Pro100-Lys330) | N-terminus | | C-terminus | |
| Accession # |
|
| N-terminal Sequence |
Ser28 |
| Structure / Form |
Disulfide-linked homodimer |
| Protein/Peptide Type |
Recombinant Proteins |
| Purity |
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining |
| Endotoxin Note |
<0.10 EU per 1 μg of the protein by the LAL method. |
Applications/Dilutions
| Dilutions |
|
| Theoretical MW |
48 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
| SDS-PAGE |
57-68 kDa, under reducing conditions |
Packaging, Storage & Formulations
| Storage |
Use a manual defrost freezer and avoid repeated freeze-thaw cycles. 12 months from date of receipt, -20 to -70 degreesC as supplied. 1 month, 2 to 8 degreesC under sterile conditions after reconstitution. 3 months, -20 to -70 degreesC under sterile conditions after reconstitution. |
| Buffer |
Lyophilized from a 0.2 μm filtered solution in PBS. |
| Purity |
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining |
| Reconstitution Instructions |
Reconstitute at 500 μg/mL in PBS. |
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Cynomolgus Lymphotoxin beta R/TNFRSF3 Fc, CF
Background
Lymphotoxin beta receptor (LT beta R), previously called TNF RIII or TNF R-related protein (TNF Rrp), is a type I transmembrane glycoprotein within the TNF receptor superfamily, designated TNFRSF3 (1-3). Cynomolgus monkey and rhesus macaque 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 cynomolgus monkey LTBR shares 65-75% aa sequence identity with human, 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, as is recombinant LT beta R, which inhibits autoimmunity (3-6). 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, 7). 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, 8-10). 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, 8 - 10). LT beta R is expressed by hepatocytes, is up-regulated in regeneration, hepatitis and hepatocellular carcinoma, and influences lipid metabolism and atherosclerosis (4, 6, 11). It regulates cell growth and can initiate inflammation-related carcinogenesis (6, 11).
- Crowe, P.D. et al. (1994) Science 264:707.
- Force, W.R. et al. (1995) J. Immunol. 155:5280.
- McCarthy, D.D. (2006) Immunol. Res. 35:41.
- Tumanov, A.V. et al. (2007) Curr. Mol. Med. 7:567.
- Boehm, T. et al. (2003) J. Exp. Med. 198:757.
- Wolf, M.J. et al. (2010) Oncogene 29:5006.
- Bista, P. et al. (2010) J. Biol. Chem. 285:12971.
- van de Pavert, S.A. et al. (2010) Nat. Rev. Immunol. 10:664.
- Mouri, Y. et al. (2011) J. Immunol. 186:5047.
- Vondenhoff, M.F. et al. (2009) J. Immunol. 182:5439.
- Haybaeck, J. et al. (2009) Cancer Cell 16:295.
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