Recombinant Mouse Lymphotoxin beta R/TNFRSF3 Fc Chimera, CF


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Reactivity MuSpecies Glossary
Applications Bioactivity

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Recombinant Mouse Lymphotoxin beta R/TNFRSF3 Fc Chimera, 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 ED50 for this effect is 15-75 ng/mL in the presence of 10 ng/mL of Recombinant Human Lymphotoxin alpha 1/ beta 2 (Catalog #
Mouse myeloma cell line, NS0-derived mouse Lymphotoxin beta R/TNFRSF3 protein
Mouse Lymphotoxin beta R
Accession # P50284
N-terminus C-terminus
Accession #
N-terminal Sequence
Structure / Form
Disulfide-linked homodimer
Protein/Peptide Type
Recombinant Proteins
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain.
Endotoxin Note
<0.01 EU per 1 μg of the protein by the LAL method.


Theoretical MW
48.7 kDa (monomer).
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.
63-67 kDa, reducing conditions
Read Publication using
1008-LR in the following applications:

Packaging, Storage & Formulations

Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
Lyophilized from a 0.2 μm filtered solution in PBS.
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain.
Reconstitution Instructions
Reconstitute at 100 μg/mL in PBS.


This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Mouse Lymphotoxin beta R/TNFRSF3 Fc Chimera, CF

  • CD18
  • D12S370
  • ltbetar
  • LT-beta-R
  • LTBR
  • lymphotoxin B receptor
  • Lymphotoxin beta R
  • lymphotoxin beta receptor (TNFR superfamily, member 3)
  • Lymphotoxin-beta receptor
  • LymphotoxinbR
  • TNF Rrp
  • TNFR superfamily, member 3
  • TNFR2-RP
  • TNFR3
  • Tumor necrosis factor C receptor
  • Tumor necrosis factor receptor 2-related protein
  • tumor necrosis factor receptor superfamily member 3
  • tumor necrosis factor receptor superfamily, member 3
  • Tumor necrosis factor receptor type III


Lymphotoxin  beta R (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, 2). Mouse LT beta R cDNA encodes 415 amino acids (aa) including a 30 aa signal peptide, a 193 aa extracellular domain (ECD), a 21 aa transmembrane domain, and a 171 aa cytoplasmic domain. The ECD contains four cysteine‑rich motifs characteristic of the TNF receptor superfamily (1). Within the ECD, mouse LT beta R shares aa sequence identity of 91% aa with rat, and 65-71% with human, 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 (2-5). A potential mouse isoform that ends at aa 218, just prior to the transmembrane domain, could also be secreted and inhibitory (6). LT beta R is expressed by visceral, lymphoid, and other stroma, epithelia and myeloid cells, but not lymphocytes (1, 3). LT beta R ligands include homotrimers of LIGHT (TNFSF14; also a ligand for HVEM) and the heterotrimeric lymphotoxin LT alpha 1/ beta 2 (2, 3, 5). 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 (5, 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 (2-4, 8-10). Secondary immune tissues are absent in LT beta R‑deficient mice (2-4). 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 (2, 8-10). LT beta R is expressed by hepatocytes, is up-regulated in regeneration, hepatitis and hepatocellular carcinoma, and influences lipid metabolism and atherosclerosis (3, 5, 11). It regulates cell growth and can initiate inflammation‑related carcinogenesis (5, 11).

  1. Force, W.R. et al. (1995) J. Immunol. 155:5280.
  2. McCarthy, D.D. (2006) Immunol. Res. 35:41.
  3. Tumanov, A.V. et al. (2007) Curr. Mol. Med. 7:567.
  4. Boehm, T. et al. (2003) J. Exp. Med. 198:757.
  5. Wolf, M.J. et al. (2010) Oncogene 29:5006.
  6. Entrez Accession # AAA81334.
  7. Bista, P. et al. (2010) J. Biol. Chem. 285:12971.
  8. van de Pavert, S.A. et al. (2010) Nat. Rev. Immunol. 10:664.
  9. Mouri, Y. et al. (2011) J. Immunol. 186:5047.
  10. Vondenhoff, M.F. et al. (2009) J. Immunol. 182:5439.
  11. Haybaeck, J. et al. (2009) Cancer Cell 16:295.

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Publications for Lymphotoxin beta R/TNFRSF3 (1008-LR)(1)

We have publications tested in 1 confirmed species: Mouse.

We have publications tested in 1 application: Flow.

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