Recombinant Human LT beta R/TNFRSF3 Fc Chimera (CHO), CF

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Summary
Reactivity HuSpecies Glossary
Applications Bioactivity
Format
Carrier-Free

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Recombinant Human LT beta R/TNFRSF3 Fc Chimera (CHO), 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 2-10 ng/mL in the presence of 10 ng/mL of Recombinant Human Lymphotoxin  alpha 1/ beta 2 (Catalog #
8884-LY).
Source
Chinese Hamster Ovary cell line, CHO-derived human Lymphotoxin beta R/TNFRSF3 protein
Human Lymphotoxin beta R
(Ser28-Met227)
Accession # NP_002333
DIEGRMD Human IgG1
(Pro100-Lys330)
N-terminus C-terminus
Accession #
N-terminal Sequence
Ser28
Structure / Form
Disulfide-linked homodimer
Protein/Peptide Type
Recombinant Proteins
Gene
LTBR
Purity
>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.

Applications/Dilutions

Theoretical MW
48.5 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.
SDS-PAGE
60-66 kDa, 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 °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.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS.
Purity
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain.
Reconstitution Instructions
Reconstitute at 100 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 Human LT beta R/TNFRSF3 Fc Chimera (CHO), 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 RIII
  • TNF Rrp
  • TNFCRTNF-RIII
  • TNFR superfamily, member 3
  • TNFR2-RP
  • TNFR3
  • TNF-R-III
  • TNFR-RP
  • TNFRSF3
  • TNFRSF3TNFR-III
  • 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

Background

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).

  1. Crowe, P.D. et al. (1994) Science 264:707.
  2. Force, W.R. et al. (1995) J. Immunol. 155:5280.
  3. McCarthy, D.D. (2006) Immunol. Res. 35:41.
  4. Tumanov, A.V. et al. (2007) Curr. Mol. Med. 7:567.
  5. Boehm, T. et al. (2003) J. Exp. Med. 198:757.
  6. Wolf, M.J. et al. (2010) Oncogene 29:5006.
  7. Entrez Accession # BAH11468 and BAG53051.
  8. Bista, P. et al. (2010) J. Biol. Chem. 285:12971.
  9. van de Pavert, S.A. et al. (2010) Nat. Rev. Immunol. 10:664.
  10. Mouri, Y. et al. (2011) J. Immunol. 186:5047.
  11. Vondenhoff, M.F. et al. (2009) J. Immunol. 182:5439.
  12. Haybaeck, J. et al. (2009) Cancer Cell 16:295.

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Bioinformatics

Gene Symbol LTBR
Uniprot