Human Lymphotoxin beta R/TNFRSF3 Antibody Summary
Accession # P36941
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Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
CXCL8/IL-8 Secretion Induced by Human Lymphotoxin beta R/TNFRSF3 Antibody. Human Lymphotoxin beta R/TNFRSF3 Monoclonal Antibody (Catalog # MAB6291) activates Lymphotoxin beta Receptor on the A375 human melanoma cell line in a dose-dependent manner which induces CXCL8/IL-8 Secretion, as measured by the Human CXCL8/IL-8 Quantikine ELISA (Catalog # D8000C). The ND50 is typically 1.5-9 ng/mL.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: Lymphotoxin beta R/TNFRSF3
Lymphotoxin beta receptor (LT beta R), also known as TNF RIII and TNF R-related protein (TNF Rrp) is a member of the TNF receptor superfamily, designated TNFRSF3. Human LT beta R cDNA encodes a 435 amino acid (aa) residue type I membrane protein with a putative 30 aa residue signal peptide, a 193 aa residue extracellular domain and a 171 aa residue cytoplasmic domain. The extracellular domain of LT beta R contains four cysteine-rich motifs characteristic of the TNF receptor superfamily. The cytoplasmic region of LT beta R shares little sequence similarity with other TNF receptor family members, suggesting that different signaling mechanisms may be used. LT beta R is expressed in a variety of tissues including visceral and lymphoid tissues. LT beta R is also expressed by cell lines of monocytic, epithelial, and fibroblastic origins but not by T and B lymphocytes. Human and mouse LT beta R share 76% aa sequence homology. The TNF family ligands that have been shown to bind and activate LT beta R include LIGHT (also a ligand for HVEM) and the heterotrimeric lymphotoxin LT alpha 1/ beta 2 or LT alpha 2/ beta 1. Depending on the cell type, activation of LT beta R has been shown to induce NF kappa B activation, chemokine production, growth arrest, and apoptosis. In vivo, LT beta R has been shown to play a critical role in controlling cellular immune functions and lymphoid organogenesis.
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- Rennert, P.D. et al. (1998) Immunity 9:71.
- Degli-Esposti, M.A. et al. (1997) J. Immunol 158:1756.
- Mackay, F. et al. (1996) J. Biol. Chem. 271:8618.
- Crowe, P.D. et al. (1994) Science 264:707.
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