Mouse LIGHT/TNFSF14 Biotinylated Antibody
Mouse LIGHT/TNFSF14 Biotinylated Antibody Summary
Accession # Q9QYH9
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.
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.
LIGHT (lymphotoxin-like, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes) is a member of the TNF superfamily and is designated TNFSF14. The gene for mouse LIGHT encodes a 239 amino acid residue (aa) type II transmembrane glycoprotein that contains a 37 aa N-terminal cytoplasmic domain, a 21 aa transmembrane region, and a 181 aa extracellular domain. A soluble form of mouse LIGHT is generated from the membrane form by proteolytic processing. Similar to other TNF ligand family members, LIGHT is assembled as a homotrimer. Mouse and human LIGHT share 71% aa sequence identity.
LIGHT is expressed by activated lymphocytes, natural killer cells, immature dendritic cells, monocytes and granulocytes. Mouse LIGHT binds and signals via two distinct TNF receptor superfamily members, including the herpes virus entry mediator (HVEM/TNFRSF14) and the lymphotoxin beta receptor (LT beta R/TNFRSF3). In humans, LIGHT also binds the soluble human decoy receptor 3 (DcR3/TNFRSF6B). Signaling from LT beta R, which also binds LT alpha beta, induces apoptosis and the production of various cytokines. LIGHT-LT beta R signaling also plays a role in mesenteric lymph node organogenesis, and restoration of secondary lymphoid structure and function. Signaling from HVEM, which also binds LT alpha, co-stimulates T-helper cell type 1 (TH1) immune responses, enhances Cytotoxic T Lymphocytes (CTL)‑mediated tumor immunity, and regulates allogeneic T cell activation and allograft rejection. Blockade of LIGHT-HVEM signaling has been shown to prevent graft versus host disease.
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