Background:  LIGHT protein is a type II transmembrane protein and a tumor necrosis factor (TNF) ligand superfamily member (TNFSF14). LIGHT is expressed on activated T cells and immature dendritic cells and its receptors have been identified as lymphotoxin-Beta receptor (LTBetaR) and the herpesvirus entry mediator (HVEM), both of which lack the cytoplasmic sequence termed as "death domain." LIGHT is first identified as HVEM ligand (HVEM-L) and a deterrent to herpesvirus infection according to its ability to compete with HSV glycoprotein D for HVEM binding. As a T cell-derived costimulatory ligand, TNFSF14 plays a crucial role in T cell activation and proliferation by LIGHT-LTBetaR interaction, and it is necessary and sufficient for LIGHT-mediated apoptosis of tumor cells. Additionally, recent studies also establish a direct role for LIGHT in NK activation/expansion via LIGHT-HVEM interaction, and thus breaking T-cell tolerance at the tumor site. Accordingly, LIGHT is suggested to be involved in CTL-mediated tumor rejection, allograft rejection and graft versus host disease. Although known as lymphotoxin-Gamma, LIGHT plays a minimal role in lymphoid tissue development in contrast with LT-Alpha and Beta. This protein was also demonstrated to inhibit TNF-Alpha-mediated but not Fas- or TRAIL-mediated apoptosis of human primary hepatocytes.

Description: Rabbit polyclonal to LIGHT

Immunogen: KLH conjugated synthetic peptide derived from LIGHT

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/200-500. Predicted Mol wt: 26 kDa;

·Immunohistochemistry (Frozen/paraffin tissue section): 1/100-500;

·Immunocytochemistry: 1/200;

·ELISA: 1/1000;

·Optimal working dilutions must be determined by the end user.