Description: LIGHT belongs to the TNF family of ligands, and can signal through the herpes virus entry mediator type A receptor (HVEM, TNFRSF14), LTβR, or bind to a decoy receptor, DcR3. It is expressed in splenocytes, activated PBL, CD+8 tumor infiltrating lymphocytes, granulocytes, and monocytes. LIGHT has the ability to active NFkB, to co-stimulate the activation of lymphocytes and to induce apoptosis in certain human tumor cells. Recombinant murine LIGHT is a 20.1 kDa protein containing 183 amino acid residues.

Description: Mouse monoclonal Kappa Light Chain antibody

Description: Human TNFSF14 Protein, also known as LIGHT, belongs to a member of the tumor necrosis factor (TNF) ligand family. It can bind to NFRSF3/LTBR. It is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and it is also known as a herpesvirus entry mediator ligand (HVEML). TNFSF14 encodes a protein with a 37 aa cytoplasmic domain, 21aa transmembrane domain and 182 aa extracellular region. The gene is predominantly expressed in the spleen and also found in the brain. Weakly expressed in peripheral lymphoid tissues and in heart, placenta, liver, lung, appendix, and kidney, and no expression seen in fetal tissues, endocrine glands, or nonhematopoietic tumor lines. TNFSF14 protein was found to probably function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. Studies have shown that this protein can prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.

Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human LIGHT . This antibody is tested and proven to work in the following applications:

Description: Human TNFSF14 Protein, also known as LIGHT, belongs to a member of the tumor necrosis factor (TNF) ligand family. It can bind to NFRSF3/LTBR. It is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and it is also known as a herpesvirus entry mediator ligand (HVEML). TNFSF14 encodes a protein with a 37 aa cytoplasmic domain, 21aa transmembrane domain and 182 aa extracellular region. The gene is predominantly expressed in the spleen and also found in the brain. Weakly expressed in peripheral lymphoid tissues and in heart, placenta, liver, lung, appendix, and kidney, and no expression seen in fetal tissues, endocrine glands, or nonhematopoietic tumor lines. TNFSF14 protein was found to probably function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. Studies have shown that this protein can prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.

Description: LIGHT Antibody: LIGHT, also known as Tumor Necrosis Factor Superfamily member 14 (TNFSF14), is a co-stimulatory molecule that can regulate T-cell activation (1) and has recently been identified as an immune checkpoint protein. LIGHT binds to two different receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin beta Receptor (LTβR). While LIGHT binding to HVEM delivers a co-stimulatory signal to T cells (1), LIGHT binding to LTβR is critical for the formation of lymphoid structures which can stimulate T cell infiltration and activation of a tumor microenvironment, leading to rapid T cell-mediated tissue destruction (2). It has been shown that targeted delivery of LIGHT to tumors, thereby causing the T cell infiltration of the tumor, can enhance the response of the PD-1/PD-L1 checkpoint blockade anti-cancer therapy (3), suggesting that LIGHT may become a potent tool in anti-cancer treatment.

Description: LIGHT Antibody: LIGHT, also known as Tumor Necrosis Factor Superfamily member 14 (TNFSF14), is a co-stimulatory molecule that can regulate T-cell activation (1) and has recently been identified as an immune checkpoint protein. LIGHT binds to two different receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin beta Receptor (LTβR). While LIGHT binding to HVEM delivers a co-stimulatory signal to T cells (1), LIGHT binding to LTβR is critical for the formation of lymphoid structures which can stimulate T cell infiltration and activation of a tumor microenvironment, leading to rapid T cell-mediated tissue destruction (2). It has been shown that targeted delivery of LIGHT to tumors, thereby causing the T cell infiltration of the tumor, can enhance the response of the PD-1/PD-L1 checkpoint blockade anti-cancer therapy (3), suggesting that LIGHT may become a potent tool in anti-cancer treatment.

Description: LIGHT Antibody: LIGHT, also known as Tumor Necrosis Factor Superfamily member 14 (TNFSF14), is a co-stimulatory molecule that can regulate T-cell activation (1) and has recently been identified as an immune checkpoint protein. LIGHT binds to two different receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin beta Receptor (LTβR). While LIGHT binding to HVEM delivers a co-stimulatory signal to T cells (1), LIGHT binding to LTβR is critical for the formation of lymphoid structures which can stimulate T cell infiltration and activation of a tumor microenvironment, leading to rapid T cell-mediated tissue destruction (2). It has been shown that targeted delivery of LIGHT to tumors, thereby causing the T cell infiltration of the tumor, can enhance the response of the PD-1/PD-L1 checkpoint blockade anti-cancer therapy (3), suggesting that LIGHT may become a potent tool in anti-cancer treatment.

Description: LIGHT Antibody: LIGHT, also known as Tumor Necrosis Factor Superfamily member 14 (TNFSF14), is a co-stimulatory molecule that can regulate T-cell activation (1) and has recently been identified as an immune checkpoint protein. LIGHT binds to two different receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin beta Receptor (LTβR). While LIGHT binding to HVEM delivers a co-stimulatory signal to T cells (1), LIGHT binding to LTβR is critical for the formation of lymphoid structures which can stimulate T cell infiltration and activation of a tumor microenvironment, leading to rapid T cell-mediated tissue destruction (2). It has been shown that targeted delivery of LIGHT to tumors, thereby causing the T cell infiltration of the tumor, can enhance the response of the PD-1/PD-L1 checkpoint blockade anti-cancer therapy (3), suggesting that LIGHT may become a potent tool in anti-cancer treatment.