LIGHT/TNFSF14 Protein, Mouse (sf9, His, solution)

LIGHT/TNFSF14 protein (CD258; TNFRSF14) is a type II transmembrane protein produced by activated T cells. It is a TNFRSF14/HVEM ligand and belongs to the tumor necrosis factor (TNF) family. LIGHT/TNFSF14 is mainly expressed in spleen, with two subtypes: membrane-bound type and soluble type ^[1]. LIGHT/TNFSF14 protein can be used as immune checkpoint molecule of tumor, and stimulate natural killer cells to produce interferon TFNγ, triggering tumor apoptosis signal ^[2]. LIGHT/TNFSF14 is also involved in the dominant LTβR-NIK-p52 NF-κB pathway promoting the expression of inflammatory gene^[3]. In addition, LIGHT/TNFSF14 protein is a co-stimulatory factor that activates lymphoid cells and has an inhibitory effect on herpes virus infection^[4]. Mouse LIGHT/TNFSF14 Protein has 239 amino acids and a transmembrane domain (38-58 a.a.). LIGHT/TNFSF14 Protein, Mouse (sf9, His, solution) is the extracellular part (D72-V239) of mouse LIGHT/TNFSF14 Protein in solution form, produced by Sf9 insect cells, with N-terminal His-tag.

LIGHT/TNFSF14 is a type II transmembrane protein produced by activated T cells, belongs to tumor necrosis factor (TNF) family. LIGHT/TNFSF14 is a TNFRSF14/HVEM (herpesvirus entry mediator) ligand, engages the receptor for the LTalphabeta heterotrimer but does not form complexes with either secreted lymphotoxin alpha (LTalpha) or LTbeta^[1].
LIGHT/TNFSF14 is predominantly expressed in the spleen but also found in the brain. It is 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^[1].
LIGHT/TNFSF14 has a transmemberane, thus it can be leaved into 2 chains: membrane form and soluble form. The soluble form of isoform 1 derives from the membrane form by proteolytic processing.
In tumor immunology, TNFSF14/LIGHT also serves as a novel immune checkpoint molecule for glioblastoma multiforme (GBM), as well as lung carcinoma, breast carcinoma, cervical cancer, and prostate cancer. TNFSF14/LIGHT can stimulate NK cells to produce IFNγ via nuclear factor-κB (NFκB) RelA/p50 signaling. TNFSF14/LIGHT sustains the function of CD8⁺ effector T cells, trigger apoptosis of various tumor cells^[2].
In cell signaling, TNFSF14/LIGHT binds to lymphotoxin-β receptor (LTβR) and HVEM for activating both of them, and disrupts the HVEM-BTLA complex in surface-bound form, and facilitates HVEM-BTLA complex formation in the soluble form^[2].
TNFSF14/LIGHT promotes an inflammatory esophageal fibroblast in vitro via a LTβR-NIK-p52 NF-κB dominant pathway with promoting inflammatory gene expression and down-regulating homeostatic factors including WNTs, BMPs and type 3 semaphorins^[3].
Beside that, TNFSF14/LIGHT protein is a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. TNFSF14/LIGHT also prevents tumor necrosis factor alpha mediated apoptosis in primary hepatocyte^[4][5].

LIGHT/TNFSF14 is homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes^[8].
LIGHT/TNFSF14 transgenic expression on T cells in mice promotes inflammation in multiple organs, including intestine^[8].
LIGHT/TNFSF14^-/- mice also shows increased accumulation of innate immune cells and higher levels of cytokines than colons from control mice, indicating a function for inflammation regulation in the colon^[8].

LIGHT/TNFSF14 (mouse; 20 μg/mL; 48 h) promotes insulin signalling in L6 skeletal muscle myotubes as indicated by increased expression of phospho-AKT^[6].
LIGHT/TNFSF14 (mouse; 100 ng/mL; 24 h) reduces palmitate-induced insulin resistance and promotes insulin secretion in vitro^[7].

Mouse

Sf9 insect cells

N-His

Q9QYH9 (D72-V239)

50930  [NCBI]

Approximately 20.5 kDa

Greater than 95% as determined by reducing SDS-PAGE.

Solution.

Supplied as a 0.2 μm filtered solution of 20 mM Tris, pH 8.0, 500 mM NaCl, 10 % gly.

<1 EU/μg, determined by LAL method.

N/A.

Stored at -80°C for 1 year. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Mauri DN, et al. LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. Immunity. 1998 Jan;8(1):21-30.  [Content Brief]

  [2]. Han M, et al. Comprehensive characterization of TNFSF14/LIGHT with implications in prognosis and immunotherapy of human gliomas. Front Immunol. 2022 Oct 20;13:1025286.  [Content Brief]

  [3]. Manresa MC, et al. LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms. Mucosal Immunol. 2022 Feb;15(2):327-337.  [Content Brief]

  [4]. Hou Y, et al. Dual Roles of Tumor Necrosis Factor Superfamily 14 in Antiviral Immunity. Viral Immunol. 2022 Nov;35(9):579-585.  [Content Brief]

  [5]. Miao X, et al. HES5-mediated repression of LIGHT transcription may contribute to apoptosis in hepatocytes. Cell Death Discov. 2021 Oct 23;7(1):308.  [Content Brief]

  [6]. Agostino M, et al. TNFSF14-Derived Molecules as a Novel Treatment for Obesity and Type 2 Diabetes. Int J Mol Sci. 2021 Sep 30;22(19):10647.  [Content Brief]

  [7]. Saunders BM, et al. Shining LIGHT on the metabolic role of the cytokine TNFSF14 and the implications on hepatic IL-6 production. Immunol Cell Biol. 2018 Jan;96(1):41-53.  [Content Brief]

  [8]. Krause P, et al. The tumor necrosis factor family member TNFSF14 (LIGHT) is required for resolution of intestinal inflammation in mice. Gastroenterology. 2014 Jun;146(7):1752-62.e4.  [Content Brief]