LIGHT/TNFSF14 蛋白, Mouse (sf9, His)

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) is the extracellular part (D72-V239) of mouse LIGHT/TNFSF14 Protein, produced by Sf9 insect cells, with N-terminal His-tag.

LIGHT/TNFSF14是由活化的T细胞产生的II型跨膜蛋白，属于肿瘤坏死因子(TNF)家族。LIGHT/TNFSF14 是 TNFRSF14/HVEM（疱疹病毒进入介质）配体，与 LTalphabeta 异三聚体受体结合，但不与分泌性淋巴毒素 α (LTalpha) 或 LTbeta^[1] 形成复合物。
LIGHT/TNFSF14 主要在脾脏中表达，但也在大脑中发现。在外周淋巴组织以及心脏、胎盘、肝脏、肺、阑尾和肾脏中微弱表达，在胎儿组织、内分泌腺或非造血肿瘤系中未见表达^[1]。
LIGHT/TNFSF14具有跨膜烷，因此可以分成2条链：膜形式和可溶形式。同工型 1 的可溶形式是通过蛋白水解加工从膜形式衍生而来。
在肿瘤免疫学中，TNFSF14/LIGHT 也可作为多形性胶质母细胞瘤 (GBM) 以及肺癌、乳腺癌、宫颈癌和前列腺癌。TNFSF14/LIGHT 可通过核因子-κB (NFκB) RelA/p50 信号传导刺激 NK 细胞产生 IFNγ。TNFSF14/LIGHT 维持 CD8⁺ 效应 T 细胞的功能，触发多种肿瘤细胞的凋亡^[2]。
在细胞信号传导中，TNFSF14/LIGHT 结合淋巴毒素-β 受体 (LTβR) 和 HVEM 可激活两者，并破坏表面结合形式的 HVEM-BTLA 复合物，并促进可溶形式的 HVEM-BTLA 复合物形成^[2]。
TNFSF14/LIGHT 通过 LTβR-NIK-p52 NF-κB 显性通路在体外促进炎症性食管成纤维细胞的形成，促进炎症基因表达并下调 WNT、BMP 和 3 型信号蛋白等稳态因子^[3]。
除此之外，TNFSF14/LIGHT 蛋白是淋巴细胞活化的共刺激因子，可阻止疱疹病毒感染。TNFSF14/LIGHT 还可预防肿瘤坏死因子 α 介导的原代肝细胞凋亡^[4][5]。

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].
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].

Mouse

Sf9 insect cells

N-His

NP_062291.1 (D72-V239)

50930  [NCBI]

Approximately 20.5 kDa

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

无菌粉末.

Lyophilized from a 0.2 μm filtered solution of 20 mM Tris, pH 8.0, 500 mM NaCl, 10 % glycerol. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [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]