Recombinant Human LIGHT/TNFSF14 Protein

Name: Recombinant Human LIGHT/TNFSF14 Protein
Brand: Beta LifeScience
SKU: BLA-0797P
Availability: InStock

Collections: Co-stimulatory receptors, Cytokines and growth factors, Recombinant proteins, Tumor necrosis factors and receptors (tnfs)

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Product Overview

Host Species	Human
Accession	O43557
Synonym	CD 258 CD258 CD258 antigen Delta transmembrane LIGHT Herpes virus entry mediator ligand Herpesvirus entry mediator A Herpesvirus entry mediator ligand herpesvirus entry mediator-ligand HVEM L HVEM-L HVEML Ligand for herpesvirus entry mediator LIGHT LTg soluble form TNF14 TNF14_HUMAN TNFSF 14 Tnfsf14 TNFSF14 protein TR 2 TR2 Tumor necrosis factor (ligand) superfamily, member 14 Tumor necrosis factor ligand superfamily member 14 Tumor necrosis factor ligand superfamily, member 14 Tumor necrosis factor receptor like 2 tumor necrosis factor receptor-like 2 Tumor necrosis factor superfamily member 14 Tumor necrosis factor superfamily member LIGHT
Description	Recombinant Human LIGHT/TNFSF14 Protein was expressed in CHO cells. It is a Protein fragment
Source	CHO cells
Molecular Weight	25 kDa including tags
Purity	>95% SDS-PAGE.
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Lyophilised
Stability	The recombinant protein samples are stable for up to 12 months at -80°C
Reconstitution	See related COA
Unit Definition	For Research Use Only
Storage Buffer	Shipped at 4°C. After reconstitution store at -20°C. Avoid freeze / thaw cycle.

Target Details

Target Function	Cytokine that binds to TNFRSF3/LTBR. Binding to the decoy receptor TNFRSF6B modulates its effects. Acts as a ligand for TNFRSF14/HVEM. Upon binding to TNFRSF14/HVEM, delivers costimulatory signals to T cells, leading to T cell proliferation and IFNG production.
Subcellular Location	[Tumor necrosis factor ligand superfamily member 14, membrane form]: Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 14, soluble form]: Secreted.; [Isoform 2]: Cytoplasm.
Protein Families	Tumor necrosis factor family
Database References	HGNC: 11930 OMIM: 604520 KEGG: hsa:8740 STRING: 9606.ENSP00000469049 UniGene: Hs.129708
Tissue Specificity	Predominantly expressed in the spleen but 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 tu

Gene Functions References

the outcomes of this study provide compelling evidence that TNFSF14 is necessary to limit relevant steps in the pathogenesis of the metabolic syndrome and support the development of agonists of TNFSF14 signaling as attractive therapeutics for treating obesity and type 2 diabetes PMID: 29359470
LIGHT is highly expressed and companied with severe inflammations in patients with coronary disease. LIGHT significantly enhanced inflammation response in oxLDL-induced THP-1 macrophages. PMID: 28642135
LIGHT and LTBR interaction increases the survival and proliferation of human bone marrow-derived mesenchymal stem cells, and therefore, LIGHT might play an important role in stem cell therapy. PMID: 27835685
Serum LIGHT levels correlate with disease progression and severity in interstitial pneumonia patients with dermatomyositis. PMID: 26448572
LIGHT, via LTbetaR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine production by bronchial epithelial cells. PMID: 25501580
LIGHT controls TSLP to drive pulmonary fibrosis. PMID: 25680454
The tumor necrosis factor superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis. PMID: 25789702
proliferation and migration would be enhanced in Tca8113 cells with over-expressed TNFSF14 PMID: 26146063
LIGHT, a TNF superfamily member, is involved in T-cell homeostasis and erosive bone disease associated with rheumatoid arthritis. PMID: 25460501
Crystal structures of LIGHT and the LIGHT:DcR3 complex reveal the structural basis for the DcR3-mediated neutralization of LIGHT. PMID: 25087510
regulation by NK cell licensing helps to safeguard against TNFSF14 production in response to healthy tissues. PMID: 25512551
The findings suggest a new molecular determinant of LIGHT-mediated pathogenic changes in human bronchial epithelial cells. PMID: 25251281
TNFSF14 has an effect on the activation of basophils and eosinophils interacting with bronchial epithelial cells PMID: 24782592
Triggering of LIGHT induced production of pro-inflammatory mediators such as interleukin-8 and matrix metalloproteinase-9 while suppressing the phagocytic activity. PMID: 24044961
GG carriers of rs1077667, of the LIGHT gene, with the highest risk for Multiple Sclerosis, had the lowest serum levels. PMID: 23037546
although a limited number of activated T-cells infiltrate the tumor and initiate an immune response, the number of LIGHT + T cells infiltrating the tumor is very low PMID: 23514280
findings show that LIGHT is not inhibited by the soluble RANKL receptor OPG and that LIGHT is a potent osteoclastogenesis factor that activates the Akt, NFkappaB and JNK pathways PMID: 23391709
TNFSF14 was significantly increased in sickle-cell anemia, SCA treated with hydroxycarbamide,& HbSC. It could contribute to endothelial activation & inflammation in SCA. PMID: 22775554
This study showed that expression of the death-triggering ligand LIGHT is increased in ALS spinal cords PMID: 22221541
increased plasma levels in patients with atopic dermatitis PMID: 22519595
INF-gamma can synergistically precede LIGHT-induced apoptotic processes through down-regulation of Bcl-2 expression, but not survivin expression. PMID: 21117871
These data clearly indicate that ZFP91 is a key regulator in LIGHT-induced activation of non-canonical NF-kappaB pathway in LTbetaR signaling. PMID: 20804734
Herpes simplex virus 1 gD interfere HVEM function by competing with its natural ligands and by downregulating HVEM. PMID: 20826693
Increased potential for LIGHT receptor signaling, coupled with increased bioavailability due to lower decoy receptor-3 (DcR3) avidity, provides a mechanism for polymorphic variants in LIGHT to contribute to the pathogenesis of inflammatory diseases. PMID: 20592286
mediates organ-specific donor T cells activation in GVHD PMID: 19826934
suppresses tumor growth by augmentation of immune response PMID: 19716382
There is over expression of genes related to immune and inflammatory responses, including cytokines such as TNFSF14 in interstitial cystitis PMID: 20096889
When highly expressed, LIGHT is capable of promoting effector T cell proliferation and differentiation even in a regulatory T (Treg) cell-enriched, suppressive intestinal environment. PMID: 20042587
These findings suggested that LIGHT might be involved in the progression of inflammatory bone destruction in rheumatoid arthritis. PMID: 19019090
Effects in transgenic mice indicate that human LIGHT may function as a major regulator of T cell activation, and implicate LIGHT signaling pathways in inflammation focused on mucosal tissues. PMID: 11714797
LIGHT (TNFSF14),5 its membrane-anchored ligand, was also present in atheromatous lesions and highest in regions rich in macrophage-derived foam cells. PMID: 11742858
Role of calcium-signaling pathway in the transcriptional control PMID: 12215452
LIGHT may act as an anti-apoptotic agent against TNFalpha-mediated liver injury by blocking the activation of both caspase-3 and caspase-8. PMID: 12393901
LIGHT, a new member of the TNF superfamily [review] PMID: 12456019
Data show that mRNA encoding LIGHT and its receptors [HVEM, LTbetaR, and TR6 (DcR3)] are present in placentas and cytotrophoblast cells at term. PMID: 12466117
Soluble LIGHT blocks TR6-Fc costimulated proliferation, lymphokine production, and cytotoxicity of T cells in the presence of T cell receptor ligation. PMID: 12471113
LIGHT-sensitized IFN-gamma-mediated apoptosis of MDA-MB-231 cells is probably through down-regulation of anti-apoptosis Bcl-2 family members; it could be caspase (especially caspase-3)-independent, even though extensive caspase activation was observed. PMID: 12767529
LIGHT signaling is mediated through both death receptor and mitochondria pathways PMID: 15115612
LIGHT-herpesvirus entry mediator mediated signaling as an important immune regulatory mechanism in mucosal inflammatory responses. PMID: 15210782
Mechanisms protecting trophoblast cells from LIGHT-mediated apoptosis were studied. PMID: 15215185
LIGHT expression by human intestinal T cells suggests the possibility that LIGHT may play a key role in regulation of the mucosal immune system. PMID: 15634882
LIGHT protein can be activated on mucosal T cells through a gut-specific CD2-dependent signaling mechanism. PMID: 15634882
Data suggest that LIGHT constitutively expressed in human melanoma cells and microvesicles may contribute to regulate T-cell responses to tumor cells. PMID: 15833878
NF-kappaB signal plays a key role in LIGHT-mediated upregulation of CD86 expression. PMID: 15895390
both LTbetaR and HVEM can discriminatively mediate the expression of different genes in cultured human umbilical vein endothelial cells, including LIGHT, a proinflammatory cytokine PMID: 15917993
A transgenic mouse model resembling Crohn's disease (CD) suggests that up-regulation of LIGHT may be an important mediator of CD pathogenesis. PMID: 15944326
LIGHT could serve as a molecular link between lipid metabolism, inflammation, and thrombus formation, which are all features of atherosclerotic plaques. PMID: 16186421
platelet-derived LIGHT is biologically active and can induce an inflammatory response in monocytes and particularly within endothelial cells measured as up-regulation of adhesion molecules and release of chemokines PMID: 16861346
Blockade of TNFSF14 signaling caused a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration factors within the islets and disrupts organization of tertiary structures, leading to prevention of diabetes. PMID: 16934497
LIGHT system may regulate early to middle stages of placental development via cell-specific, temporally programmed expression of the ligand and its receptors, and may also assist in preserving placental immune privilege. PMID: 17010447

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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