Mouse Tumor necrosis factor ligand superfamily member 14(TNFSF14) ELISA kit

Code CSB-EL023991MO
Size 96T,5×96T,10×96T
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Product Details

Target Name
tumor necrosis factor (ligand) superfamily, member 14
Alternative Names
Tnfsf14 ELISA kit; LightTumor necrosis factor ligand superfamily member 14 ELISA kit; CD antigen CD258) [Cleaved into: Tumor necrosis factor ligand superfamily member 14 ELISA kit; membrane form; Tumor necrosis factor ligand superfamily member 14 ELISA kit; soluble form] ELISA kit
Abbreviation
TNFSF14
Uniprot No.
Species
Mus musculus (Mouse)
Sample Types
serum, plasma, tissue homogenates
Detection Range
25 pg/mL-1600 pg/mL
Sensitivity
6.25 pg/mL
Assay Time
1-5h
Sample Volume
50-100ul
Detection Wavelength
450 nm
Research Area
Others
Assay Principle
quantitative
Measurement
Sandwich
Troubleshooting
and FAQs
Storage
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx
Description

CUSABIO's mouse TNFSF14 ELISA kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of mouse TNFSF14 in serum, plasma, or tissue homogenates. This assay uses the sandwich enzyme immunoassay technique in combination with the enzyme-substrate chromogenic reaction to quantify the analyte in the sample. The color develops positively to the amount of TNFSF14 in samples. The color intensity is measured at 450 nm via a microplate reader.

TNFSF14, also known as LIGHT, is a component of the cytokine network that regulates innate and adaptive immune responses, which promote the homeostasis of lymphoid organs, liver, and bone. It functions as a costimulatory factor to activate lymphocytes and induces pro-inflammatory gene expression via activating NF-κB. Studies have demonstrated that TNFSF14 plays a broader role in mucosal and systemic immunity, and is linked to dysregulated mucosal function. TNFSF14 is involved in dysregulated mucosal function or pulmonary diseases, such as pneumonia, non-small cell lung cancer, asthma, and lung fibrosis. Depletion of TNFSF14 or either receptor inhibits myoblast differentiation and promotes apoptosis. In addition to being expressed on activated immune cells, TNFSF14 is also expressed on some tumor cells. TNFSF14 is a pivotal regulator both for recruiting and activating immune cells in tumor lesions.

Citations

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Target Background

Function
(From Uniprot)
Cytokine that binds to TNFRSF3/LTBR. Binding to the decoy receptor TNFRSF6B modulates its effects. Activates NFKB and stimulates the proliferation of T-cells. 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.
Gene References into Functions
  1. bone marrow cells from Tnfsf14 deficient mice appeared to promote diet-induced obesity, insulin resistance and reduced FGF21 levels in white adipose tissue and liver PMID: 29359470
  2. Blockade of LIGHT markedly suppressed airway smooth muscle hyperplasia and inflammatory responses, which might be modulated through HVEM-NFkappaB or c-JUN pathways. PMID: 29460021
  3. The LIGHT (Tumour necrosis factor ligand superfamily member 14, TNFSF14)/Lymphotoxin beta-Receptor(LTbeta-R) pathway, which is involved in T-cell and macrophage activation, was diminished in plasma and in apoE-/-Irs2+/-HL-/- atheromas. PMID: 27172975
  4. LIGHT promote myeloid differentiation of Hematopoietic stem/progenitor cells via LIGHT receptor signaling. PMID: 28422285
  5. LIGHT signalling pathway combined with IFN-gamma induces beta cells apoptosis via an NF-kappaB/Bcl2-dependent mitochondrial pathway. PMID: 27241100
  6. Increasing LIGHT expression increased T-cell proliferation, activation, and infiltration, resulting in enhanced tumor-specific immune-mediated tumor regressions in primary tumors and colorectal liver metastases. PMID: 28249900
  7. Together, these results demonstrate that the LIGHT signaling pathway is not only required for inflammatory cytokine production as part of the host response to chlamydial infection, but also influences the differentiation of CD4(+) CD25(+) FoxP3(+) Treg cells, both of which may be essential for control of C. psittaci respiratory tract infection. PMID: 27725282
  8. These results expose the relevance of LIGHT/LTbetaR/HVEM interaction for the potential therapeutic control of the allogeneic immune responses mediated by alloreactive CD8 T cells that can contribute to prolong allograft survival. PMID: 26752542
  9. Mechanistically, intratumoral LIGHT induces pericyte differentiation and normalization via Rho kinase signaling. Minute amounts of LIGHT act in a paracrine fashion to trigger an amplifying cascade involving transforming growth factor beta (TGF-beta) from peri-vascular macrophages. PMID: 26711337
  10. localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt signaling. PMID: 26720335
  11. LIGHT-HVEM interactions stimulate IL-12 production by DCs during Leishmania donovani infection. Blockade of LIGHT-LTbetaR interactions dramatically enhanced early anti-parasitic immunity. PMID: 21998581
  12. LIGHT controls TSLP to drive pulmonary fibrosis. PMID: 25680454
  13. The tumor necrosis factor superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis. PMID: 25789702
  14. LIGHT signal pathway is not correlated with protection against Chlamydia muridarum urogenital tract infection. PMID: 26211324
  15. LIGHT protein is rapidly and transiently expressed after T-cell activation, and this expression is stronger on CD8 T cells than on CD4 T cells PMID: 25226173
  16. Chronic wounds in TNFSF14 KO mice could be induced by exacerbating the redox imbalance by further inhibiting the antioxidant enzymes and by infecting the wounds with biofilm-forming bacteria isolated from the chronic wounds that developed naturally in these mice. PMID: 25313558
  17. Tnfsf14(-/-) mice develop more severe colitis than control mice. LIGHT signals through the lymphotoxin beta receptor in the colon to regulate the innate immune response and mediate recovery from intestinal inflammation. PMID: 24560868
  18. Expression of LIGHT on donor cells is not required for disease induction; however, its expression on host cells is a decisive factor to limit disease progression and tissue damage. PMID: 23720813
  19. interaction of LIGHT with LTbetaR on hepatocytes, but not Kupffer cells, is sufficient to down regulate hepatic lipase expression and that this effect can be independent of LIGHT's costimulatory function. PMID: 23355893
  20. LIGHT promoted MSCs differentiation into adipocyte which was confirmed by Oil Red O Staining Assay. Since either MSCs or adipocytes are the major cell population in bone marrow niche, we then suggest that LIGHT regulate bone marrow niche PMID: 22930663
  21. Here we show that deletion of tumor necrosis factor superfamily member 14 (TNFSF14/LIGHT) leads to impaired wounds in mice that have the characteristics of nonchronic and chronic ulcers. PMID: 22564230
  22. LIGHT regulation of Lymph node hypertrophy in the generation of an adaptive immune response PMID: 21572030
  23. expression of tumor necrosis factor superfamily member 14 and lymphotoxin-beta receptor by motoneurons in vivo correlates with the preferential expression of interferon-gamma at disease onset and symptomatic stage in amyotrophic lateral sclerosis mice PMID: 21072055
  24. Trimerization of soluble mLIGHT is essential for its biological activity. PMID: 21400099
  25. LIGHT is expressed on lung inflammatory cells after allergen exposure. LIGHT-deficient mice also show an impairment in fibrosis and smooth muscle accumulation. PMID: 21499267
  26. LIGHT interaction with the LTbetaR plays a critical role in liver inflammation but is not required for LIGHT-mediated adeno-associated virus clearance. PMID: 20498840
  27. LIGHT enhances the expression of SOCS3 during stimulating BMDC maturation. PMID: 17718431
  28. LIGHT could potentiate the proliferation of T lymphocytes and induction of T CD8(+) cells performing by measuring Granzyme B, a specific marker of cell mediated immunity and virus neutralization antibody titer. PMID: 20097089
  29. LIGHT-deficient mice display reduced signs of intestinal inflammation in the model of dextran sodium sulphate-induced colitis PMID: 20067544
  30. T cell to T cell-mediated LIGHT/HVEM-dependent costimulation is a significant component of the host response leading to cardiac allograft rejection PMID: 11901205
  31. LIGHT selectively plays a role in CD8+ T cell activation but is not required for Th cell-dependent humoral responses. PMID: 11994431
  32. targeted disruption causes defects in costimulatory T cell activation and reveals cooperation with lymphotoxin beta in mesenteric lymph node genesis PMID: 12070288
  33. LIGHT, signaling via lymphotoxin beta-specific receptor, in supporting the development and maintenance of the lymphoid microenvironment PMID: 12115617
  34. LIGHT, although a ligand, can receive LIGHT cross-linking enhanced p44/42 mitogen-activated protein kinase activation after TCR ligation. This study reveals a new function and signaling event of LIGHT. PMID: 12384428
  35. LIGHT, a new member of the TNF superfamily [review] PMID: 12456019
  36. LIGHT plays a role in negative selection of thymocytes via inducing the apoptosis of thymocytes bearing high affinity T cell receptors. PMID: 12682226
  37. forced expression of LIGHT in the tumor environment induces a massive infiltration of naive T lymphocytes that correlates with an upregulation of both chemokine production and expression of adhesion molecules PMID: 14704792
  38. In graft arterial disease, the LIGHT pathway plays important roles in the regulation not only of T-cell activation but also of SMC proliferation. PMID: 15178556
  39. Inhibition of LIGHT/herpes simplex virus entry mediator and LIGHT/lymphotoxin beta receptor interactions decreases mortality in MHC class I and II disparate graft-vs-host disease. PMID: 15814693
  40. The expression of LIGHT inside tumors leads to rapid rejection in a natural killer-dependent manner. PMID: 16223768
  41. Our studies thus identify a what we believe to be a novel function of soluble LIGHT in vivo and offer a potential target for therapeutic interventions in hepatic inflammatory diseases PMID: 16557300
  42. We identified lymphotoxin (LT) and LIGHT, tumor necrosis factor cytokine family members that are primarily expressed on lymphocytes, as critical regulators of key enzymes that control lipid metabolism PMID: 17431181
  43. selective blockade of LIGHT-lymphotoxin beta receptor signaling protects mice from experimental cerebral malaria caused by Plasmodium berghei ANKA PMID: 19017933
  44. The inflammatory interaction between LIGHT & PAR-2 may be operating in vivo within an atherosclerotic lesions in ApoE(-) mice. LIGHT/PAR-2-driven inflammation could be a pathogenic loop in atherogenesis. PMID: 19023130
  45. LIGHT/HVEM signaling negatively regulates neurite growth from developing sensory neurons via NF-kappa B inhibition. PMID: 19211867

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Subcellular Location
Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 14, soluble form]: Secreted.
Protein Families
Tumor necrosis factor family
Database Links
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