Tumor Necrosis Factor (Ligand) Superfamily, Member 14 (TNFSF14) ELISA Kits

The protein encoded by TNFSF14 is a member of the tumor necrosis factor (TNF) ligand family. Additionally we are shipping TNFSF14 Antibodies (203) and TNFSF14 Proteins (42) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
TNFSF14 8740 O43557
TNFSF14 301133  
TNFSF14 50930 Q9QYH9
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Top TNFSF14 ELISA Kits at antibodies-online.com

Showing 8 out of 46 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 7.81 pg/mL 31.2-2000 pg/mL Typical standard curve 96 Tests Log in to see 15 to 18 Days
$788.33
Details
Mouse 6.0 pg/mL 15.6 pg/mL - 1000 pg/mL 96 Tests Log in to see 13 to 16 Days
$682.11
Details
Rat 3.91 pg/mL 15.6-1000 pg/mL   96 Tests Log in to see 13 to 16 Days
$788.33
Details
Pig 18.75 pg/mL 31.25-2000 pg/mL   96 Tests Log in to see 12 to 14 Days
$715.00
Details
Rabbit 0.75 pg/mL 1.25-80 pg/mL   96 Tests Log in to see 12 to 14 Days
$715.00
Details
Chicken 0.938 pg/mL 1.563-100 pg/mL   96 Tests Log in to see 12 to 14 Days
$715.00
Details
Monkey 18.75 pg/mL 31.25-2000 pg/mL   96 Tests Log in to see 12 to 14 Days
$715.00
Details
Sheep 9.375 pg/mL 15.625 pg/mL - 1000 pg/mL   96 Tests Log in to see 11 to 18 Days
$824.38
Details

More ELISA Kits for TNFSF14 Interaction Partners

Human Tumor Necrosis Factor (Ligand) Superfamily, Member 14 (TNFSF14) interaction partners

  1. 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

  2. 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.

  3. 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.

  4. Serum LIGHT levels correlate with disease progression and severity in interstitial pneumonia patients with dermatomyositis.

  5. LIGHT, via LTbetaR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine production by bronchial epithelial cells.

  6. LIGHT controls TSLP to drive pulmonary fibrosis.

  7. The tumor necrosis factor superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis.

  8. proliferation and migration would be enhanced in Tca8113 cells with over-expressed TNFSF14

  9. LIGHT, a TNF superfamily member, is involved in T-cell homeostasis and erosive bone disease associated with rheumatoid arthritis.

  10. Crystal structures of LIGHT and the LIGHT:DcR3 complex reveal the structural basis for the DcR3-mediated neutralization of LIGHT.

  11. regulation by NK cell licensing helps to safeguard against TNFSF14 production in response to healthy tissues.

  12. The findings suggest a new molecular determinant of LIGHT-mediated pathogenic changes in human bronchial epithelial cells.

  13. TNFSF14 has an effect on the activation of basophils and eosinophils interacting with bronchial epithelial cells

  14. Triggering of LIGHT induced production of pro-inflammatory mediators such as interleukin-8 and matrix metalloproteinase-9 while suppressing the phagocytic activity.

  15. GG carriers of rs1077667, of the LIGHT gene, with the highest risk for Multiple Sclerosis, had the lowest serum levels.

  16. 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

  17. 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

  18. TNFSF14 was significantly increased in sickle-cell anemia, SCA treated with hydroxycarbamide,& HbSC. It could contribute to endothelial activation & inflammation in SCA.

  19. This study showed that expression of the death-triggering ligand LIGHT is increased in ALS spinal cords

  20. increased plasma levels in patients with atopic dermatitis

Mouse (Murine) Tumor Necrosis Factor (Ligand) Superfamily, Member 14 (TNFSF14) interaction partners

  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

  2. Blockade of LIGHT markedly suppressed airway smooth muscle hyperplasia and inflammatory responses, which might be modulated through HVEM-NFkappaB or c-JUN pathways.

  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.

  4. LIGHT promote myeloid differentiation of Hematopoietic stem/progenitor cells via LIGHT receptor signaling.

  5. LIGHT signalling pathway combined with IFN-gamma induces beta cells apoptosis via an NF-kappaB/Bcl2-dependent mitochondrial pathway.

  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.

  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.

  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.

  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.

  10. localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt signaling.

  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.

  12. LIGHT controls TSLP to drive pulmonary fibrosis.

  13. The tumor necrosis factor superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis.

  14. Although LIGHT is critical for maintenance of primary Th1 response, it is dispensable during secondary anti-Leishmania immunity in the presence of functional CD40 signaling.

  15. LIGHT signal pathway is not correlated with protection against Chlamydia muridarum urogenital tract infection.

  16. 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

  17. 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.

  18. 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.

  19. 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.

  20. 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.

TNFSF14 Antigen Profile

Antigen Summary

The protein encoded by this gene is a member of the tumor necrosis factor (TNF) ligand family. This protein is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and which is also known as a herpesvirus entry mediator (HVEM). This protein may function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. This protein has been shown to stimulate the proliferation of T cells, and trigger apoptosis of various tumor cells. This protein is also reported to prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.

Gene names and symbols associated with TNFSF14

  • TNF superfamily member 14 (TNFSF14) antibody
  • TNF superfamily member 14 (Tnfsf14) antibody
  • tumor necrosis factor (ligand) superfamily, member 14 (Tnfsf14) antibody
  • CD258 antibody
  • HVEM-L antibody
  • HVEML antibody
  • LIGHT antibody
  • LTg antibody
  • Ly113 antibody
  • TNFSF14 antibody
  • TR2 antibody

Protein level used designations for TNFSF14

tumor necrosis factor ligand superfamily, member 14 , tumor necrosis factor (ligand) superfamily, member 14 , delta transmembrane LIGHT , herpes virus entry mediator ligand , herpesvirus entry mediator A , herpesvirus entry mediator ligand , herpesvirus entry mediator-ligand , ligand for herpesvirus entry mediator , tumor necrosis factor ligand superfamily member 14 , tumor necrosis factor receptor-like 2 , tumor necrosis factor superfamily member LIGHT , tumor necrosis factor superfamily member 14 , tumor necrosis factor superfamily, member 14

GENE ID SPECIES
468687 Pan troglodytes
701451 Macaca mulatta
8740 Homo sapiens
301133 Rattus norvegicus
611306 Canis lupus familiaris
100519468 Sus scrofa
505521 Bos taurus
50930 Mus musculus
100347876 Oryctolagus cuniculus
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