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The protein encoded by TNFSF14 is a member of the tumor necrosis factor (TNF) ligand family. Additionally we are shipping TNFSF14 Antibodies (166) and TNFSF14 Kits (34) and many more products for this protein.
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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.
LIGHT and LTBR (show LTBR Proteins) 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.
LIGHT, via LTbetaR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine (show CCL1 Proteins) production by bronchial epithelial cells.
LIGHT controls TSLP (show TSLP Proteins) to drive pulmonary fibrosis.
The tumor necrosis factor (show TNF Proteins) superfamily molecule LIGHT promotes keratinocyte activity and skin fibrosis.
proliferation and migration would be enhanced in Tca8113 cells with over-expressed TNFSF14
LIGHT, a TNF (show TNF Proteins) superfamily member, is involved in T-cell homeostasis and erosive bone disease associated with rheumatoid arthritis.
Crystal structures of LIGHT and the LIGHT:DcR3 complex reveal the structural basis for the DcR3 (show TNFRSF6B Proteins)-mediated neutralization of LIGHT.
regulation by NK cell licensing helps to safeguard against TNFSF14 production in response to healthy tissues.
TNFSF14 has an effect on the activation of basophils and eosinophils interacting with bronchial epithelial cells
The LIGHT (Tumour necrosis factor (show TNF Proteins) ligand superfamily member 14, TNFSF14)/Lymphotoxin beta-Receptor (show LTBR Proteins)(LTbeta (show LTB Proteins)-R) pathway, which is involved in T-cell and macrophage activation, was diminished in plasma and in apoE (show APOE Proteins)-/-Irs2 (show IRS2 Proteins)+/-HL-/- atheromas.
LIGHT signalling pathway combined with IFN-gamma (show IFNG Proteins) induces beta cells apoptosis via an NF-kappaB (show NFKB1 Proteins)/Bcl2 (show BCL2 Proteins)-dependent mitochondrial pathway.
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 (show CD4 Proteins)(+) CD25 (show IL2RA Proteins)(+) FoxP3 (show FOXP3 Proteins)(+) Treg cells, both of which may be essential for control of C. psittaci respiratory tract infection.
These results expose the relevance of LIGHT/LTbetaR/HVEM (show TNFRSF14 Proteins) interaction for the potential therapeutic control of the allogeneic immune responses mediated by alloreactive CD8 (show CD8A Proteins) T cells that can contribute to prolong allograft survival.
Mechanistically, intratumoral LIGHT induces pericyte differentiation and normalization via Rho kinase (show ROCK2 Proteins) signaling. Minute amounts of LIGHT act in a paracrine fashion to trigger an amplifying cascade involving transforming growth factor beta (TGF-beta) from peri (show POSTN Proteins)-vascular macrophages.
localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt (show AKT1 Proteins) signaling.
LIGHT-HVEM (show TNFRSF14 Proteins) interactions stimulate IL-12 (show IL12A Proteins) production by DCs during Leishmania donovani infection. Blockade of LIGHT-LTbetaR interactions dramatically enhanced early anti-parasitic immunity.
Although LIGHT is critical for maintenance of primary Th1 (show HAND1 Proteins) response, it is dispensable during secondary anti-Leishmania immunity in the presence of functional CD40 (show CD40 Proteins) signaling.
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.
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