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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 Kits (25) and TNFSF14 Proteins (20) and many more products for this protein.
Showing 10 out of 124 products:
Human Monoclonal TNFSF14 Primary Antibody for FACS - ABIN2663234
Mauri, Ebner, Montgomery, Kochel, Cheung, Yu, Ruben, Murphy, Eisenberg, Cohen, Spear, Ware: LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. in Immunity 1998
Show all 5 references for ABIN2663234
Human Monoclonal TNFSF14 Primary Antibody for FACS, IP - ABIN2661013
Morel, Schiano de Colella, Harrop, Deen, Holmes, Wattam, Khandekar, Truneh, Sweet, Gastaut, Olive, Costello: Reciprocal expression of the TNF family receptor herpes virus entry mediator and its ligand LIGHT on activated T cells: LIGHT down-regulates its own receptor. in Journal of immunology (Baltimore, Md. : 1950) 2000
Show all 5 references for ABIN2661013
Human Polyclonal TNFSF14 Primary Antibody for EIA, WB - ABIN452686
Cohavy, Zhou, Ware, Targan: LIGHT is constitutively expressed on T and NK cells in the human gut and can be induced by CD2-mediated signaling. in Journal of immunology (Baltimore, Md. : 1950) 2005
LIGHT, via LTbetaR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine (show CCL1 Antibodies) production by bronchial epithelial cells.
LIGHT controls TSLP (show TSLP Antibodies) to drive pulmonary fibrosis.
The tumor necrosis factor (show TNF Antibodies) 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 Antibodies) 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 Antibodies)-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
Triggering of LIGHT induced production of pro-inflammatory mediators such as interleukin-8 (show IL8 Antibodies) and matrix metalloproteinase-9 (show MMP9 Antibodies) while suppressing the phagocytic activity.
findings show that LIGHT is not inhibited by the soluble RANKL (show TNFSF11 Antibodies) receptor OPG (show TNFRSF11B Antibodies) and that LIGHT is a potent osteoclastogenesis factor that activates the Akt (show AKT1 Antibodies), NFkappaB (show NFKB1 Antibodies) and JNK (show MAPK8 Antibodies) pathways
localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt (show AKT1 Antibodies) signaling.
LIGHT-HVEM (show TNFRSF14 Antibodies) interactions stimulate IL-12 (show IL12A Antibodies) 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 Antibodies) response, it is dispensable during secondary anti-Leishmania immunity in the presence of functional CD40 (show CD40 Antibodies) signaling.
LIGHT protein is rapidly and transiently expressed after T-cell activation, and this expression is stronger on CD8 (show CD8A Antibodies) T cells than on CD4 (show CD4 Antibodies) T cells
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.
Tnfsf14(-/-) mice develop more severe colitis than control mice. LIGHT signals through the lymphotoxin beta receptor (show LTBR Antibodies) in the colon to regulate the innate immune response and mediate recovery from intestinal inflammation.
interaction of LIGHT with LTbetaR on hepatocytes, but not Kupffer cells, is sufficient to down regulate hepatic lipase (show LIPC Antibodies) expression and that this effect can be independent of LIGHT's costimulatory function.
Here we show that deletion of tumor necrosis factor (show TNF Antibodies) superfamily member 14 (TNFSF14/LIGHT) leads to impaired wounds in mice that have the characteristics of nonchronic and chronic ulcers.
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