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The protein encoded by TNFSF14 is a member of the tumor necrosis factor (TNF) ligand family. Zusätzlich bieten wir Ihnen TNFSF14 Kits (32) und TNFSF14 Proteine (26) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 159 products:
Human Monoclonal TNFSF14 Primary Antibody für 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
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Human Monoclonal TNFSF14 Primary Antibody für FACS - ABIN4897779
Celik, Langer, Stellos, May, Shankar, Kurz, Katus, Gawaz, Dengler: Platelet-associated LIGHT (TNFSF14) mediates adhesion of platelets to human vascular endothelium. in Thrombosis and haemostasis 2007
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Human Monoclonal TNFSF14 Primary Antibody für ELISA (Capture), FACS - ABIN4900484
Wang, Wen, Routy, Bernard, Sekaly, Watts et al.: 4-1BBL induces TNF receptor-associated factor 1-dependent Bim modulation in human T cells and is a critical component in the costimulation-dependent rescue of functionally impaired HIV-specific CD8 T ... in Journal of immunology (Baltimore, Md. : 1950) 2007
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Human Monoclonal TNFSF14 Primary Antibody für FACS - ABIN4897778
Holmes, Wilson, Black, Benest, Vaz, Tan, Tanavde, Cook: Licensed human natural killer cells aid dendritic cell maturation via TNFSF14/LIGHT. in Proceedings of the National Academy of Sciences of the United States of America 2014
Human Polyclonal TNFSF14 Primary Antibody für ELISA, WB - ABIN4330966
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 is highly expressed and companied with severe inflammations in patients with coronary disease. LIGHT significantly enhanced inflammation response in oxLDL-induced THP-1 (zeige GLI2 Antikörper) macrophages.
LIGHT and LTBR (zeige LTBR Antikörper) 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 (zeige CCL1 Antikörper) production by bronchial epithelial cells.
LIGHT controls TSLP (zeige TSLP Antikörper) to drive pulmonary fibrosis.
The tumor necrosis factor (zeige TNF Antikörper) 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 (zeige TNF Antikörper) 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 (zeige TNFRSF6B Antikörper)-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
LIGHT signalling pathway combined with IFN-gamma (zeige IFNG Antikörper) induces beta cells apoptosis via an NF-kappaB (zeige NFKB1 Antikörper)/Bcl2 (zeige BCL2 Antikörper)-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 (zeige CD4 Antikörper)(+) CD25 (zeige IL2RA Antikörper)(+) FoxP3 (zeige FOXP3 Antikörper)(+) 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 (zeige TNFRSF14 Antikörper) interaction for the potential therapeutic control of the allogeneic immune responses mediated by alloreactive CD8 (zeige CD8A Antikörper) T cells that can contribute to prolong allograft survival.
Mechanistically, intratumoral LIGHT induces pericyte differentiation and normalization via Rho kinase (zeige ROCK2 Antikörper) signaling. Minute amounts of LIGHT act in a paracrine fashion to trigger an amplifying cascade involving transforming growth factor beta (TGF-beta) from peri (zeige POSTN Antikörper)-vascular macrophages.
localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt (zeige AKT1 Antikörper) signaling.
LIGHT-HVEM (zeige TNFRSF14 Antikörper) interactions stimulate IL-12 (zeige IL12A Antikörper) 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 (zeige HAND1 Antikörper) response, it is dispensable during secondary anti-Leishmania immunity in the presence of functional CD40 (zeige CD40 Antikörper) signaling.
LIGHT protein is rapidly and transiently expressed after T-cell activation, and this expression is stronger on CD8 (zeige CD8A Antikörper) T cells than on CD4 (zeige CD4 Antikörper) T cells
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