Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
Untreated children with IBD have higher percentage of DR3(+) PBMCs.
In addition to apoptosis, DR3 can robustly trigger necroptotic cell death and provide evidence for TL1A (show TNFSF15 ELISA Kits)-induced, DR3-mediated necrosome assembly. DR3-mediated necroptosis critically depends on receptor-interacting protein 1 (RIP1 (show RIPK1 ELISA Kits)) and RIP3 (show RIPK3 ELISA Kits), the core components of the necroptotic machinery, which activate the pseudo-kinase mixed lineage kinase domain-like, the prototypic downstream effector molecule of necroptosis.
Data suggest that human regulatory T-lymphocytes express DR3 and demonstrate DR3/TL1A (show TNFSF15 ELISA Kits)-mediated activation of signaling via MAP kinases and NFkappaB (show NFKB1 ELISA Kits). (DR3 = death receptor 3; TL1A/TNFSF15 (show TNFSF15 ELISA Kits) = tumor necrosis factor (show TNF ELISA Kits) [ligand] superfamily, member 15)
These results raise the possibility for involvement of TL1A (show TNFSF15 ELISA Kits)/DR3/DR3-mediated mechanisms in epithelial-mesenchymal interactions and the development of inflammation-induced intestinal fibrosis in Crohn's disease.
Activation of DR3 is accompanied by inhibition of apoptosis of naive T-lymphocytes in children with acute infectious mononucleosis.
Biologics beyond TNF-alpha (show TNF ELISA Kits) inhibitors and the effect of targeting the homologues TL1A (show TNFSF15 ELISA Kits)-DR3 pathway in chronic inflammatory disorders.
Higher DR3 levels were associated with early stage chronic lymphocytic leukemia.
DR3 is efficiently activated by soluble TL1A (show TNFSF15 ELISA Kits) trimers.
These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition.
Human memory IL-18Ralpha and DR3 CD4 (show CD4 ELISA Kits)+ T cells may contribute to antigen-independent innate responses at barrier surfaces.
This work describes both a novel function and essential requirement for the DR3/TL1A (show TNFSF15 ELISA Kits) pathway in acute, resolving, and chronic inflammation in the peritoneal cavity.
this study shows that DR3 signaling protects mice from acute dextran sodium sulfate colitis because DR3-/- mice showed more severe mucosal inflammation and increased mortality
the critical effect of the state of T-cell activation on clinical outcomes after activation of DR3, is reported.
Data indicate that death receptor 3 (DR3) depletion gives rise to an increased anti-apoptotic potential.
these data identify TL1A (show TNFSF15 ELISA Kits)-DR3 interactions as a novel pathway that promotes Th9 differentiation and pathogenicity. TL1A (show TNFSF15 ELISA Kits) may be a potential therapeutic target in diseases dependent on IL-9 (show IL9 ELISA Kits).
TL1A (show TNFSF15 ELISA Kits) induces NF-kappaB (show NFKB1 ELISA Kits) activation in EC in renal and cardiac tissue from wild type but not DR3 knock-out mice.
Both in supernatant and as purified fusion protein, TL1A (show TNFSF15 ELISA Kits)-Ig binds to TNFRSF25 transfected--but not untransfected--P815 tumor cells as determined by flow cytometry.
TNFRSF25 agonists expand Tregs in vivo and delay cardiac allograft rejection.
TNFRSF25 agonistic antibody and galectin-9 (show LGALS9 ELISA Kits) combination therapy controls herpes simplex virus-induced immunoinflammatory lesions
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is expressed preferentially in the tissues enriched in lymphocytes, and it may play a role in regulating lymphocyte homeostasis. This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domain containing adaptor proteins. Knockout studies in mice suggested the role of this gene in the removal of self-reactive T cells in the thymus. Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, most of which are potentially secreted molecules. The alternative splicing of this gene in B and T cells encounters a programmed change upon T-cell activation, which predominantly produces full-length, membrane bound isoforms, and is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation.
tumor necrosis factor receptor superfamily, member 25
, apoptosis inducing receptor
, apoptosis-inducing receptor AIR
, apoptosis-mediating receptor DR3
, apoptosis-mediating receptor TRAMP
, death domain receptor 3 soluble form
, death receptor beta
, lymphocyte-associated receptor of death
, protein WSL-1
, tumor necrosis factor receptor superfamily member 25
, tumor necrosis factor receptor superfamily, member 12 (translocating chain-association membrane protein)
, tumor necrosis factor receptor superfamily, member 12
, translocating chain-association membrane protein
, tumor necrosis factor receptor superfamily, member12