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Knockdown death receptor 6 by shRNA in human pDCs cell line GEN2.2 significantly diminished the CpG-ODN induced IFN-regulatory factor 7 nuclear localization and IFN-I production.
data identify a new mechanism underlying tumour cell extravasation and metastasis, and suggest endothelial DR6-mediated necroptotic signalling pathways as targets for anti-metastatic therapies
Increase in the expression levels of mRNA and protein for the death receptor 6 is associated with various types of gynaecological malignancy.
Circulating levels of DR6 and Gpm6B (show GPM6B ELISA Kits) correlate with breast cancer tumor grade.
The present findings suggested that DR6 is involved in the pathogenesis of endometriosis by creating the proliferative and anti-apoptotic characteristics of endometriosis.
Our results support the view that DR6 functions with APP (show APP ELISA Kits) to modulate synaptic density in the adult CNS
These results provide direct support for the model that APP (show APP ELISA Kits) and DR6 function cell autonomously and in the same pathway to control pruning
our findings provide new insight into a novel mechanism by which DR6 induces downstream signaling in response to an agonist antibody.
DR6 knockout mice are viable and fertile, and show hyperproliferation of T cells when stimulated.
DR6 mediates T cell proliferation and differentiation in mice.
miR-17-5p induction was verified during renal ischemia-reperfusion injury. The induction was mediated by p53 (show TP53 ELISA Kits) and, following induction, this microRNA may repress death receptor 6 (DR6) to protect kidney cells and tissues from injury.
Transmembrane APP (show APP ELISA Kits) expressed by tumor cells binds to endothelial DR6 to trigger necroptosis, and targeting DR6-mediated endothelial cell necroptosis may be a potential therapeutic strategy
This study demonistrated that DR6 to contribute to axonal pruning occurring during experience-dependent cortical plasticity throughout life.
A DR6/p75(NTR (show NGFR ELISA Kits)) complex is responsible for beta-amyloid-induced cortical neuron death.
Pla2g7 (show Lp-PLA2 ELISA Kits) and Tnfrsf21 have been identified as genetic susceptibility to influenza genes in mice.
findings show that DR6 expression is significantly but transiently upregulated only in activated both CD4 (show CD4 ELISA Kits)+ and CD8 (show CD8A ELISA Kits)+ T cells in NF-kappaB (show NFKB1 ELISA Kits) and NF-AT (show NFATC3 ELISA Kits) dependent manner with a contribution of PI3K-dependent signaling
T cells lacking the DR6 receptor generate a severe form of acute graft-versus-host disease with accelerated onset, increased severity, rapid weight loss, and earlier organ damage and mortality.
Enhanced B cell expansion, survival, and humoral responses by targeting death receptor 6.
Death receptor 6 plays an important role in regulating leukocyte infiltration and function in the induction and progression of experimental autoimmune encephalomyelitis.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor has been shown to activate NF-kappaB and MAPK8/JNK, and induce cell apoptosis. Through its death domain, this receptor interacts with TRADD protein, which is known to serve as an adaptor that mediates signal transduction of TNF-receptors. Knockout studies in mice suggested that this gene plays a role in T-helper cell activation, and may be involved in inflammation and immune regulation.
tumor necrosis factor receptor superfamily, member 21
, tumor necrosis factor receptor superfamily member 21-like
, TNFR-related death receptor 6
, death receptor 6
, tumor necrosis factor receptor superfamily member 21
, Death receptor 6
, TNFR-related death receptor-6