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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 (显示 GPM6B ELISA试剂盒) 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 (显示 APP ELISA试剂盒) to modulate synaptic density in the adult CNS
These results provide direct support for the model that APP (显示 APP ELISA试剂盒) 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 (显示 TP53 ELISA试剂盒) and, following induction, this microRNA may repress death receptor 6 (DR6) to protect kidney cells and tissues from injury.
Transmembrane APP (显示 APP ELISA试剂盒) 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 (显示 NGFR ELISA试剂盒)) complex is responsible for beta-amyloid-induced cortical neuron death.
Pla2g7 (显示 Lp-PLA2 ELISA试剂盒) 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 (显示 CD4 ELISA试剂盒)+ and CD8 (显示 CD8A ELISA试剂盒)+ T cells in NF-kappaB (显示 NFKB1 ELISA试剂盒) and NF-AT (显示 NFATC3 ELISA试剂盒) 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