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Hepatitis C virus modulates DR6 signaling pathway for viral propagation.DR6 is not involved in the entry, replication, and translation steps of the HCV life cycle.Hepatitis C virus NS5A protein specifically interacts with DR6.
MiR20a5p functioned as an oncogene in HNSCC by downregulating TNFRSF21.
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 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 to modulate synaptic density in the adult CNS
These results provide direct support for the model that APP 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.
DR6-induced apoptosis occurs through a new pathway that is different from the type I and type II pathways through interacting with Bax.
DR6 serum protein may be a tool to aid in the diagnosis of some sarcomatous tumors to improve treatment planning.
SAXS measurements on the ectodomain suggested that a dimer defines the minimal physical unit of an unliganded DR6 molecule in solution.
findings show that DR6 expression is significantly but transiently upregulated only in activated both CD4+ and CD8+ T cells in NF-kappaB and NF-AT dependent manner with a contribution of PI3K-dependent signaling
The model is used to provide a satisfying structural and energetic interpretation of DR6-growth factor-like domain of NAPP binding and to suggest the possibility of and a mechanism for spontaneous apoptosis.
androgen signaling pathway might cross talk with apoptosis signaling pathway through the interaction between ARA267-alpha and DR6
MMP-14 and DR6 are part of a mechanism tumor cells can employ to actively escape detection by the immune system by affecting the generation of antigen presenting cells
N-glycosylation of the extracellular part might participate in directing DR6 into lipid raft membrane microdomains.
DR6 contributes to autoimmunity in lupus-prone mice.
An orphan receptor, death receptor 6 (DR6), is required to drive Wallerian axon degeneration after axotomy in sympathetic and sensory neurons cultured in microfluidic devices.
miR-17-5p induction was verified during renal ischemia-reperfusion injury. The induction was mediated by p53 and, following induction, this microRNA may repress death receptor 6 (DR6) to protect kidney cells and tissues from injury.
This study demonistrated that DR6 to contribute to axonal pruning occurring during experience-dependent cortical plasticity throughout life.
A DR6/p75(NTR) complex is responsible for beta-amyloid-induced cortical neuron death.
Pla2g7 and Tnfrsf21 have been identified as genetic susceptibility to influenza genes in mice.
role in oligodendrocyte survival, differentiation and myelination
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.
point to a critical role of DR6 in regulating airway inflammation in the ovalbumin-induced mouse model of asthma
results indicate that APP and DR6 are components of a neuronal self-destruction pathway, and suggest that an extracellular fragment of APP, acting via DR6 and caspase 6, contributes to Alzheimer's disease
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