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Human TNFRSF21 Protein expressed in Human Cells - ABIN2002244
Kasof, Lu, Liu, Speer, Mongan, Gomes, Lorenzi: Tumor necrosis factor-alpha induces the expression of DR6, a member of the TNF receptor family, through activation of NF-kappaB. in Oncogene 2001
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Cynomolgus TNFRSF21 Protein expressed in Human Cells - ABIN2010155
Pan, Bauer, Haridas, Wang, Liu, Yu, Vincenz, Aggarwal, Ni, Dixit: Identification and functional characterization of DR6, a novel death domain-containing TNF receptor. in FEBS letters 1998
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Human TNFRSF21 Protein expressed in Human Cells - ABIN2002248
Zhao, Yan, Wang, Erickson, Grewal, Dixit: Impaired c-Jun amino terminal kinase activity and T cell differentiation in death receptor 6-deficient mice. in The Journal of experimental medicine 2001
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Mouse (Murine) TNFRSF21 Protein expressed in Human Cells - ABIN2007584
Liu, Heuer, Na, Galbreath, Zhang, Yang, Glasebrook, Song: Accelerated onset and increased severity of acute graft-versus-host disease following adoptive transfer of DR6-deficient T cells. in Journal of immunology (Baltimore, Md. : 1950) 2002
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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 Proteins) 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 Proteins) to modulate synaptic density in the adult CNS
These results provide direct support for the model that APP (show APP Proteins) 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.
This study demonistrated that DR6 to contribute to axonal pruning occurring during experience-dependent cortical plasticity throughout life.
A DR6/p75(NTR (show NGFR Proteins)) complex is responsible for beta-amyloid-induced cortical neuron death.
Pla2g7 (show Lp-PLA2 Proteins) 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 Proteins)+ and CD8 (show CD8A Proteins)+ T cells in NF-kappaB (show NFKB1 Proteins) and NF-AT (show NFATC3 Proteins) 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.
point to a critical role of DR6 in regulating airway inflammation in the ovalbumin (show OVA Proteins)-induced mouse model of asthma
results indicate that APP (show APP Proteins) and DR6 are components of a neuronal self-destruction pathway, and suggest that an extracellular fragment of APP (show APP Proteins), acting via DR6 and caspase 6 (show CASP6 Proteins), 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