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Hypermethylation of the proapoptotic genes BCL2 L11 and TNFRSF25 is observed in pleomorphic adenoma of the salivary glands. However, this phenomenon did not impact mRNA transcription.
the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.
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-induced, DR3-mediated necrosome assembly. DR3-mediated necroptosis critically depends on receptor-interacting protein 1 (RIP1) and RIP3, 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-mediated activation of signaling via MAP kinases and NFkappaB. (DR3 = death receptor 3; TL1A/TNFSF15 = tumor necrosis factor [ligand] superfamily, member 15)
These results raise the possibility for involvement of TL1A/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 inhibitors and the effect of targeting the homologues TL1A-DR3 pathway in chronic inflammatory disorders.
Higher DR3 levels were associated with early stage chronic lymphocytic leukemia.
DR3 is efficiently activated by soluble TL1A trimers.
These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition.
Human memory IL-18Ralpha and DR3 CD4+ T cells may contribute to antigen-independent innate responses at barrier surfaces.
DR3 is expressed by IL-22-producing human group 3 innate lymphoid cells (ILC3s).
These results suggested that TL1A could promote Th17 differentiation in rheumatoid arthritis via the activation of RORc, and this effect may be mediated by the binding of TL1A with DR3.
Silencing of the DR3 gene affect levels of apoptosis antigen3 ligand in cells.
DR3 is expressed in some interstitial vascular endothelial cells in human kidney in situ. These EC also respond to TL1A by activating NF-kappaB. Very low levels of DR3 are seen on the cell surface of HUVEC, which do not respond to TL1A.
The changes in frequency of occurrence of spliced variants of DR3/LARD mRNA were directed towards modulation of apoptosis and restraint of antiviral immune response.
Distinctions in occurrence of spectrums of DR3/LARD mRNA at healthy volunteers and colon cancer patients can define a different susceptibility of immunocompetent and tumor cells for apoptosis
DR-3 drives early cartilage destruction in the antigen-induced model of inflammatory arthritis through the release of CXCL1, maximizing neutrophil recruitment to the joint and leading to enhanced local production of cartilage-destroying enzymes.
Suggest tectochrysin leads to apoptotic cell death in NSCLC cells through activation of DR3 and Fas expression via inhibition of STAT3 phosphorylation.
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.
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
, tumor necrosis factor receptor superfamily, member 25
, translocating chain-association membrane protein
, tumor necrosis factor receptor superfamily, member12