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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.
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the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.
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Untreated children with IBD have higher percentage of DR3(+) PBMCs.
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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.
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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)
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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.
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Activation of DR3 is accompanied by inhibition of apoptosis of naive T-lymphocytes in children with acute infectious mononucleosis.
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Biologics beyond TNF-alpha inhibitors and the effect of targeting the homologues TL1A-DR3 pathway in chronic inflammatory disorders.
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Higher DR3 levels were associated with early stage chronic lymphocytic leukemia.
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DR3 is efficiently activated by soluble TL1A trimers.
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These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition.
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Human memory IL-18Ralpha and DR3 CD4+ T cells may contribute to antigen-independent innate responses at barrier surfaces.
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DR3 is expressed by IL-22-producing human group 3 innate lymphoid cells (ILC3s).
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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.
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Silencing of the DR3 gene affect levels of apoptosis antigen3 ligand in cells.
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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.
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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.
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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
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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.
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Suggest tectochrysin leads to apoptotic cell death in NSCLC cells through activation of DR3 and Fas expression via inhibition of STAT3 phosphorylation.
