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TNFRSF18 encodes a member of the TNF-receptor superfamily. Additionally we are shipping TNFRSF18 Antibodies (321) and TNFRSF18 Kits (19) and many more products for this protein.
Showing 10 out of 30 products:
Human TNFRSF18 Protein expressed in HEK-293 Cells - ABIN2181162
Gurney, Marsters, Huang, Pitti, Mark, Baldwin, Gray, Dowd, Brush, Heldens, Schow, Goddard, Wood, Baker, Godowski, Ashkenazi: Identification of a new member of the tumor necrosis factor family and its receptor, a human ortholog of mouse GITR. in Current biology : CB 1999
GITR appears as a potential target for intervention during infection by the parasite Toxoplasma gondii, even though further studies are still necessary to better characterize the immune response triggered by GITR activation during T. gondii infection
our data suggest a critical role for GITR in Treg cell homeostasis and indicate that Ptpn22 (show PTPN22 Proteins) independently affects the differentiation status of Treg cells and their homeostatic behavior
These findings provide further support for the continued development of agonist anti-GITR antibodies as an immunotherapeutic strategy for osteosarcoma. We suggest that our proposed immunotherapy could be developed further to improve osteosarcoma treatment
Th9 cells and iTregs are developmentally linked and GITR can subvert tolerogenic conditions to boost Th9 immunity.
GITR is a crucial player in differentiation of thymic regulatory T cells and expansion of regulatory T cells, including both thymic regulatory T cells and peripheral regulatory T cells.
enhanced GITR-triggering mediates its protective, anti-viral effect on the CD8 (show CD8A Proteins) T cell compartment by boosting CD4 (show CD4 Proteins) T cell help.
A CD4 (show CD4 Proteins) T cell-intrinsic role for GITR in sustaining early CD8 (show CD8A Proteins) and late humoral responses to collectively promote control of chronic LCMV clone 13 infection.
GITRL (show TNFSF18 Proteins) expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR-dependent actions. The GITRL (show TNFSF18 Proteins)-GITR pathway might represent a novel target for the treatment of neuropathic pain.
Data show that GITR agonist antibody alters Treg lineage stability inducing an inflammatory effector T cell phenotype. The resultant loss of lineage stability causes Treg to lose their intra-tumor immune suppressive function.
Gene expression in the Gitr locus is regulated by NF-kappaB (show NFKB1 Proteins) and Foxp3 (show FOXP3 Proteins) through an enhancer.
Aberrant expression of GITR may contribute to systemic lupus erithematosus pathogenesis. Glucocorticoid may achieve its therapeutic effect partly by inducing GITR expression on Tresps rather than Tregs, which initiates the apoptosis of Tresp cells in SLE patients.
GITR expression can enhance the sensitivity to Bortezomib by inhibiting Bortezomib-induced NF-kappaB (show NFKB1 Proteins) activation.
Data may suggest a key role of regulatory GITR+CD25 (show IL2RA Proteins) low/-CD4 (show CD4 Proteins)+ T cells subset in the modulation of the abnormal immune response in lupus erythematosus (SLE) patients.
results suggest that the GITR rs3753348 polymorphism may be involved in the development and susceptibility of CWP.
these results show a higher susceptibility to apoptosis in patients' versus controls' T(reg (show EXTL3 Proteins)) cells, suggesting that GITR is a T(reg (show EXTL3 Proteins))-cell marker that would be primarily involved in T(reg (show EXTL3 Proteins))-cell survival rather than in their suppressor function.
Our findings indicate the possible involvement of GITR-GITRL (show TNFSF18 Proteins) pathway in the pathogenesis of pSS (show CDSN Proteins).
GITR acts as a potential tumor suppressor in MM.
Data indicate that the mRNAs of CTLA-4 (show CTLA4 Proteins) and GITR genes were expressed at lower levels in CVID (show TNFRSF13B Proteins) patients compared to control group.
GITR is pathologically expressed on Treg cells in systemic lupus erythematosus.
This gene encodes a member of the TNF-receptor superfamily. The encoded receptor has been shown to have increased expression upon T-cell activation, and it is thought to play a key role in dominant immunological self-tolerance maintained by CD25(+)CD4(+) regulatory T cells. Knockout studies in mice also suggest the role of this receptor is in the regulation of CD3-driven T-cell activation and programmed cell death. Three alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.
tumor necrosis factor receptor superfamily member 18
, glucocorticoid-induced TNFR-related
, tumor necrosis factor receptor superfamily, member 18
, glucocorticoid-induced TNFR-related protein
, TNF receptor superfamily activation-inducible protein
, activation-inducible TNFR family receptor