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TNFRSF18 encodes a member of the TNF-receptor superfamily. Zusätzlich bieten wir Ihnen TNFRSF18 Proteine (35) und TNFRSF18 Kits (19) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 340 products:
Human Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN4896950
Godfrey, Spoden, Ge, Baker, Liu, Levine, June, Blazar, Porter: Cord blood CD4(+)CD25(+)-derived T regulatory cell lines express FoxP3 protein and manifest potent suppressor function. in Blood 2005
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Human Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN4896944
Mandapathil, Hilldorfer, Szczepanski, Czystowska, Szajnik, Ren, Lang, Jackson, Gorelik, Whiteside: Generation and accumulation of immunosuppressive adenosine by human CD4+CD25highFOXP3+ regulatory T cells. in The Journal of biological chemistry 2010
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Human Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN4896942
Tuyaerts, Van Meirvenne, Bonehill, Heirman, Corthals, Waldmann, Breckpot, Thielemans, Aerts: Expression of human GITRL on myeloid dendritic cells enhances their immunostimulatory function but does not abrogate the suppressive effect of CD4+CD25+ regulatory T cells. in Journal of leukocyte biology 2007
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Mouse (Murine) Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN4895259
Cobb, Hertweck, Smith, OConnor, Graf, Cook, Smale, Sakaguchi, Livesey, Fisher, Merkenschlager: A role for Dicer in immune regulation. in The Journal of experimental medicine 2006
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Mouse (Murine) Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN320239
Cobbold, Castejon, Adams, Zelenika, Graca, Humm, Waldmann: Induction of foxP3+ regulatory T cells in the periphery of T cell receptor transgenic mice tolerized to transplants. in Journal of immunology (Baltimore, Md. : 1950) 2004
Human Monoclonal TNFRSF18 Primary Antibody für FACS, ELISA - ABIN610417
Fallon, Moreau, Croft, Labib, Gu, Fon: Parkin and CASK/LIN-2 associate via a PDZ-mediated interaction and are co-localized in lipid rafts and postsynaptic densities in brain. in The Journal of biological chemistry 2002
Mouse (Murine) Monoclonal TNFRSF18 Primary Antibody für FACS - ABIN4895260
Fecci, Sweeney, Grossi, Nair, Learn, Mitchell, Cui, Cummings, Bigner, Gilboa, Sampson: Systemic anti-CD25 monoclonal antibody administration safely enhances immunity in murine glioma without eliminating regulatory T cells. in Clinical cancer research : an official journal of the American Association for Cancer Research 2006
Human Polyclonal TNFRSF18 Primary Antibody für WB - ABIN2792139
Liu, Li, Mahesh, Pantanelli, Hwang, Siu, Nussenblatt: Glucocorticoid-induced tumor necrosis factor receptor negatively regulates activation of human primary natural killer (NK) cells by blocking proliferative signals and increasing NK cell apoptosis. in The Journal of biological chemistry 2008
Human Polyclonal TNFRSF18 Primary Antibody für IHC, WB - ABIN2792138
Clark, Gurney, Abaya, Baker, Baldwin, Brush, Chen, Chow, Chui, Crowley, Currell, Deuel, Dowd, Eaton, Foster, Grimaldi, Gu, Hass, Heldens, Huang, Kim, Klimowski, Jin, Johnson, Lee, Lewis, Liao, Mark et al.: The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment. ... in Genome research 2003
Expression of human GITR was comparable with that of mouse GITR in tumor-infiltrating Tregs despite being drastically lower in other human TILs and in many human peripheral blood populations.
anti-GITR mAb shifts Treg populations to enable immune attack on tumors, with clinical implications for molecular markers to modify emerging treatments.
Continuous GITR stimulation through B cell Gitrl (zeige TNFSF18 Antikörper) acts protective in a mouse model of atherosclerosis by regulating the balance between regulatory and effector memory CD4 (zeige CD4 Antikörper)(+) T cells.
these results indicate that blockade of GITR signaling can ameliorate arthritis progression mainly by modulating the follicular helper T cell response
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 (zeige PTPN22 Antikörper) 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 (zeige CD8A Antikörper) T cell compartment by boosting CD4 (zeige CD4 Antikörper) T cell help.
HTLV-1 infection can modify the expression of main functional transcription factors, FOXP3 (zeige FOXP3 Antikörper) and GITR
a novel molecular mechanism by which MBD4 (zeige MBD4 Antikörper) inhibits GITR expression in a DNMT1 (zeige DNMT1 Antikörper)-dependent manner
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 (zeige NFKB1 Antikörper) activation.
Data may suggest a key role of regulatory GITR+CD25 (zeige IL2RA Antikörper) low/-CD4 (zeige CD4 Antikörper)+ 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 (zeige EXTL3 Antikörper)) cells, suggesting that GITR is a T(reg (zeige EXTL3 Antikörper))-cell marker that would be primarily involved in T(reg (zeige EXTL3 Antikörper))-cell survival rather than in their suppressor function.
Our findings indicate the possible involvement of GITR-GITRL (zeige TNFSF18 Antikörper) pathway in the pathogenesis of pSS (zeige CDSN Antikörper).
GITR acts as a potential tumor suppressor in MM.
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