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Validated All-in-One™ qPCR Primer for TNFRSF18(NM_148901.2) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is a member of the TNF-receptor superfamily. This 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. [provided by RefSeq].
Gene References into function
- GITR rapidly recruits TNF receptor-associated factor 2 (TRAF2) in a ligand-dependent manner; data indicate that the cytoplasmic domain of GITR contains a single TRAF binding site where acidic residues 202/203 and 211-213 are critical for this interaction
- Since regulatory T-cells are localized in the vicinity of GITRL-expressing cells in atopic dermatitis skin, the GITR/GITRL interaction may serve to perpetuate the inflammation locally.
- This protein has been shown to stimulate T cell-mediated antitumor immunity in mice, and now in a human tumor cell line.
- These data suggest that, despite abnormal GITR expression during HIV infection, GITR triggering enhances HIV-specific CD4(+) T cell cytokine expression and protects HIV-specific CD4(+) T cells from apoptosis.
- although GITR is an activation marker for NK cells similar to that for T cells, GITR serves as a negative regulator for NK cell activation
- CD4(+)CD25(+) effector memory T-cells expressing CD134 and GITR seem to play a role in disease mechanisms, as suggested by their close association with disease activity and their participation in the inflammatory process in Wegener's granulomatosis.
- mechanism of IgG4 induction by regulatory cells involves GITR-GITR-L interactions, IL-10 and TGF-beta.
- Data show that in humans GITRL expression subverts NK cell immunosurveillance of AML.