|Application ||WB, ICC, E|
|Other Accession||Q9UNG2, 13124621|
|Calculated MW||22724 Da|
|Application Notes||GITRL antibody can be used for the detection of GITRL by Western blot at 1 µg/mL. Antibody can also be used for immunocytochemistry starting at 10 µg/mL.|
|Other Names||GITRL Antibody: TL6, AITRL, GITRL, hGITRL, TL6, UNQ149/PRO175, Tumor necrosis factor ligand superfamily member 18, Activation-inducible TNF-related ligand, tumor necrosis factor (ligand) superfamily, member 18|
|Reconstitution & Storage||GITRL antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||GITRL Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||AITRL, GITRL, TL6|
|Function||Cytokine that binds to TNFRSF18/AITR/GITR. Regulates T- cell responses. Can function as costimulator and lower the threshold for T-cell activation and T-cell proliferation. Important for interactions between activated T-lymphocytes and endothelial cells. Mediates activation of NF-kappa-B. Triggers increased phosphorylation of STAT1 and up-regulates expression of VCAM1 and ICAM1 (PubMed:23892569). Promotes leukocyte adhesion to endothelial cells (PubMed:23892569). Regulates migration of monocytes from the splenic reservoir to sites of inflammation (By similarity).|
|Cellular Location||Cell membrane; Single-pass type II membrane protein|
|Tissue Location||Expressed at high levels in the small intestine, ovary, testis, kidney and endothelial cells|
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Provided below are standard protocols that you may find useful for product applications.
GITRL Antibody: The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation, differentiation, and survival through regulating the activation of the transcription factor NF-κB and various mitogen-activated protein kinases. The glucocorticoid-induced tumor necrosis factor receptor (GITR) is an emerging member of this family that is expressed on CD4+ CD25+ regulatory T cells and appears to have crucial immune regulation functions. Its ligand GITRL is expressed in endothelial and antigen-presenting cells and can activate NF-κB, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR. Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-κB activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.
Gaur U, Aggarwal BB. Regulation of proliferation, survival and apoptosis by members of the TNF superfamily. Biochem. Pharmacol. 2003; 66:1403-8.
Ronchetti S, Nocentini G, Riccardi C, et al. Role of GITR in activation response of T lymphocytes.Blood 2002; 100:350-2.
Shimizu J, Yamakai S, Takahashi T, et al. Stimulation of CD25(+) CD4(+) regulatory T cells through GITR breaks immunological self- tolerance. Nat. Immunol. 2002;3:135-42.
Gurney AL, Marsters SA, Huang A, et al. Identification of a new member of the tumor necrosis factor family and its receptor, a human ortholog of mouse GITR. Curr. Biol. 1999; 9:215-218.
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