Datasheet

GITRL Antibody
CATALOG NUMBER: 3591

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Specifications
Properties
Additional Info
Background

Specifications

SPECIES REACTIVITY:Human, Mouse
TESTED APPLICATIONS:ELISA, ICC, WB
APPLICATIONS: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.

Antibody validated: Immunocytochemistry in human samples. All other applications and species not yet tested.
USER NOTE:Optimal dilutions for each application to be determined by the researcher.
POSITIVE CONTROL:1) Cat. No. 1208 - THP-1 Cell Lysate
 2) Cat. No. 17-008 - THP-1 Cell Slide
IMMUNOGEN:GITRL antibody was raised against purified recombinant human GITR ligand.
HOST SPECIES:Rabbit

Properties

PURIFICATION:GITRL Antibody is affinity chromatography purified via peptide column.
PHYSICAL STATE:Liquid
BUFFER:GITRL Antibody is supplied in PBS containing 0.02% sodium azide.
CONCENTRATION:1 mg/mL
STORAGE CONDITIONS:GITRL antibody can be stored at 4˚C for three months and -20˚C, 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.
CLONALITY:Polyclonal
ISOTYPE:IgG
CONJUGATE:Unconjugated

Additional Info

ALTERNATE NAMES:GITRL Antibody: TL6, AITRL, GITRL, hGITRL, TL6, UNQ149/PRO175, Tumor necrosis factor ligand superfamily member 18, Activation-inducible TNF-related ligand
ACCESSION NO.:Q9UNG2
PROTEIN GI NO.:13124621
OFFICIAL SYMBOL:TNFSF18
GENE ID:8995

Background

BACKGROUND: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.
REFERENCES: 1) Gaur U, Aggarwal BB. Regulation of proliferation, survival and apoptosis by members of the TNF superfamily. Biochem. Pharmacol. 2003; 66:1403-8.
2) Ronchetti S, Nocentini G, Riccardi C, et al. Role of GITR in activation response of T lymphocytes.Blood 2002; 100:350-2.
3) 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.
4) 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.

For Research Use Only