癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
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GITRL Antibody
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Application 
| WB, ICC, E |
|---|---|
| Primary Accession | Q9UNG2 |
| Other Accession | Q9UNG2, 13124621 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 20308 Da |
| Concentration (mg/ml) | 1 mg/mL |
| Conjugate | Unconjugated |
| 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. |
| Gene ID | 8995 |
|---|---|
| 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 |
| Target/Specificity | TNFSF18; |
| 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. |
| Name | TNFSF18 (HGNC:11932) |
|---|---|
| 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 |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
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
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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