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。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
GITR / Tnfrsf18 (mouse) Antibody - With BSA and Azide
Rat Monoclonal Antibody [Clone DTA-1 ]
- 产品详情
- 实验流程
- 背景知识
Application 
| IF, FC |
|---|---|
| Primary Accession | O35714 |
| Other Accession | 21936 (Mouse), 3180 (Mouse), 482508 (Mouse) |
| Reactivity | Mouse |
| Host | Rat |
| Clonality | Monoclonal |
| Isotype | Rat / IgG2b, lambda |
| Clone Names | DTA-1 |
| Calculated MW | 25334 Da |
| Gene ID | 21936 |
|---|---|
| Other Names | Tumor necrosis factor receptor superfamily member 18, Glucocorticoid-induced TNFR-related protein, CD357, Tnfrsf18, Gitr |
| Application Note | IF~~1:50~200 FC~~1:10~50 |
| Storage | Store at 2 to 8°C.Antibody is stable for 24 months. |
| Precautions | GITR / Tnfrsf18 (mouse) Antibody - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | Tnfrsf18 |
|---|---|
| Synonyms | Gitr |
| Function | Receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway (By similarity). |
| Cellular Location | [Isoform A]: Cell membrane; Single-pass type I membrane protein [Isoform C]: Cell membrane; Single-pass type I membrane protein |
| Tissue Location | Preferentially expressed in activated T lymphocytes |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
GITR (glucocorticoid-induced TNFR-related gene) is a member of the TNF-receptor superfamily, also known as TNFRSF18. It is expressed at low levels on resting T lymphocytes and at high levels on CD25+ĀCD4+ĀTregs. The expression of GITR on T cells can be upregulated upon activation. Interaction of GITR with its ligand (GITRL) has been demonstrated to augment T cell activation, proliferation, cytokine production as well as MAPKs and NF-ĪŗB activation, and abrogate the inhibitory function ofĀCD25+ĀCD4+ĀTregs. In vivoĀactivation of GITR causes development of autoimmune diseases and restores the suppressed immune response.
REFERENCES
Stephens GL, et al. 2004. J. Immunol. 173:5008. | Tone M, et al. 2003. Proc. Natl. Acad. Sci. USA 100:15059
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