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。
mGLUR8 Antibody
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application 
| WB |
|---|---|
| Primary Accession | O00222 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 101741 Da |
| Gene ID | 2918 |
|---|---|
| Other Names | Metabotropic glutamate receptor 8, mGluR8, GRM8, GPRC1H, MGLUR8 |
| Target/Specificity | KLH-conjugated synthetic peptide encompassing a sequence within the C-term region of human mGLUR8. The exact sequence is proprietary. |
| Dilution | WB~~1:1000 |
| Format | 0.01M PBS, pH 7.2, 0.09% (W/V) Sodium azide, Glycerol 50% |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
| Name | GRM8 |
|---|---|
| Synonyms | GPRC1H, MGLUR8 |
| Function | G-protein coupled receptor for glutamate. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase activity. |
| Cellular Location | Cell membrane; Multi-pass membrane protein. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
G-protein coupled receptor for glutamate. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase activity.
REFERENCES
Scherer S.W.,et al.Genomics 44:232-236(1997).
Wu S.,et al.Brain Res. Mol. Brain Res. 53:88-97(1998).
Malherbe P.,et al.Brain Res. Mol. Brain Res. 67:201-210(1999).
Stormann T.M.,et al.Submitted (APR-2004) to the EMBL/GenBank/DDBJ databases.
Kaighin V.A.,et al.Submitted (DEC-2007) to the EMBL/GenBank/DDBJ databases.
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