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。
FADD Rabbit mAb
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- 实验流程
- 背景知识
Application 
| WB, IHC-P, FC, IP |
|---|---|
| Primary Accession | Q61160 |
| Reactivity | Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 22960 Da |
| Gene ID | 14082 |
|---|---|
| Other Names | Fadd |
| Dilution | WB~~1:500-1:1000 IHC-P~~1:50~200 FC~~1:10~50 IP~~N/A |
| Format | Liquid in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Name | Fadd {ECO:0000303|PubMed:8649383, ECO:0000312|MGI:MGI:109324} |
|---|---|
| Function | Apoptotic adapter molecule that recruits caspases CASP8 or CASP10 to the activated FAS/CD95 or TNFRSF1A/TNFR-1 receptors. The resulting aggregate called the death-inducing signaling complex (DISC) performs CASP8 proteolytic activation. Active CASP8 initiates the subsequent cascade of caspases mediating apoptosis. Involved in interferon-mediated antiviral immune response, playing a role in the positive regulation of interferon signaling. |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:Q13158}. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Apoptotic adaptor molecule that recruits caspase-8 or caspase-10 to the activated Fas (CD95) or TNFR-1 receptors. The resulting aggregate called the death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation. Active caspase-8 initiates the subsequent cascade of caspases mediating apoptosis . Involved in interferon-mediated antiviral immune response, playing a role in the positive regulation of interferon signaling .
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