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。
Phospho-BID (Ser78) Antibody
Rabbit Polyclonal Antibody
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC |
|---|---|
| Primary Accession | P55957 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 21995 Da |
| Gene ID | 637 |
|---|---|
| Positive Control | WB: mouse spleen, rat spleen lysates; IHC: human brain tissue |
| Application & Usage | WB; 1:500 – 1:2000, IHC; 1:50 – 1:200 |
| Alias Symbol | BID |
| Other Names | BH3-interacting domain death agonist, p22 BID, BID |
| Appearance | Colorless liquid |
| Formulation | In 0.42% Potassium phosphate; 0.87% Sodium chloride; pH 7.3; 30% glycerol and 0.01% sodium azide |
| Reconstitution & Storage | -20 °C |
| Background Descriptions | |
| Precautions | Phospho-BID (Ser78) Antibody 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 | BID |
|---|---|
| Function | Induces caspases and apoptosis (PubMed:14583606). Counters the protective effect of BCL2 (By similarity). |
| Cellular Location | Cytoplasm. Mitochondrion membrane. Mitochondrion outer membrane. Note=When uncleaved, it is predominantly cytoplasmic. [BH3-interacting domain death agonist p13]: Mitochondrion membrane {ECO:0000250|UniProtKB:P70444}. Note=Associated with the mitochondrial membrane. {ECO:0000250|UniProtKB:P70444} [Isoform 3]: Cytoplasm |
| Tissue Location | [Isoform 2]: Expressed in spleen, pancreas and placenta (at protein level). [Isoform 4]: Expressed in lung and pancreas (at protein level). |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Bid, a BH3 domain-containing proapoptotic Bcl-2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase-8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl-2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In the animal model studies, Bid-deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas.
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