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。
API5 Antibody
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IP, IHC-P |
|---|---|
| Primary Accession | Q9BZZ5 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 59005 Da |
| Gene ID | 8539 |
|---|---|
| Other Names | Apoptosis inhibitor 5, API-5, Antiapoptosis clone 11 protein, AAC-11, Cell migration-inducing gene 8 protein, Fibroblast growth factor 2-interacting factor, FIF, Protein XAGL, API5 |
| Dilution | WB~~1:1000 IP~~N/A IHC-P~~N/A |
| 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 | API5 (HGNC:594) |
|---|---|
| Function | Antiapoptotic factor that may have a role in protein assembly. Negatively regulates ACIN1. By binding to ACIN1, it suppresses ACIN1 cleavage from CASP3 and ACIN1-mediated DNA fragmentation. Also known to efficiently suppress E2F1-induced apoptosis. Its depletion enhances the cytotoxic action of the chemotherapeutic drugs. |
| Cellular Location | Nucleus. Cytoplasm. Note=Mainly nuclear. Can also be cytoplasmic |
| Tissue Location | Expressed in all tissues tested, including heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas Highest levels in heart, pancreas and placenta. Highly expressed in several cancers. Preferentially expressed in squamous cell carcinoma versus adenocarcinoma in non-small cell lung cancer |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Antiapoptotic factor that may have a role in protein assembly. Negatively regulates ACIN1. By binding to ACIN1, it suppresses ACIN1 cleavage from CASP3 and ACIN1-mediated DNA fragmentation. Also known to efficiently suppress E2F1-induced apoptosis. Its depletion enhances the cytotoxic action of the chemotherapeutic drugs.
REFERENCES
Tewari M.,et al.Cancer Res. 57:4063-4069(1997).
Gianfrancesco F.,et al.Cytogenet. Cell Genet. 84:164-166(1999).
Van den Berghe L.,et al.Mol. Endocrinol. 14:1709-1724(2000).
Kim J.W.,et al.Submitted (JUN-2003) to the EMBL/GenBank/DDBJ databases.
Kalnine N.,et al.Submitted (MAY-2003) to the EMBL/GenBank/DDBJ databases.
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