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。
APC2 Rabbit pAb
- 产品详情
- 实验流程
Application 
| IHC-P, IHC-F, IF, E |
|---|---|
| Primary Accession | Q9UJX6 |
| Other Accession | Q9UJX6 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 93828 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human APCL/APC2 |
| Epitope Specificity | 1-100/2303 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SIMILARITY | Belongs to the adenomatous polyposis coli (APC) family. Contains 6 ARM repeats. |
| SUBUNIT | Interacts with PSRC1 (By similarity). Interacts with APC, CTNNB1, MAPRE1, MAPRE3, TP53BP2 and possibly with AXIN2. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The adenomatous polyposis syndromes, familial adenomatous polyposis (FAP) and Gardner’s syndrome (GS), are characterized by numerous adenomatous polyps throughout the entire colon. These polyps invariably progress to colon cancer in addition to other extracolonic manifestations. The cloning of the APC gene revealed a ubiquitously expressed protein, 2843 amino acids in length, which is frequently mutated in patients suffering from FAP and GS. APC has been found to be associated with structural components of intracellular junctions. b-catenin and g-catenin (also called plakoglobin) are involved in the regulation of cellular adhesion. APC and E cadherin compete for binding to specific internal regions of both b- and g-catenin. Interactions between cytoskeleton and the APC, E cadherin, b/g catenin complex are mediated by a-catenin. |
| Gene ID | 29882 |
|---|---|
| Other Names | APC2; 9230107K09Rik; Emi4; Imi4; mKIAA1406; ANC2_HUMAN; ANAPC2; Cyclosome subunit 2; KIAA1406; ANC2_MOUSE; anaphase promoting complex subunit 2 |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500,ELISA=1:5000-10000 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | ANAPC2 |
|---|---|
| Synonyms | APC2, KIAA1406 |
| Function | Component of the anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated E3 ubiquitin ligase that controls progression through the cell cycle (PubMed:11739784, PubMed:18485873, PubMed:27120157, PubMed:27509861). Together with the RING-H2 protein ANAPC11, forms the catalytic component of the E3 ubiquitin ligase complex (PubMed:11739784, PubMed:18485873, PubMed:27120157, PubMed:27509861). APC/C acts by mediating ubiquitination and subsequent degradation of target proteins: it mainly mediates the formation of 'Lys-11'-linked polyubiquitin chains and, to a lower extent, the formation of 'Lys-48'- and 'Lys-63'-linked polyubiquitin chains (PubMed:11739784, PubMed:18485873). APC/C catalyzes assembly of branched 'Lys-11'-/'Lys-48'-linked branched ubiquitin chains on target proteins (PubMed:29033132). APC/C is activated by CDC20 in the metaphase/anaphase transition of cell cycle, targeting the degradation of cyclin B and securin (PubMed:27120157, PubMed:27509861). APC/C is regulated by the mitotic checkpoint complex (MCC), which inhibits APC/C and delays chromosome segregation (PubMed:27509861). The CDC20-APC/C complex positively regulates the formation of synaptic vesicle clustering at active zone to the presynaptic membrane in postmitotic neurons (By similarity). CDC20-APC/C-induced degradation of NEUROD2 drives presynaptic differentiation (By similarity). |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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