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。
Anti-WASP Picoband Antibody
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- 背景知识
Application 
| WB, IHC-P, IHC-F, ICC |
|---|---|
| Primary Accession | P42768 |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Clonality | Polyclonal |
| Format | Lyophilized |
| Description | Rabbit IgG polyclonal antibody for Wiskott-Aldrich syndrome protein(WAS) detection. Tested with WB, IHC-P, IHC-F, ICC in Human;Mouse;Rat. |
| Reconstitution | Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
| Gene ID | 7454 |
|---|---|
| Other Names | Wiskott-Aldrich syndrome protein, WASp, WAS, IMD2 |
| Calculated MW | 52913 Da |
| Application Details | Immunocytochemistry , 0.5-1 µg/ml, Human, - Immunohistochemistry(Frozen Section), 0.5-1 µg/ml, Human, - Immunohistochemistry(Paraffin-embedded Section), 0.5-1 µg/ml, Human, By Heat Western blot, 0.1-0.5 µg/ml, Human, Mouse, Rat |
| Subcellular Localization | Cytoplasm, cytoskeleton. |
| Tissue Specificity | Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen. . |
| Source | Eukaryota |
| Protein Name | Wiskott-Aldrich syndrome protein |
| Contents | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3. |
| Immunogen | A synthetic peptide corresponding to a sequence at the C-terminus of human WASP (129-156aa ADEDEAQAFRALVQEKIQKRNQRQSGDR), different from the related mouse sequence by two amino acids. |
| Purification | Immunogen affinity purified. |
| Cross Reactivity | No cross reactivity with other proteins |
| Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time.Avoid repeated freezing and thawing. |
| Sequence Similarities | Contains 1 CRIB domain. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | WAS |
|---|---|
| Synonyms | IMD2 |
| Function | Effector protein for Rho-type GTPases that regulates actin filament reorganization via its interaction with the Arp2/3 complex (PubMed:12235133, PubMed:12769847, PubMed:16275905). Important for efficient actin polymerization (PubMed:12235133, PubMed:16275905, PubMed:8625410). Possible regulator of lymphocyte and platelet function (PubMed:9405671). Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria (PubMed:18650809). In addition to its role in the cytoplasmic cytoskeleton, also promotes actin polymerization in the nucleus, thereby regulating gene transcription and repair of damaged DNA (PubMed:20574068). Promotes homologous recombination (HR) repair in response to DNA damage by promoting nuclear actin polymerization, leading to drive motility of double-strand breaks (DSBs) (PubMed:29925947). |
| Cellular Location | Cytoplasm, cytoskeleton. Nucleus |
| Tissue Location | Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen. |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known.
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