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。
EYA4 Rabbit pAb
- 产品详情
- 实验流程
Application 
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | O95677 |
| Other Accession | O95677 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 69505 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human EYA4 |
| Epitope Specificity | 131-230/639 |
| 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 HAD-like hydrolase superfamily. EYA family. |
| DISEASE | Defects in EYA4 are the cause of deafness autosomal dominant type 10 (DFNA10) [MIM:601316]. DFNA10 is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. Defects in EYA4 are the cause of cardiomyopathy dilated type 1J (CMD1J) [MIM:605362]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | A gene of chromosome 6q23 encodes the 640 amino acid protein, EYA4 (eyes absent) (1). EYA is one of four members of the eyes absent family (1). A 271 amino acid domain at the carboxyl terminal is highly conserved amongst the members of the eyes absent family (1). EYA4 is expressed in the craniofacial mesenchyme, the dermamyotome, and the limb (1). The conserved region in other EYA proteins interacts with SIX, DACH, and G-proteins, which regulate transcription in early embryonic development (1,2,3,4). SIX translocates EYA1-3 to the nucleus, and G-proteins can stop this interaction (3,4). Premature stop codon mutations in EYA4 cause postlingual, progressive autosomal dominant hearing loss in humans (2). This shows that EYA4 is also vital to the mature organ of Corti (2). EYA4 may cause oculo-dento-digital syndrome, based on its expression pattern and map postion (1). |
| Gene ID | 2070 |
|---|---|
| Other Names | CMD1J; DFNA10; B130023L16Rik; EYA4_HUMAN; EYA4; Eyes absent homolog 4; 3.1.3.48; EYA4_MOUSE; EYA transcriptional coactivator and phosphatase 4; eyes absent (Drosophila) homolog 4; eyes absent homolog 4 (Drosophila) |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| 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 | EYA4 |
|---|---|
| Function | Tyrosine phosphatase that specifically dephosphorylates 'Tyr- 142' of histone H2AX (H2AXY142ph). 'Tyr-142' phosphorylation of histone H2AX plays a central role in DNA repair and acts as a mark that distinguishes between apoptotic and repair responses to genotoxic stress. Promotes efficient DNA repair by dephosphorylating H2AX, promoting the recruitment of DNA repair complexes containing MDC1. Its function as histone phosphatase probably explains its role in transcription regulation during organogenesis. May be involved in development of the eye (By similarity). |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:Q99502}. Nucleus {ECO:0000250|UniProtKB:Q99502} |
| Tissue Location | Highly expressed in heart and skeletal muscle. |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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