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。
XRCC4 Recombinant Mouse mAb
XRCC4 Recombinant Mouse mAb
- 产品详情
- 实验流程
- 背景知识
Application 
| WB |
|---|---|
| Reactivity | Human |
| Host | Mouse |
| Clonality | Recombinant |
| Physical State | Liquid |
| Isotype | IgG2B/lambda |
| Purity | affinity purified by Protein G |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Nucleus. |
| SIMILARITY | Belongs to the XRCC4 family. |
| SUBUNIT | Homodimer and homotetramer in solution. The homodimer associates with LIG4, and the LIG4-XRCC4 complex associates in a DNA-dependent manner with the DNA-PK complex formed by the Ku p70/p86 dimer (XRCC6/XRCC5) and PRKDC. Seems to interact directly with PRKDC but not with the Ku p70/86 dimer. Interacts with XLF/Cernunnos. Interacts with APTX and APLF. |
| Post-translational modifications | Phosphorylated by PRKDC. The phosphorylation seems not to be necessary for binding to DNA. Phosphorylation by CK2 promotes interaction with APTX. Monoubiquitinated. Sumoylation at Lys-210 is required for nuclear localization and recombination efficiency. Has no effect on ubiquitination. |
| DISEASE | The disease is caused by mutations affecting the gene represented in this entry. Disease descriptionA disease characterized by short stature and microcephaly apparent at birth, progressive post-natal growth failure, and endocrine dysfunction. In affected adults endocrine features include hypergonadotropic hypogonadism, multinodular goiter, and diabetes mellitus. Variable features observed in some patients are progressive ataxia, and lymphopenia or borderline leukopenia. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The x-ray repair cross-complementing (XRCC) proteins are responsible for efficiently repairing and maintaining genetic stability following DNA base damage. These genes share sequence similarity with the yeast DNA repair protein Rad51. XRCC1 is a protein that facilitates the DNA base excision repair pathway by interacting with DNA ligase III and DNA polymerase to repair DNA single-strand breaks. XRCC2 and XRCC3 are both involved in maintaining chromosome stability during cell division. XRCC2 is required for efficient repair of DNA double-strand breaks by homologous recombination between sister chromatids, and XRCC3 interacts directly with Rad51 to cooperate with Rad51 during recombinational repair. XRCC4 is an accessory factor of DNA ligase IV that preferentially binds DNA with nicks or broken ends. XRCC4 binds to DNA ligase IV and enhances its joining activity, and it is also involved in V(D)J recombination. Any defect in one of the known components of the DNA repair/V(D)J recombination machinery (Ku-70, Ku-80, DNA-PKCS, XRCC4 and DNA ligase IV) leads to abortion of the V(D)J rearrangement process and early block in both T and B cell maturation. |
| Target/Specificity | Widely expressed. |
|---|---|
| Dilution | WB=1:500-1000 |
| 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.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The x-ray repair cross-complementing (XRCC) proteins are responsible for efficiently repairing and maintaining genetic stability following DNA base damage. These genes share sequence similarity with the yeast DNA repair protein Rad51. XRCC1 is a protein that facilitates the DNA base excision repair pathway by interacting with DNA ligase III and DNA polymerase to repair DNA single-strand breaks. XRCC2 and XRCC3 are both involved in maintaining chromosome stability during cell division. XRCC2 is required for efficient repair of DNA double-strand breaks by homologous recombination between sister chromatids, and XRCC3 interacts directly with Rad51 to cooperate with Rad51 during recombinational repair. XRCC4 is an accessory factor of DNA ligase IV that preferentially binds DNA with nicks or broken ends. XRCC4 binds to DNA ligase IV and enhances its joining activity, and it is also involved in V(D)J recombination. Any defect in one of the known components of the DNA repair/V(D)J recombination machinery (Ku-70, Ku-80, DNA-PKCS, XRCC4 and DNA ligase IV) leads to abortion of the V(D)J rearrangement process and early block in both T and B cell maturation.
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