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。
NHEJ1 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | Q9H9Q4 |
| Other Accession | NP_079058.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 33337 Da |
| Antigen Region | 268-296 aa |
| Gene ID | 79840 |
|---|---|
| Other Names | Non-homologous end-joining factor 1, Protein cernunnos, XRCC4-like factor, NHEJ1, XLF |
| Target/Specificity | This NHEJ1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 268-296 amino acids from the C-terminal region of human NHEJ1. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | NHEJ1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | NHEJ1 {ECO:0000303|PubMed:17191205, ECO:0000312|HGNC:HGNC:25737} |
|---|---|
| Function | DNA repair protein involved in DNA non-homologous end joining (NHEJ); it is required for double-strand break (DSB) repair and V(D)J recombination and is also involved in telomere maintenance (PubMed:16439204, PubMed:16439205, PubMed:17317666, PubMed:17470781, PubMed:17717001, PubMed:18158905, PubMed:18644470, PubMed:20558749, PubMed:26100018, PubMed:28369633). Plays a key role in NHEJ by promoting the ligation of various mismatched and non-cohesive ends (PubMed:17470781, PubMed:17717001, PubMed:19056826). Together with PAXX, collaborates with DNA polymerase lambda (POLL) to promote joining of non-cohesive DNA ends (PubMed:25670504, PubMed:30250067). May act in concert with XRCC5-XRCC6 (Ku) to stimulate XRCC4-mediated joining of blunt ends and several types of mismatched ends that are non- complementary or partially complementary (PubMed:16439204, PubMed:16439205, PubMed:17317666, PubMed:17470781). In some studies, has been shown to associate with XRCC4 to form alternating helical filaments that bridge DNA and act like a bandage, holding together the broken DNA until it is repaired (PubMed:21768349, PubMed:21775435, PubMed:22228831, PubMed:22287571, PubMed:26100018, PubMed:27437582, PubMed:28500754). Alternatively, it has also been shown that rather than forming filaments, a single NHEJ1 dimer interacts through both head domains with XRCC4 to promote the close alignment of DNA ends (By similarity). The XRCC4-NHEJ1/XLF subcomplex binds to the DNA fragments of a DSB in a highly diffusive manner and robustly bridges two independent DNA molecules, holding the broken DNA fragments in close proximity to one other (PubMed:27437582, PubMed:28500754). The mobility of the bridges ensures that the ends remain accessible for further processing by other repair factors (PubMed:27437582). Binds DNA in a length-dependent manner (PubMed:17317666, PubMed:18158905). |
| Cellular Location | Nucleus. Chromosome. Note=Localizes to site of double-strand breaks; recruitment is dependent on XRCC5-XRCC6 (Ku) heterodimer |
| Tissue Location | Ubiquitously expressed. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Double-strand breaks in DNA result from genotoxic stresses and are among the most damaging of DNA lesions. This gene encodes a DNA repair factor essential for the nonhomologous end-joining pathway, which preferentially mediates repair of double-stranded breaks. Mutations in this gene cause different kinds of severe combined immunodeficiency disorders.
REFERENCES
Malivert, L., et al. J. Biol. Chem. 285(34):26475-26483(2010)
Briggs, F.B., et al. Am. J. Epidemiol. 172(2):217-224(2010)
Okada, Y., et al. Hum. Mol. Genet. 19(11):2303-2312(2010)
Andres, S.N., et al. Mol. Cell 28(6):1093-1101(2007)
Tsai, C.J., et al. Proc. Natl. Acad. Sci. U.S.A. 104(19):7851-7856(2007)
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