|Application ||WB, E|
|Calculated MW||33337 Da|
|Antigen Region||268-296 aa|
|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.|
|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.|
|Function||DNA repair protein involved in DNA nonhomologous end joining (NHEJ) required for double-strand break (DSB) repair and V(D)J recombination. May serve as a bridge between XRCC4 and the other NHEJ factors located at DNA ends, or may participate in reconfiguration of the end bound NHEJ factors to allow XRCC4 access to the DNA termini. It may act in concert with XRCC6/XRCC5 (Ku) to stimulate XRCC4-mediated joining of blunt ends and several types of mismatched ends that are noncomplementary or partially complementary (PubMed:16439204, PubMed:16439205, PubMed:17470781). Binds DNA in a length-dependent manner (PubMed:17317666).|
|Tissue Location||Ubiquitously expressed.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
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.
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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