XRCC4 Antibody #23908
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 50 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
XRCC4 Antibody recognizes endogenous levels of total XRCC4 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro268 of human XRCC4 protein. Antibodies are purified by peptide affinity chromatography.
Background
DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells recognize and repair DSBs via two distinct but partly overlapping signaling pathways: non-homologous end joining (NHEJ) and homologous recombination (HR). DNA repair via the HR pathway is restricted to S and G2 phases of the cell cycle, while NHEJ can occur during any phase. NHEJ machinery is also utilized in V(D)J recombination, a process that generates diversity in immunoglobulin and T cell receptor genes. Defects in both pathways have been associated with human disease, including cancer (1).
DNA repair through the NHEJ pathway involves a core group of proteins that includes the Ku heterodimer (Ku70/Ku80), DNA-PKcs, DNA ligase IV, X-ray repair cross-complementing protein 4 (XRCC4), XLF, and PAXX (Paralog of XRCC4 and XLF, also known as C9orf142 or XLS). XRCC4 interacts with XLF and promotes the ligation of DNA strands by DNA ligase IV (2).
Mutations and polymorphisms in XRCC4 have been linked to human disease, including microcephaly, dwarfism, and cancer susceptibility (3-5). Knockdown of XRCC4 expression in hepatocellular carcinoma (HCC) cells and triple-negative breast cancer cells increases sensitivity to doxorubicin and ionizing radiation, respectively (6,7).
DNA repair through the NHEJ pathway involves a core group of proteins that includes the Ku heterodimer (Ku70/Ku80), DNA-PKcs, DNA ligase IV, X-ray repair cross-complementing protein 4 (XRCC4), XLF, and PAXX (Paralog of XRCC4 and XLF, also known as C9orf142 or XLS). XRCC4 interacts with XLF and promotes the ligation of DNA strands by DNA ligase IV (2).
Mutations and polymorphisms in XRCC4 have been linked to human disease, including microcephaly, dwarfism, and cancer susceptibility (3-5). Knockdown of XRCC4 expression in hepatocellular carcinoma (HCC) cells and triple-negative breast cancer cells increases sensitivity to doxorubicin and ionizing radiation, respectively (6,7).
- Hartlerode, A.J. and Scully, R. (2009) Biochem J 423, 157-68.
- Tsai, C.J. et al. (2007) Proc Natl Acad Sci USA 104, 7851-6.
- Murray, J.E. et al. (2015) Am J Hum Genet 96, 412-24.
- Bee, L. et al. (2015) EMBO Mol Med 7, 918-29.
- Saadat, M. and Saadat, S. (2015) J Med Biochem 34, 409-413.
- Lu, J. et al. (2017) Oncotarget 8, 87955-87970.
- Wen, Y. et al. (2019) Biosci Rep 39, BSR20180893. doi: 10.1042/BSR20180893.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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