|Positive WB detected in||HepG2 cells, COLO 320 cells|
|Positive IP detected in||HepG2 cells|
|Positive IHC detected in||human breast cancer tissue, rat testis tissue, rat small intestine tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
15817-1-AP targets XRCC4 in WB, IP, IHC,ELISA applications and shows reactivity with human, rat samples.
|Tested Reactivity||human, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||XRCC4 fusion protein Ag8606|
|Full Name||X-ray repair complementing defective repair in Chinese hamster cells 4|
|Calculated molecular weight||310 aa, 35 kDa|
|Observed molecular weight||55 kDa|
|GenBank accession number||BC005259|
|Gene ID (NCBI)||7518|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
There are at least two pathways for eukaryotes to repair DNA double-strand breaks: homologous recombination and nonhomologous end joining(NHEJ). XRCC4 is one of the core machiney of NHEJ that required for double-strand break repair and V(D)J recombination. The DNA ligase IV(LIG4)-XRCC4 complex is responsible for the NHEJ ligation step, and XRCC4 enhances the joining activity of LIG4.
Silencing of XRCC4 increases radiosensitivity of triple-negative breast cancer cells.
RNase L facilitates the repair of DNA double-strand breaks through the nonhomologous end-joining pathway.
5-Azacytidine Enhances the Radiosensitivity of CNE2 and SUNE1 Cells In Vitro and In Vivo Possibly by Altering DNA Methylation.
Toxicol Appl Pharmacol
Polychlorinated biphenyl quinone induces oxidative DNA damage and repair responses: The activations of NHEJ, BER and NER via ATM-p53 signaling axis.
Cell Death Differ
LRIK interacts with the Ku70-Ku80 heterodimer enhancing the efficiency of NHEJ repair.
Inhibition of ATM Induces Hypersensitivity to Proton Irradiation by Upregulating Toxic End Joining.