Anti-Ku70

0.5mg/ml if reconstituted with 0.2ml sterile DI water. XRCC6 (X-Ray Repair, Complementing Defective, In Chinese Hamster, 6), also called Ku70, G22P1 or TLAA, is a protein that in humans, is encoded by the XRCC6 gene. The XRCC6 gene encodesthe subunit p70 of the p70/p80 autoantigen which consists of two proteins of molecular mass of approximately 70,000 and 80,000 daltons that dimerize to form a 10 S DNA-binding complex. XRCC6 and Mre11 are differentially expressed during meiosis. XRCC6 interacts with Baxa, a mediator of mitochondrial-dependent apoptosis. Disruption of both FANCC and XRCC6/Ku70 suppressed sensitivity to crosslinking agents, diminished chromosome breaks, and reversed defective homologous recombination. Ku70 binds directly to free DNA ends, committing them to NHEJ repair. In early meiotic prophase, however, when meiotic recombination is most probably initiated, Mre11 was abundant, whereas Ku70 was not detectable. Protein function: Single-stranded DNA-dependent ATP-dependent helicase. Has a role in chromosome translocation. The DNA helicase II complex binds preferentially to fork-like ends of double-stranded DNA in a cell cycle-dependent manner. It works in the 3'-5' direction. Binding to DNA may be mediated by XRCC6. Involved in DNA non-homologous end joining (NHEJ) required for double-strand break repair and V(D)J recombination. The XRCC5/6 dimer acts as regulatory subunit of the DNA-dependent protein kinase complex DNA-PK by increasing the affinity of the catalytic subunit PRKDC to DNA by 100-fold. The XRCC5/6 dimer is probably involved in stabilizing broken DNA ends and bringing them together. The assembly of the DNA-PK complex to DNA ends is required for the NHEJ ligation step. Required for osteocalcin gene expression. Probably also acts as a 5'-deoxyribose-5-phosphate lyase (5'-dRP lyase), by catalyzing the beta-elimination of the 5' deoxyribose- 5-phosphate at an abasic site near double-strand breaks. 5'-dRP lyase activity allows to 'clean' the termini of abasic sites, a class of nucleotide damage commonly associated with strand breaks, before such broken ends can be joined. The XRCC5/6 dimer together with APEX1 acts as a negative regulator of transcription. [The UniProt Consortium]