CtIP (D76F7) Rabbit mAb

DNA damage checkpoints are critical for regulated repair of damaged DNA and genome maintenance. CtIP/RBBP8 (CtBP-interacting protein), initially characterized as a binding partner for the trancription factor CtBP, has emerged as a regulator of both cell cycle progression and repair of DNA double strand breaks (DSB). Along with the DSB-sensing MRN complex (MRE11-RAD50-NBS1), CtIP functions in the generation of single stranded DNA at DSBs, a process required for signaling to DNA repair machinery (reviewed in 1). CtIP is thought to be critical in the transition between sensing of DSBs and repair by homologous recombination (HR) (2,3).In addition to HR, DSBs can also be repaired through nonhomologous end joining (NHEJ), and CtIP has been shown to have a role in signaling to the NHEJ pathway independently of its function in DSB end resection (4).CtIP is also involved in cellular tolerence of topoisomerase inhibitors camptothecin and etoposide, which are used to treat cancer through their ability to introduce DSBs in cycling cells (5). 1.You, Z. and Bailis, J.M. (2010) Trends Cell Biol 20, 402-9. 2.You, Z. et al. (2009) Mol Cell 36, 954-69. 3.Eid, W. et al. (2010) EMBO Rep 11, 962-8. 4.Quennet, V. et al. (2010) Nucleic Acids Res, Epub ahead of print. 5.Nakamura, K. et al. (2010) PLoS Genet 6, e1000828.