Description | Specificity: Specific for endogenous levels of the ~100 kDa CtIP protein phosphorylated at Ser326. Immunolabeling is completely eliminated by treatment with lambda-Ptase. CtIP, C-terminal binding protein-interacting protein, is a DNA endonuclease activated by double stranded breaks (DSBs). DSB repairs can be performed by either one of two mechanisms; non-homologous end joining (NHEJ) or homologous recombination (HR). NHEJ is the predominant DSB repair pathway throughout the entire cell cycle, most importantly in the G1 phase (Rothkamm et al, 2003); while HR is important for repairing DSBs in S and G2 phases (Beucher et al, 2009). CtIP controls DSB resection; an event that only occurs in HR during G2-phase. Phosphorylation of Thr847 dictates |
Product Specific References | Rothkamm K, Kruger I, Thompson LH, Lobrich M (2003) Pathways of DNA double-strand break repair during the mammalian cell cycle. Mol Cell Biol., 23, 5706-5715.Beucher A, Birraux J, tchouandong L, Baron O, Shibata A, Conrad S, Goodarzi AA, Krempler A, Jeggo PA, Lobrich M (2009) ATM and Artemis promote homologous recombination of radiation-inducted DNA double-strand breaks in G2. EMBO J., 28, 3413-3427.Huertas P, Jackson SP (2008) Human CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair. J. Biol. Chem, 284: 9558-9565.Olivia Barton, Steffen C Naumann, Ronja Diemer-Biehs, Julia Kunzel, Monika Steinlage, Sandro Conrad, Nodar Makharashili, Jiadong Wang, Lin Fent,Bernard S. Lopez, Tanya T. Paull, Junjie Chen, Penny A Jeggo, and Markus Lobrich (2014) Polo-like Kinase 3 regulates CtIP during DNA double-strand break repair in G1. JCB, Nov 7;206(7): 877-894. |