Note: Genetic dissection of vertebrate 53BP1: A major role in non-homologous end joining of DNA double strand breaks
Note: Genetic dissection of vertebrate 53BP1: A major role in non-homologous end joining of DNA double strand breaks (doi: http://dx.doi.org/10.1016/j.dnarep.2006.03.008 ) mutation of 53BP1 in mammalian causing 1.cellular sensitivity toward radiation. 2.defect in checkpoint But DT40-53BP1(-/-) 1.intra-S phase checkpoint was normal 2.G2-M checkpoint was normal once there is the DSB -- 53BP1 is the earliest protein to recruit and form foci. In mammalian, defect in 53BP1 causes the cell cycle delays after the damage. The sequence of NHEJ; 1. Ku70/80 2.DNA-PK --> phosphorylate Artemis nuclease Artemis in IR break fixing is required more studies. Late S-G2; HR and NHEJ play role in "IR-induced" double strand break G1-early S; NHEJ is dominant AA from 203-1716 was removed. Sensitivity toward irradiation with asynchronously growing 53BP1-/- -->biphasic pattern. 53BP1(-/-) also increased the rate of HR --> this mean th...