The nuclear protein kinase ATM is the chief activator of the massive cellular response to double strand breaks in the DNA. specific HDAC inhibitors ATM orchestrates a complex signaling network comprising cell cycle checkpoints, repair systems, apoptotic pathways, and a great many other stress responses that cause the cell to repair and survival, or apoptosis. After the induction of DSBs, ATM is activated and phosphorylates amultitude of downstream targets, each ofwhich subsequently modulates one or more response pathways. Reduction or inactivation of ATM due to ATM variations leads to a prototype genomic instability problem, ataxiatelangiectasia. A T is seen as an neuronal damage, immunodeficiency, genomic uncertainty, sensitivity to ionizing radiation and cancer predisposition. A Ts major feature is the Lymph node cerebellar ataxia, which gradually develops in to serious neuromotor dysfunction and appears in early infancy. The ataxia displays gradual degeneration of the cerebellar cortex and gradual lack of Purkinje and granule cells; the rest of the nervous system may possibly show degenerative changes at a later age. Knowledge the neuronal damage, A Ts prominent function, needs elucidating the functions of ATM in nerves. While there’s a wealth of data on ATMs mobilization of the DSB result in growing cells, itwas suggested that ATM in nerves is cytoplasmic and features in other volumes. This idea severed ATMs well recorded purpose from the major symptom due to its inactivation and obscured the molecular basis of the neurodegeneration in A T. Previous work in our laboratory added genetic molecular evidence that MK-2206 the neurodegeneration in A T does indeed derive from defective DSB result. Therefore, we analyzed ATMs subcellular localization in human neuron like cells obtained by neuronal differentiation of neuroblastoma cells, and discovered that in this model system of human nerves, ATM is largely nuclear. We further showed that, like with proliferating cells, therapy of NLCs with DSB causing agents activates nuclear ATM and consequently the ATM mediated system. These results suggested that ATM in individual neurons might be nuclear and perform a similar work as in growing cells. In our work we wanted to establish this conclusion by analyzing ATMs subcellular localization and function in the DSB answer in two additional and special types of human nerves. The initial one is obtained by in vitro differentiation of pluripotent human embryonic stem cells into neural precursors that further differentiate into the three neural lineages, including adult neurons. The next model is based on a line of neural stem cells.