Hu et al. Identified an regulation of Pyruvate kinase isozymes M1 M2 in ATCL8 cells weighed against AT5BIVA due to 3 hours of irradiation. Moreover, in just one of ATP-competitive Chk inhibitor proteomic study previously suggested, the authors isolated PKM2 via a large scale proteomic analysis of proteins phosphorylated in response to DNA damage on agreement sites acknowledged by ATM and ATR. Intriguingly is known in literature a translocation of PKM2 in response to various apoptotic stimuli and this nuclear translocation is enough to cause programmed cell death. Our results and the reported published evidences confirmthe theory that PKM2 could be regarded as one of the ATM target protein. None the less, we observed an of PKM2 in L6 ATM reconstituted cell line only in basal condition and not following the MG132 treatment. We could hypothesize that in the absence of ATM this protein is more degraded by the Ub proteasome system and after the proteasome congestion there is an accumulation of the ubiquitylated protein in both cell point explaining the absence of different appearance Cellular differentiation involving the two treated cell lines in our study. The final checked metabolite, lactate, was observed more concentrated in presence of ATM according to the larger amount of its precursor pyruvate. Usually, lactate is generated inmammalian organismwhen the oxygen availability is reduced in a reaction that generates NAD from NADH and H. In our mobile process we hypothesize that the lactate greater amount depends on its functions as thermodynamic driving force to push the glycolytic step of the Glyceraldehyde 3 phosphate dehydrogenase which will be enzymatically acting in near equilibrium situation. Ataxia Telangiectasia is a genetic infection characterized by cerebellar ataxia buy FK228 and immunodeficiency. A T is linked to the loss of ATM protein function, a serine/threonine kinase main in DNA damage response. ATM modulates also the activity of E3 ubiquitin ligases, affecting the balance of target proteins. Consequently, ATM deficit may significantly impinge on the cellular proteome structure resulting in defective signaling pathways. Actually, there are increasing evidence that this protein could have an important part in the get a grip on of target proteins of the ubiquitin system. Stagni and colleagues have recently shown that ATM modulates the proteasome dependent down regulation of c FLIP. In today’s study, we have pursued a thorough proteomic investigation to judge the biological effects of ATM expression on the control of protein quality and security. To this purpose, protein expression profiling were also evaluated in the existence of the proteasome inhibitor MG132 to emphasize these proteins whose expression is modulated by ATM most likely through the ubiquitin.