proteasome program and whose half life is particularly small and their ATM dependentmodulation levels on the whole proteomewould be partiallymasked in a primary study. By name free nLC MSE approach, a total of 53 and 62 differentially expressed proteins were determined in the 2 analyzed comparison. Twelve proteins are controlled in the in an identical way in both experimental dataset and we could Hedgehog inhibitor speculate that their appearance is affected by the presence/absence of ATM but this event occurs independently of the ubiquitin?proteasome system involvement. Extremely one of these, Plastin 3, differentially controlled in both dataset of the shotgun proteomic tests, has already been known as phosphorylated upon DNA damage, probably by ATM or ATR, and its levels are reduced in Spinal Muscular Atrophy mouse model. Other three proteins were analyzed by western Plastid blot by us whose levels were influenced by ATM phrase and MG132 treatment: STAT1, Lamin B1 and Matrin 3 to verify the regulation noticed through proteomic evaluation in both L6 treated cell lines. Activator and signal Transducer of Transcription 1 has been previously identified as a possible substrate of ATM in nuclear extracts from irradiated HeLa cells implementing the concept that thismember of the STAT protein family is actually a immediate target of ATM. In our study STAT1 is down regulated after proteasome impediment in L6 ATM when compared with L6, an evidence that would be ultimately explained by proteasome dependent degradation of STAT1 in ATM good cells. In response to cytokines (-)-MK 801 and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form dimers that translocate to the cell nucleus where they behave as transcription activators of a variety of genes, which can be thought to be important for cell viability in response to different cell toys and pathogens. There are several evidences in literature which glow a light on the interaction between ATM and STAT1 in the response to the DNA damage, that reinforce our findings. Furthermore, we observed a loss of Lamin B1 in L6 ATM treated cells, recently Barascu and colleagues demonstrated an of Lamin B1 in A T cells acquire. The authors stressed the point that LMNB1 overexpression is enough to senescence in wild type cells and produce nuclear shape changes. A T patients suffer from premature ageing and this observation led to the theory that Lamin B1 dysregulation can take into account senescence in A T cells. LMNB1 accumulation was related by the authors to A T connected DDR problems, oxidative stress and nuclear form modifications. Finally, with a systematic analysis of individual protein complexes to spot chromosome segregation meats, ATMand LMNB1 were found as trap prey interactors from appreciation refinement mass spectrometry experiments.