Fig. 1
From: Influence of cellular models and individual factor in the biological response to head CT scan exams
The radiation-induced ATM nucleoshuttling: RIANS model and its current biomarkers. a In the frame of the RIANS model, IR induce the monomerisation of the ATM dimers in cytoplasm. The resulting ATM monomers diffuse in the nucleus and phosphorylate the H2AX histone variant molecular (γH2AX) at DSB sites, which triggers the formation of nuclear γH2AX foci, easily quantifiable by immunofluorescence. This is the recognition step. The recognised DSB are repaired by the non-homologous end-joining, the major DSB repair pathway in humans (see refs. [8, 16,17,18,19,20,21]). During the DSB repair process, two ATM monomers reassociate on the DSB sites and form the nuclear autophophorylated ATM (pATM) foci, also visible by immunofluorescence. b In the kinetics of γH2AX or pATM foci appearance, the early (10 min, 1 h) post-irradiation times provide information on the functionality of the DSB recognition step while the late (24 h) ones provide information on the functionality of the DSB repair step. ATM Ataxia telangiectasia mutated gene/protein, DSB Deoxyribonucleic acid double-strand breaks, RIANS Radiation-induced nucleoshuttling of the ATM protein, γH2AX Phosphorylated forms of the H2AX histone variant molecular