Mombach, José CMBugs, Cristhian AChaouiya, Claudine2015-10-012015-10-012014-10-27http://hdl.handle.net/10400.7/339DNA damage (single or double-strand breaks) triggers adapted cellular responses. These responses are elicited through signalling pathways, which activate cell cycle checkpoints and basically lead to three cellular fates: cycle arrest promoting DNA repair, senescence (permanent arrest) or cell death. Cellular senescence is known for having a tumour-suppressive function and its regulation arouses a growing scientific interest. Here, we advance a qualitative model covering DNA damage response pathways, focusing on G1/S checkpoint enforcement, supposedly more sensitive to arrest than G2/M checkpoint.engSignalling networkLogical modellingSenescenceDNA-damageCell fateCell cycle checkpointjournal article10.1186/1471-2164-15-S7-S710.1186/1471-2164-15-S7-S7