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Fig. 2 | Theoretical Biology and Medical Modelling

Fig. 2

From: Fanconi anemia cells with unrepaired DNA damage activate components of the checkpoint recovery process

Fig. 2

FA network simulations. a The current information regarding the FA/BRCA pathway have not uncovered the mechanism that allows the resolution of the G2/M checkpoint after DNA damage and further cell division. b Trajectories and attractor of the wild type FA/BRCA network under an ICL pulse. In this simulation wild type cells repair DNA damage through the FA/BRCA pathway and arrive to CCP attractor after activating the CHKREC node once the damage has been fixed. The inclusion of the CHKREC node, as a checkpoint negative regulator, allows to explore the mechanisms behind cell division after checkpoint resolution. c In response to a continuous ICL DNA damage, wild type cells arrive to a CCA attractor with activation of the checkpoint and DNA damage repair nodes,the CHKREC node becomes eventually activated in this attractor. d Under and ICL pulse FAcore mutant cells activate the NHEJ pathway to repair DNA damage and arrive to a CCP attractor. e In response to a continuous ICL DNA damage, FAcore mutant cells concomitantly activate the checkpoint and the CHKREC nodes. Node names are indicated at the topmost row. The leftmost column indicates simulation time steps in arbitrary units. Time steps corresponding to trajectories are indicated and time steps corresponding to attractors are indicated by shaded gray and “ATT”. For illustrative purpose cyclic attractors are represented twice

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