Figure 5.

Model presenting the interplay between oncogene activation, FANCD2 and cathepsin expression. An unscheduled and permanent oncogene activation leads to a burst of cells in S-phase associated to DNA damage and replication stress that activates the DNA damage response. FANCD2, which activation is integrated in the DDR network, acts to not only allow DNA repair and replication rescue but also delay the potential establishment of a permanent growth arrest signaling network that drives the cells into senescence by opposing to CTSL1 activity that, per se, affects, directly or indirectly, FANCD2 expression.