David Cortez lab
Replication stress response is a crucial and complex system that evolved to sustain genomic stability in the face of DNA damage. DNA-PK, ATM and ATR are three prominent protein kinases involved in activating and regulating such response. This may lead to subsequent fork stalling and structural rearrangements of the replication fork such as fork reversal to facilitate fork protection while allowing time for fork processing and restart. We study how such intricate dynamic changes to the fork are regulated and maintained through a wide variety of biochemical techniques.