Replication stress has emerged as a key driver of oncogenesis but also represents an Achilles' heel of cancer cells. Newly reported SUMO binding and SUMO ligase functions of the DNA repair protein SLX4 that influence the outcome of replication stress open new avenues for investigating the roles played by SLX4 in tumorigenesis.
Keywords: BTB domain; Chromosome stability; DNA damage response; E3 SUMO ligase; Fanconi anemia; SLX4; SUMO; SUMO Interaction Motifs; XPF-ERCC1; oncogenesis; replication stress; signal transduction; structure-specific endonuclease; tumor suppressor.