DNA damage or incomplete replication of DNA results in the inhibition of cell cycle progression at the G1 to S or the G2 to M phase transition by conserved regulatory mechanisms known as cell cycle checkpoints. Checkpoint proteins include Rad17, which is involved in regulating cell cycle progression at the G1 checkpoint as well as Chk1, Chk2, Rad1, Rad9 and Hus1, which are involved in regulating cell cycle arrest at the G2 checkpoint. In response to DNA damage, ATM and ATR kinases are important for cell cycle checkpoint response signalling. ATR-interacting protein (ATRIP), also designated ATM and Rad3-related-interacting protein, is required for checkpoint signaling after DNA damage. It is also important for ATR expression, which regulates DNA replication and damage checkpoint responses. ATRIP is a ubiquitously expressed protein that can form heterodimers with ATR. After dimerization they bind the RPA complex and are recruited to single stranded DNA. ATRIP is a nuclear protein that may also play a role in protein stabilization.