ATM/ATR

ATM (Ataxia Telangiectasia Mutated) and ATR (ATM and Rad3-Related) are crucial proteins in the cellular DNA damage response. Both function as serine/threonine kinases that activate in response to DNA damage, particularly DNA double-strand breaks (ATM) and replication stress (ATR). They play pivotal roles in signaling pathways that halt the cell cycle, allowing time for DNA repair, or initiating apoptosis if the damage is irreparable. Given their central role in maintaining genomic stability, ATM and ATR are important targets in cancer therapy. Inhibiting these kinases can sensitize cancer cells to radiation and chemotherapy by preventing effective DNA damage repair, thus enhancing the treatment's efficacy and targeting tumor cells more precisely.