Abstract
ATM is a member of a family of proteins that share a phosphatidylinositol 3-kinase (PI3K) domain. This group includes the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), A-T and rad3-related protein (ATR), and proteins in other organisms responsible for DNA damage recognition or cell cycle control. ATM kinase is rapidly activated by ionizing radiation to phosphorylate a series of substrates involved in radiation signaling. However, evidence also exists to show that ATM can be regulated at both the transcriptional and translational levels. A more widespread role for ATM in events other than DNA damage recognition exists including receptor signaling, cellular proliferation, K + channel activity, and insulin signaling pathways. It is possible that ATM plays a direct role in these processes, or that in its absence cellular homeostasis is altered by oxidative stress or some other form of perturbation, leading to the myriad of defects described in A-T cells. This chapter focuses on the function of ATM; its role in DNA damage recognition and its relationship to other DNA damage recognition systems; intermediates phosphorylated; and pathways activated to help coordinate the cellular response to radiation. A possible role in more general signaling is discussed later.
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