ATR

Ataxia telangiectasia mutated (ATM) encodes a serine/threonine protein kinase that coordinates cellular signaling after DNA double-strand breaks, oxidative stress, and cell-cycle checkpoint activation[1]. Mechanistically, ATM and ATR (ATM-Rad3-related) act as proximal DNA damage response kinases, but ATM is central to double-strand-break signaling, whereas ATR leads a parallel cascade activated by replication stress[2][3]. In disease contexts, ATM mutation causes ataxia-telangiectasia, a multisystem disorder involving neurodegeneration, immunodeficiency, radiosensitivity, cancer susceptibility, and genetic instability[4][5]. Compared with ATR, ATM deficiency creates experimental dependence on ATR in some cancer models, supporting ATR inhibition as a synthetic-lethal strategy in ATM-deficient prostate cancer and colorectal xenograft models[6][7]. For research applications, ATM inhibitors such as KU-55933 help interrogate ATM-dependent DNA damage signaling and have reduced HSV-1 replication and stromal keratitis severity in experimental corneal models[8].
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