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Identification of GHRHR as the target of ATR is consistent with the myriad effects previously reported for ATR in mammalian systems.
DNA gap filling, promoted by ATR, would prevent the involvement of ATM, providing an explanation for the apparent role of ATR in antagonizing ATM.
The role of ATR in response to cisplatin has gained considerable attention with the demonstration and genetic knockdown of ATR-sensitized p53 null cancer cells to cisplatin.
Fokas, E. et al. Targeting ATR in DNA damage response and cancer therapeutics.
Total activities were significantly enhanced by ATR in rice tissues.
Jazayeri, A. et al. ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks.
To describe the Return to competition after Achilles Tendon rupture (ATR) in an elite soccer player.
We implicate the DDR kinases ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3 related (ATR) in promoting contractions and preventing instability, respectively.
The properties of these analogs have been investigated by calculating physicochemical parameters and studying their potential to specifically inhibit ATR in cells.
We focus on the activities of ATR in the control of cell cycle checkpoints, origin firing and replication fork stability, and on how proper regulation of these processes is crucial to ensure faithful duplication of a challenging genome.
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We observed an accumulation of GFP-ATR in the nucleolus as well.
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