ETP-46464 is a potent and selective inhibitor of the DNA damage response kinase Ataxia telangiectasia-mutated (ATM) - and Rad3-related (ATR) with an IC50 of 25 nM. ETP-46464 shows moderate activity against PI3K and is a potent inhibitor of mTor, but is selective for ATR versus ATM and DNA -dependent protein kinase (DNA -PKcs) even at high doses. ETP-46464 inhibited phosphorylation of Chk1, the downstream kinase of ATR, but did not affect ionizing radiation–induced γH2AX formation, which is jointly controlled by ATM and DNA-PKc.
ETP-46464 is a potent and selective inhibitor of the DNA damage response kinase Ataxia telangiectasia-mutated (ATM) - and Rad3-related (ATR).
DNA replication errors generate complex chromosomal rearrangements and thereby contribute to tumorigenesis and other human diseases. One mechanism that triggers these errors is mitotic entry before the completion of DNA replication. To address how mitosis might affect DNA replication, we
The repair of DNA double-strand breaks (DSBs) is essential for safeguarding genome integrity. When a DSB forms, the PI3K-related ATM kinase rapidly triggers the establishment of megabase-sized, chromatin domains decorated with phosphorylated histone H2AX (γH2AX), which act as seeds for
Covalent DNA-protein cross-links (DPCs) impede replication fork progression and threaten genome integrity. Using Xenopus egg extracts, we previously showed that replication fork collision with DPCs causes their proteolysis, followed by translesion DNA synthesis. We show here that when DPC proteolysis
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