A point mutation in the FAT domain constitutively increases the kinase activity of Rad3ATR and bypasses the requirement for 9-1-1 phosphorylation to activate the DNA replication checkpoint - PubMed
5 hours ago
- #DNA replication checkpoint
- #ATR kinase
- #allosteric regulation
- A point mutation (E1369K) in the FAT domain of Rad3ATR constitutively increases its kinase activity.
- This mutation bypasses the need for 9-1-1 complex phosphorylation specifically in the DNA replication checkpoint.
- The findings suggest an allosteric activation mechanism via the FAT domain, distinct from the canonical PRD model.
- This mechanism is likely conserved in higher eukaryotes.