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

Journal:
PLOS Genetics
Published:
DOI:
10.1371/journal.pgen.1012213
Affiliations:
1
Authors:
5
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Institutions Authors Share
Wright State University, United States of America (USA)
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