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Identification of early replicating fragile sites that contribute to genome instability.
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Coordinated control of replication and transcription by a SAPK protects genomic integrity.
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Senataxin associates with replication forks to protect fork integrity across RNA-polymerase-II-transcribed genes.
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Increased replication initiation and conflicts with transcription underlie Cyclin E-induced replication stress.
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The complex basis underlying common fragile site instability in cancer.
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Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription.
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A genome-wide siRNA screen reveals diverse cellular processes and pathways that mediate genome stability.
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Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study.
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