Fig. 9 | Nature Communications

Fig. 9

From: A requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancers

Fig. 9The alternative text for this image may have been generated using AI.

Model depicting the role of the cohesin complex during replication fork procession. In normal cells with intact STAG2 (left), cohesin dynamically associates with the pre-replication complex and replication machinery to stabilize the replication fork. In cancer cells with STAG2 inactivation (right), disruption of the cohesin interaction with PCNA and DNA polymerases results in failure to establish SMC3 acetylation, replication fork collapse, DNA double-strand breaks, and enhanced sensitivity to DNA damaging chemotherapeutic agents

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