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. 2011 Dec 13;287(5):3366–3380. doi: 10.1074/jbc.M111.311241

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© 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 8. — RAD51C regulates intra-S-phase checkpoint through CHK2 activation in response to replication-associated DSBs. A, knocking down RAD51C in HeLa cells leads to loss of intra-S-phase checkpoint control after CPT (1 μm for 2 h) treatment as measured by BrdU incorporation. B, RAD51C depletion in HeLa cells decreases CHK2 phosphorylation after CPT treatment. Control as well as cells transfected with RAD51C shRNA were treated with 1 μm CPT for the indicated time. C, overexpression of various RAD51C variants affect CHK2 activation after CPT treatment. HeLa cells were transfected with 1 μg of WTRAD51C and RAD51C variants treated with 1 μm CPT for the indicated time. D, model to explain RAD51C-regulated HR and intra-S-phase checkpoint in response to ICL and replicative stress.