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. 2008 Oct 9;105(42):16125–16130. doi: 10.1073/pnas.0802727105

Fig. 5.

Fig. 5.

Model for persistence of Ub-PCNA. (A) On blocking of the replication fork at a lesion (X), PCNA becomes ubiquitinated (U). (Note that only one ubiquitin molecule is shown for simplicity, but it is likely that all three monomers of the homotrimeric ring become ubiquitinated.) (B) A new replication apparatus is assembled beyond the lesion, leaving a gap. (C) The process is repeated at the next lesion. (D) Some time later, the gap opposite the first lesion is filled, as indicated by the thick line.