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1 eplication soon after UVC irradiation (i.e., postreplication repair).
2 protein ligase that has crucial functions in postreplication repair.
3 on serves as a molecular mark to orchestrate postreplication repair.
4 illess H2A/H3 mutant, indicating a defect in postreplication repair.
5 into recombination-dependent and error-free postreplication repair.
6 n the RAD18 epistasis group, which regulates postreplication repair.
7 -cycle response to UV is to provide time for postreplication repair.
8 on in the RING finger motif are defective in postreplication repair.
9 multiple DNA damaging agents and a defect in postreplication repair.
10 er eukaryotes, Rad18 plays a crucial role in postreplication repair.
11 to maintenance of genomic stability through postreplication repair.
12 DNA damage signaling and (iii) facilitating postreplication repair.
13 s that perhaps determine the fidelity of DNA postreplication repair.
14 s 10 and 13 lie in or near genes involved in postreplication repair, a DNA damage-tolerance pathway.
15 is necessary to restore normal survival and postreplication repair after ultraviolet irradiation in
17 itin-conjugating enzyme, and a key player in postreplication repair and induced mutagenesis in the ye
18 ecombination and nucleotide excision repair, postreplication repair, and checkpoints in the repair an
19 rough homologous recombinational repair, not postreplication repair, and confirm findings of a G1 che
21 induced by ultraviolet light, and defective postreplication repair, but normal nucleotide excision r
22 ion synthesis DNA polymerase, the Mms2-Ubc13 postreplication repair complex, downstream DNA-damage ch
23 include DNA replication, DNA damage repair, postreplication repair, damage checkpoint activation, ch
25 nhomologous end joining, excision repair, or postreplication repair enhanced sensitivity to Top2 targ
26 ite damaged DNA during replication, and this postreplication repair function depends on its HIRAN dom
28 tolerance process in eukaryotes (also called postreplication repair) has existed for more than two de
29 odification central to DNA damage bypass and postreplication repair in both yeast and vertebrates.
30 poorly defined RAD6-RAD18-RAD5 mechanism of postreplication repair in eukaryotes occurs by an analog
31 combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3'-t
32 ide excision repair, recombinational repair, postreplication repair including translesional synthesis
33 ranslesion synthesis, one of the pathways of postreplication repair, is thought to account for some r
34 or-free translesion synthesis by Poleta, and postreplication repair of discontinuities by a Rad5-depe
35 in-conjugating enzymes that are required for postreplication repair of DNA and damage-induced mutagen
36 ated as a participant in the recombinational postreplication repair of these replication products.
38 umor suppressor gene that might operate in a postreplication repair or a cell cycle checkpoint functi
39 encodes a DNA helicase that is active in the postreplication repair pathway and homologous recombinat
40 ons to promote recombination through a novel postreplication repair pathway and the structure-specifi
42 in nucleotide excision repair (NER) (rad14), postreplication repair (PRR) (rad6, rad18, mms2, and rad
44 NA polymerases eta or zeta or Rad5-dependent postreplication repair (PRR) in which error-free replica
45 in conjugating enzymes that are required for postreplication repair (PRR) of DNA and damage-induced m
47 First, we show that genes in the error-free postreplication repair (PRR) pathway prevent fusion of i
49 e damage whereas the recombination (REC) and postreplication repair (PRR) pathways bypass the damage,
50 f1 and different gene products implicated in postreplication repair (PRR) pathways in the suppression
54 have evolved lesion bypass pathways such as postreplication repair (PRR) to resolve these arrested f
56 that, in addition to its established role in postreplication repair, RAD18 is also required for the o
57 HR, resolution of branched HR intermediates, postreplication repair, sumoylation in response to DNA d
58 at, in addition to homologous recombination, postreplication repair, the Fanconi anemia pathway, poly
59 ecognized as an essential step in initiating postreplication repair, the mechanistic relevance of thi
61 repair, homologous recombination repair, or postreplication repair when compared with platin control
62 lesion, and homology-dependent repair (HDR; postreplication repair), which is based on the homologou