ライフサイエンスコーパス: replication fork collapse

1 mechanism of S phase DPC repair that avoids replication fork collapse.

2 interaction with the sliding clamp, driving replication fork collapse.

3 es, unscheduled origin firing, and increased replication fork collapse.

4 ut has no obvious effect on RPA2-P following replication fork collapse.

5 checkpoint proteins Cds1 and Mrc1 to prevent replication fork collapse.

6 on DNA replication, and can be explained by replication fork collapse.

7 upon FEN1 depletion are the direct result of replication fork collapse.

8 ession of the replisome, possibly leading to replication fork collapse.

9 the point of the DNA lesion before complete replication fork collapse.

10 ting double-strand break formation, and thus replication fork collapse.

11 is during replication elongation, suggesting replication fork collapse.

12 small replication intermediates and eventual replication fork collapse.

13 viability but is essential for recovery from replication fork collapse.

14 lap recombination intermediate downstream of replication fork collapse.

15 possibly re-initiation of replication after replication fork collapse.

16 -directed repair (5' to 3' resected ends) or replication fork collapse.

17 tabilizes DNA replication forks and prevents replication fork collapse, a cause of DNA breaks and apo

18 We propose that replication fork collapse accompanies episodic hypermuta

19 during DNA replication, these lesions cause replication fork collapse and are transformed into subst

20 nd breaks (DSB) occur in chromatin following replication fork collapse and chemical or physical damag

21 This prevents replication fork collapse and controls their progression

22 s with the transcription apparatus can cause replication fork collapse and genomic instability.

23 tants with replication inhibitors results in replication fork collapse and inappropriate partitioning

24 Progerin sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in

25 Implications of these results for replication fork collapse and recovery are discussed.

26 des across lesions, thereby limiting stalled replication fork collapse and the potential for cell dea

27 a-induced nucleotide depletion by preventing replication fork collapse and the segregation of unrepli

28 of a functional S-phase checkpoint, stalled replication forks collapse and give rise to chromosome b

29 nsitivity to DNA-damaging agents that induce replication fork collapse, and exhibit slower fork recov

30 generated at conventional DSBs or following replication fork collapse are therefore intrinsically di

31 These observations establish replication fork collapse as a dynamic process that cont

32 and DNA breaks may arise as a consequence of replication fork collapse at sites of oxidative damage,

33 controls the S-phase checkpoint and prevents replication fork collapse at slow zones of DNA replicati

34 NA triggers chromosomal fragmentation due to replication fork collapse at uracil-excision intermediat

35 racil-triggered chromosomal fragmentation is replication fork collapse at uracil-excision nicks.

36 DNA synthesis or reprime DNA synthesis after replication fork collapse, but the origin of this activi

37 endonuclease may play a more direct role in replication fork collapse by catalysing the cleavage of

38 In contrast, replication forks collapsed by prolonged replication blo

39 re a potent block to replication, leading to replication fork collapse, double-strand DNA breaks, and

40 Thus, replication fork collapse following ATR inhibition is a

41 Interestingly, SCE produced by replication fork collapse following DNA DSBs creation is

42 NA double-strand breaks (DSBs), or following replication fork collapse from HR substrates assembled a

43 tion fork collisions that ultimately lead to replication fork collapse, growth stasis and/or cell dea

44 ng replication fork integrity and preventing replication fork collapse in the presence of triplex str

45 ments for proteins involved in recovery from replication fork collapse, including the gammaH2AX-bindi

46 the intra-S-phase checkpoint, which prevents replication fork collapse, late origin firing and stabil

47 fragmentation patterns not only support the replication fork collapse model, but also reveal another

48 xpression technology assay), suggesting that replication fork collapse occurs more frequently in mutA

49 DSBs that arise by replication fork collapse or by erosion of uncapped telo

50 We propose that a replication fork "collapse point" in HU-treated cells de

51 an increase in replication fork stalling or replication fork collapse that activates the G2 DNA dama

52 The double-strand DNA breaks resulting from replication fork collapse were inefficiently repaired, c

53 fect in RAD51 recruitment and SCE induced by replication fork collapse when ATR is depleted.

54 combination-dependent DNA intermediates when replication forks collapse, which leads to increased rDN

55 ng radiation (IR)-induced DSBs and following replication fork collapse, yet, is essential for RAD-51