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

1 mplexes can impede DNA replication and cause replication fork collapse.

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

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

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

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

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

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

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

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

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

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

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

13 is during replication elongation, suggesting replication fork collapse.

14 small replication intermediates and eventual replication fork collapse.

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

16 lap recombination intermediate downstream of replication fork collapse.

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

18 d before replication termination, to prevent replication fork collapse.

19 and nucleoprotein complexes that can lead to replication fork collapse.

20 his process that must be overcome to prevent replication fork collapse.

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

22 We propose that replication fork collapse accompanies episodic hypermuta

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

24 he repair of uracil-induced gaps, increasing replication fork collapse and cell death.

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

26 This prevents replication fork collapse and controls their progression

27 lobal replisome disassembly that can trigger replication fork collapse and DNA rearrangements.

28 end joining (NHEJ), DSBs generated following replication fork collapse and DSBs present owing to stal

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

30 cription factor (HLTF), causing irreversible replication fork collapse and hyperaccumulation of ssDNA

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

32 breaks (DSBs) by inducing lamin B1-dependent replication fork collapse and inhibition of homologous r

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

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

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

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

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

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

39 s can result in RNA polymerase stalling, DNA replication fork collapse, and hyperactivation of the SS

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

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

42 We show that replication fork collapse at leading-strand nicks genera

43 t mechanisms of DNA breakage are implicated: replication fork collapse at natural replication barrier

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

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

46 pombe for studying recombination induced by replication fork collapse at the site-specific protein-D

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

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

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

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

51 In contrast, replication forks collapsed by prolonged replication blo

52 lication catastrophe, a form of irreversible replication fork collapse caused by excessive single-str

53 on and nonhomologous end joining, leading to replication fork collapse, chromosomal instability, and

54 e on genomic hmdU, leading to PARP trapping, replication fork collapse, DNA break formation, and apop

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

56 Thus, replication fork collapse following ATR inhibition is a

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

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

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

60 predominant role of this enzyme in avoiding replication fork collapse in all three plant genomes, bo

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

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

63 DAC8 and checkpoint kinases led to extensive replication fork collapse, irreversible cell-cycle arres

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

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

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

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

68 regions of single-stranded DNA arising from replication fork collapse or resection of DNA double str

69 the polymerization of DNA or RNA, leading to replication fork collapse or transcription arrest, or ca

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

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

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

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

74 g3-mediated ligation, causing dose-dependent replication fork collapse, which is detrimental to eryth

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

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