ライフサイエンスコーパス: cleavable complex

1 the enzyme in covalent linkage with DNA (the cleavable complex).

2 d measuring the formation of the topo II-DNA cleavable complex.

3 y disabling the formation of the topo II-DNA cleavable complex.

4 omerase II and prevents the formation of the cleavable complex.

5 tion of ParE prevented the formation of this cleavable complex.

6 on of a process(es) downstream from the TOP1 cleavable complex.

7 ormation of etoposide-stabilized topo II-DNA cleavable complex.

8 c inhibition of top-II or stabilization of a cleavable complex.

9 n in the absence of drugs that stabilize the cleavable complex.

10 le complex or inhibited camptothecin-induced cleavable complex.

11 out the fate of cellular TOP1 trapped in the cleavable complex.

12 ormation of etoposide stabilized topo II-DNA cleavable complex.

13 izing the Top1-DNA intermediate or cleavage (cleavable) complex.

14 ide kill cells by trapping covalent TOP2-DNA cleavable complexes.

15 -position of CPT would result in more stable cleavable complexes.

16 ase (topo) II without stabilizing DNA-topoII cleavable complexes.

17 ability to trap human DNA topoisomerase I in cleavable complexes.

18 hout damaging DNA or stabilizing DNA-topo II cleavable complexes.

19 ATP and involves the formation of reversible cleavable complexes.

20 ks, which include stable DNA-topoisomerase I cleavable complexes.

21 topo) II that does not stabilize DNA-topo II cleavable complexes.

22 piridol did not induce topoisomerase I or II cleavable complex activity.

23 that a VM-26-stabilized topoisomerase II-DNA cleavable complex acts as a replication fork barrier at

24 they resulted from the collision between the cleavable complex and DNA polymerase of S-phase cells.

25 IIalpha inhibitors are unable to induce DNA-cleavable complexes and cell death.

26 te that DNA damage can efficiently trap top1-cleavable complexes and enhance top1-mediated DNA recomb

27 isons than CPT and produce long lasting top1 cleavable complexes and greater cytotoxicity than CPT in

28 and 7-CM-EDO-CPT are more potent inducers of cleavable complexes and more cytotoxic than CPT.

29 efining chemosensitivity to CPT-induced top1-cleavable complexes and that CPT appears to have two cyt

30 own to trap DNA topoisomerase I on DNA, form cleavable complexes, and generate DNA breaks upon collis

31 Pathways influencing the repair of cleavable complexes are expected to be major determinant

32 ell lines indicate that events downstream of cleavable complexes are more relevant.

33 ere targeted to potential free 3' termini of cleavable complexes, as determined by mapping of cleavag

34 ore potent than camptothecin in the in vitro cleavable complex assay.

35 potencies were docked into the hypothetical cleavable complex binding site to test and refine the mo

36 rs are used to describe the induction of the cleavable complex by MccB17 analogs containing modified

37 Rb facilitates processing and repair of TOP2-cleavable complexes by recruiting proteins like BRCA1 to

38 sistent with the reversible trapping of top1 cleavable complexes by the indenoisoquinolines.

39 religation, resulting in an increase of top1 cleavable complexes, camptothecin did not reduce recombi

40 poisomerase I (top1) poison which traps top1 cleavable complexes; e.g. top1-linked DNA single-strand

41 metabolites antagonized etoposide-stabilized cleavable complex formation and inhibited topo II-DNA bi

42 no-4'-O-demethyl Epipodophyllotoxin (W2)] on cleavable complex formation and top I degradation.

43 Although all five drugs induced cleavable complex formation, two of the drugs, NB506 and

44 uction in VP-16-induced TOPO II-mediated DNA cleavable complex formation.

45 ase in the level of etoposide-stabilized DNA cleavable complex formation.

46 not affect etoposide-stabilized topo II-DNA cleavable complex formation.

47 topoisomerase I for the observed increase in cleavable complex formation.

48 general model for the ternary drug-DNA-TOP1 cleavable complex formed with camptothecin (CPT) and its

49 tment under hypoxic conditions, and that the cleavable complexes formed by TPZ are more stable over t

50 lated to the total amount of drug-stabilized cleavable complexes formed in VM-26-treated cells.

51 showed DNA cleavage with etoposide, and the cleavable complexes formed with etoposide showed greater

52 Compounds 19, 21, 24, and 25 were "cleavable-complex"-forming DNA topoisomerase II inhibito

53 o further understand the mechanisms by which cleavable complex-forming topoisomerase II inhibitors in

54 that the replication fork arrest induced by cleavable complex-forming topoisomerase II inhibitors le

55 II and etoposide that stabilizes enzyme/DNA cleavable complexes) have been used to probe the role of

56 tive technique to detect in vivo CPT-induced cleavable complexes; (ii) investigate the frequency and

57 he reduced formation of VP-16-stabilized DNA cleavable complex in the HL-60/DOX 0.05 cells was not du

58 top1 cleavage site irreversibly trapped top1 cleavable complexes in the absence of camptothecin and p

59 omerase I-catalyzed camptothecin-induced DNA cleavable complexes in the ovarian cell line, which was

60 Topoisomerase I (top1)-mediated cleavable complexes in the presence of CPT, measured by

61 A significant reduction in cleavable complexes in the resistant cells could be obse

62 merase II and prevent the resolution of the "cleavable complex," in which one DNA duplex is passed th

63 The reversal of the cleavable complexes induced by 7-E-MDO-CPT, 7-CM-MDO-CPT

64 In the current studies, we show that TOP2 cleavable complexes induced by the prototypic TOP2 poiso

65 cells, which suggested that VM-26-stabilized cleavable complexes interfered with the movement of DNA

66 transcription arrest and conversion of TOP1 cleavable complexes into 'irreversible' strand breaks.

67 scales and we conclude that formation of the cleavable complex is a prerequisite for polymerase block

68 ility of TOPO II to form drug-stabilized DNA cleavable complex is related to the phosphorylated state

69 hat independent of DNA replication, the TOP1 cleavable complex is ubiquitinated and destroyed in cell

70 Rb1-mediated processing and repair of TOP2-cleavable complexes is genetically separable from its ab

71 siological stresses are known to induce TOP2 cleavable complexes leading to apoptotic cell death and

72 We observe that degradation of trapped TOP2-cleavable complexes, liberation of DNA strand breaks, an

73 By contrast, CPT-stabilized TOP1 cleavable complexes located on the non-template strand w

74 gating T7 RNA polymerase is arrested by TOP1 cleavable complexes located on the template but not the

75 a model in which collision between the TOP1-cleavable complexes located on the template strand and t

76 CPT-stabilized TOP1 cleavable complexes located on the template strand withi

77 with a model in which the repair of TOP2beta cleavable complexes may involve transcription-dependent

78 The results suggest that a ternary cleavable complex might be stabilized by several hydroge

79 dimensional model for the postulated ternary cleavable complex of topoisomerase I (top1), DNA, and ca

80 ines tested induced topoisomerase I-mediated cleavable complex or inhibited camptothecin-induced clea

81 yeast to determine whether stabilization of cleavable complexes plays a role in doxorubicin action a

82 ross-links (including topoisomerase I and II cleavable complexes) produce stalling and collapse of re

83 he molecular mechanism(s) for repair of TOP2 cleavable complexes remains unclear.

84 DNA topoisomerase II (TOP2) cleavable complexes represent an unusual type of DNA dam

85 s led to slightly reduced rate constants for cleavable complex reversal.

86 mplexes with DNA and topoisomerase I (termed cleavable complexes) show greater activity in their abil

87 These analogs showed increasing cleavable complex stability as the number of hydroxyl gr

88 Our data indicate that in vitro cleavable complex stability, as determined by the appare

89 But, in no case was cleavable complex stabilization observed and the metabol

90 from events invoked for leukemogenic topo II cleavable complex-stabilizing antitumor agents.

91 Analysis of the levels of TOP1 cleavable complexes, SUMO-1-TOP1 conjugates, and ubiquit

92 k and the frozen topoisomerase converted the cleavable complex to a nonreversible form but did not ge

93 s to the formation of an increased number of cleavable complexes ultimately resulting in rise in DNA

94 otent inducers of topoisomerase (topo) I-DNA cleavable complexes using purified recombinant human DNA

95 This greater stability of the top1 cleavable complexes was contributed by the 7-alkyl and t

96 ture of the human topoisomerase I (TOP1)-DNA cleavable complex, we have developed a general model for

97 of a covalent enzyme-DNA complex termed the 'cleavable complex.' We have used yeast to determine whet

98 which enoxacin induces formation of a novel "cleavable" complex, whereas CcdB protein traps a very ra

99 n (7-E-MDO-CPT) also induced reversible top1 cleavable complexes, which were markedly more stable to

100 motherapeutic, etoposide, to trap topo II in cleavable complexes with DNA, thereby preventing DNA str

101 The concentration required to produce cleavable complexes with purified topoisomerase I in 50%

102 the hairpin cleavage rate and to form active cleavable complexes with Rnt1p.

103 produce double-strand breaks by trapping of cleavable complexes would, likewise, induce mutations sp