ライフサイエンスコーパス: Topo II

1 Topo II 3'-UTR sequence analysis and RNA-protein binding

2 Topo II activity is a suggested predictive marker in can

3 Topo II activity was detected via the numeric release of

4 Topo II can be poisoned by common chemotherapeutics (suc

5 Topo-II localized to the perimeter of mitotic chromosome

6 bited 47% Topo I (camptothecin, 34%) and 20% Topo II (etoposide 24%) at 20 muM.

7 3l inhibited 61% Topo II (etoposide 24%) at 20 muM.

8 But here, we define a Topo II-dependent G2/M checkpoint in a genetically amena

9 gnificantly reduced by coadministration of a Topo-II poison.

10 ent the signatures of inhibition of HDAC and Topo II in both cell-free and whole-cell assays.

11 HDAC and Topo II modify each other's activity in vitro and in viv

12 of combination chemotherapy with Topo I and Topo II inhibitors.

13 , RFC, RFA, DNA ligase I, NDH II, Topo I and Topo II) and cell cycle proteins (Cyclins A, B1, D1, D2,

14 Topoisomerase I (Topo I) and Topo II inhibitors can selectively inhibit Epstein-Barr

15 Examination of the structure of Topo IA and Topo II and modeling of the Toprim domains of the primas

16 juxtaposed, and inserts seen in Topo IA and Topo II.

17 We propose that PICH and Topo II cooperate to prevent chromosome missegregation e

18 Because Topo II gene expression is regulated posttranscriptional

19 2 and metaphase cell cycle delays induced by Topo II poisons have been proposed to be the result of c

20 , and this enhances the growth inhibition by Topo II drugs.

21 ion; by contrast, non-DNA-damaging catalytic Topo II inhibitors such as ICRF-187 and merbarone do not

22 Finally, the catalytic Topo II inhibitor ICRF-187 suppressed VM-26-induced-FasL

23 nd cleavage core of Saccharomyces cerevisiae Topo II (also known as Top2) and a gate-DNA segment.

24 Thus, compromised Topo II function activates a yeast checkpoint system tha

25 Complexes containing Topo II possess HDAC activities, and complexes containin

26 -untranslated region (3'-UTR) in controlling Topo II mRNA accumulation.

27 pport the hypothesis that cell cycle-coupled Topo II gene expression is regulated by interaction of t

28 increased binding correlated with decreased Topo II mRNA levels.

29 enhanced in G(1), correlating with decreased Topo II mRNA levels.

30 lls demonstrated that, similar to endogenous Topo II mRNA levels, the mRNA levels of reporter genes c

31 Finally, Topo II and Sgo1 are equally important for Ipl1 recruitm

32 nimal PET of animals with L1210 tumors (high Topo-II expressing) showed excellent tumor accumulation

33 f breast cancer cells with topoisomerase II (Topo II) drugs, whereas paclitaxel (Taxol) does not have

34 ents of the life essential topoisomerase II (Topo II) enzyme activity.

35 one deacetylase (HDAC) and topoisomerase II (Topo II) inhibitors, respectively.

36 Topoisomerase II (Topo II) performs topological modifications on double-st

37 Topoisomerase II (Topo II) poisons such as etoposide can induce abortive D

38 potential to interact with topoisomerase II (Topo II) than did the other Ginkgo biloba constituents;

39 nes identified encoded DNA topoisomerase II (Topo II), an enzyme known to have a role in transcriptio

40 itivity to an inhibitor of Topoisomerase II (Topo II), ICRF-193.

41 s not due to inhibition of topoisomerase II (Topo II).

42 de (VP16), an inhibitor of topoisomerase II (Topo II).

43 Topoisomerase II (Topo-II) is an essential enzyme in the DNA replication p

44 and colocalized with topoisomerase IIalpha (Topo II) and scaffold protein II (ScII).

45 Mammalian topoisomerase IIalpha (Topo II) is a highly regulated enzyme essential for many

46 l domain (CTD) of DNA topoisomerase IIalpha (Topo II) provides a novel function at inner centromeres

47 In Topo II knockdown cells, DNA damage triggered by Ginkgo

48 otecan results in a compensatory increase in Topo II alpha levels associated with increasing sensitiv

49 Cs) are potent antitumor agents that inhibit Topo-II.

50 d with that of animals with PC-3 tumors (low Topo-II expressing), and the L1210 tumor uptake was sign

51 ited to increase the therapeutic activity of Topo II drugs.

52 trongly stimulates the catalytic activity of Topo II in vitro.

53 n is distinct from the catalytic activity of Topo II.

54 ed product enabled quantitative detection of Topo II activity at the single decatenation event level

55 promoting solely the structural function of Topo II.

56 The Ca2+-induced inhibition of Topo II catalytic activity and direct binding of Ca2+ to

57 tially decondensed chromosomes and a loss of Topo II and ScII, but not hCAP-C and histones.

58 ase (Topo) I inhibitors in the modulation of Topo II levels and sensitivity to Topo II-directed drugs

59 the described highly sensitive monitoring of Topo II activity may add considerably to the toolbox of

60 d in vitro genotoxicity may be the result of Topo II inhibition.

61 l (64)Cu-TSC complexes and the expression of Topo-II activity.

62 ounds is related to the expression levels of Topo-II in tumor tissue.

63 ere compared with the activity and levels of Topo-II, as determined by a commercially available assay

64 mors, which expressed high and low levels of Topo-II, respectively.

65 complexes containing HDAC1 or HDAC2 possess Topo II activities.

66 We conclude that by retarding Topo II-driven decatenation, cohesin mediates sister chr

67 For instance, complex-stabilizing Topo II inhibitors such as etoposide, teniposide, and do

68 firmed by using a biochemical assay to study Topo II enzyme inhibition.

69 el organisms has excluded genetic proof that Topo II checkpoints exist and are separable from the con

70 Furthermore, we show that Topo II alpha levels decline 5 days after the last dose

71 netic and biochemical evidence suggests that Topo II recruits Ipl1 via the Haspin-histone H3 threonin

72 mRNA levels of reporter genes containing the Topo II 3'-UTR varied during the cell cycle and were max

73 or camptothecin and, to a lesser extent, the Topo II inhibitor etoposide are potent inhibitors of the

74 y checkpoint components are required for the Topo II checkpoint, but checkpoint activation is not the

75 its levels affected cell sensitivity to the Topo II-targeting drug etoposide.

76 y of tumors to subsequent treatment with the Topo II inhibitor etoposide.

77 lytic activity and direct binding of Ca2+ to Topo II by a fluorescent filter-binding assay supports a

78 ion of FasL promoter activity in response to Topo II inhibitors such as VM-26 mimicked endogenous Fas

79 ulation of Topo II levels and sensitivity to Topo II-directed drugs, athymic mice bearing SW480 human

80 increased susceptibility and sensitivity to Topo II-induced DNA double-strand breaks, thereby reveal

81 to investigate effects of DNA topoisomerase (Topo) II inhibitors on FasL promoter activity.

82 n induce abortive DNA strand breaks in which Topo II remains covalently bound to a 5' DNA strand term

83 ate that HDAC1 and HDAC2 are associated with Topo II in vivo under normal physiological conditions.

84 that DNA damage is directly associated with Topo II.