ライフサイエンスコーパス: microtubule inhibitor

1 ases a DNA cross-linking agent rather than a microtubule inhibitor.

2 ld artificially in G2-phase by addition of a microtubule inhibitor.

3 tosis or in cells blocked at prometaphase by microtubule inhibitors.

4 arrest in the face of kinetochore defects or microtubule inhibitors.

5 c checkpoint function and chemoresistance to microtubule inhibitors.

6 were either sensitive or resistant to known microtubule inhibitors.

7 (PBMC) in their responses to treatment with microtubule inhibitors.

8 y that is activated by vinblastine and other microtubule inhibitors.

9 f sister chromatids in the presence of these microtubule inhibitors.

10 s such, they represent downstream targets of microtubule inhibitors.

11 Because microtubule inhibitors activate JNK, we sought to determ

12 evealed a compound with higher activity as a microtubule inhibitor and cytotoxic agent in comparison

13 its inviability after transient exposure to microtubule inhibitors and its precocious dissociation o

14 spindle checkpoint activation, and thus how microtubule inhibitors and other antimitotic drugs ultim

15 Moreover, the data identify microtubule inhibitors and protein synthesis inhibitors

16 Src kinase inhibitors, microtubule inhibitors, and PGE(2) prevented the T cell

17 s are identified, including glucocorticoids, microtubule inhibitors, and protein synthesis inhibitors

18 cells exhibit no motility in the presence of microtubule inhibitors, at concentrations that disassemb

19 d that upon spindle checkpoint activation by microtubule inhibitors benomyl or nocodazole, wild-type

20 ed predominantly in G1 and to respond not to microtubule inhibitor but to mitogenic stimulus.

21 and Bcl-2 are phosphorylated in response to microtubule inhibitors, but the kinase(s) responsible an

22 s required for the M phase arrest induced by microtubule inhibitors, but the protein is not essential

23 Paclitaxel (PTX) and other microtubule inhibitors cause mitotic arrest.

24 agents that induced Bcl-xL phosphorylation (microtubule inhibitors) caused loss of the 150-kDa form,

25 tacks are unique in their sensitivity to the microtubule inhibitor colchicine, contrasted with their

26 -expressing tumor cells was augmented by the microtubule inhibitor, colchicine.

27 ication to the chemical structure of a known microtubule inhibitor, combretastatin A-4, Borowiak et a

28 -treatment with ATM and vincristine (VCR), a microtubule inhibitor currently used in rhabdomyosarcoma

29 ation of ubiquitination at specific sites by microtubule inhibitors, demonstrating the effectiveness

30 Nocodazole, a microtubule inhibitor, did not disperse aggregates.

31 In contrast, the cytotoxic microtubule inhibitor docetaxel increased glycerophospho

32 together, our results show that these novel microtubule inhibitors have promising anticancer activit

33 on and that combination therapy with ATM and microtubule inhibitors holds promise for the treatment o

34 Eribulin (E7389), a mechanistically unique microtubule inhibitor in phase III clinical trials for c

35 inical efficacy data for vinflunine, a novel microtubule inhibitor, in MPM.

36 These microtubule inhibitors increased osteoblast differentiat

37 rexate (antimetabolites), and vinblastine (a microtubule inhibitor) induced the same site-specific cl

38 cerning the role of Bcl-2 phosphorylation in microtubule inhibitor-induced apoptosis.

39 t the JNK pathway plays an essential role in microtubule inhibitor-induced apoptosis.

40 identify specific p53 residues necessary for microtubule inhibitor-induced phosphorylation.

41 Moreover, these cells underwent microtubule inhibitor-induced reduplication, leading to

42 ough MSC function, prototypically induced by microtubule inhibitors, is active selectively during mit

43 ery of cytotoxics, 1C1 was conjugated to the microtubule inhibitor monomethylauristatin phenylalanine

44 oint function would sensitize tumor cells to microtubule inhibitor (MTI)-induced apoptosis, we examin

45 orms in cells increased after treatment with microtubule inhibitors (MTIs) and that the pattern of p5

46 sented herein show that after treatment with microtubule inhibitors (MTIs), cells deficient in the Cd

47 ER reorganisation is also prevented by the microtubule inhibitor nocodazole and by the inhibition o

48 missiveness was impaired upon treatment with microtubule inhibitor nocodazole, which was identified a

49 elatively low concentration of nuclei or the microtubule inhibitor nocodazole.

50 after prolonged treatment of cells with the microtubule inhibitor nocodazole.

51 Cells treated with the microtubule inhibitors nocodazole, colchicine, vincristi

52 In contrast, the microtubule inhibitor, nocodazole, prevented development

53 Here we show that, unlike many other microtubule inhibitors, noscapine does not significantly

54 enzotrifluoride (chloralin) (2), an in vitro microtubule inhibitor of several Leishmania species, hav

55 ting these responses, we examined effects of microtubule inhibitors on the hedgehog (Hh) pathway, sin

56 Moreover, application of colchicine, a microtubule inhibitor, or paclitaxel, a microtubule stab

57 sis thaliana roots to moderate levels of the microtubule inhibitor, oryzalin.

58 Microtubule inhibitors paclitaxel and demecolcine inhibi

59 rethamine), anthracylines (doxorubicin), and microtubule inhibitors (paclitaxel).

60 ggest that Bcl-xL phosphorylation induced by microtubule inhibitors plays a key pro-apoptotic role at

61 perhaps other signaling pathways altered by microtubule inhibitors reflect perturbations of normal m

62 Cytochalasin D and vinblastine, actin and microtubule inhibitors, respectively, failed to complete

63 to aid in the design of effective parasitic microtubule inhibitors, several novel dinitroaniline ana

64 Experiments with microtubule inhibitors show that the retracted microtubu

65 Microtubule inhibitors slowed but did not prevent membra

66 pathy; and, third, that structurally diverse microtubule inhibitors stimulate OXPHOS transcription wh

67 the antiangiogenic effects of 2-ME and other microtubule inhibitors such as Taxol, vincristine, and c

68 of Bcl-xL phosphorylation induced by several microtubule inhibitors tested.

69 analog of the natural product maytansine, a microtubule inhibitor that by itself has limited clinica

70 uct Dolastatin 10, are ultrapotent cytotoxic microtubule inhibitors that are clinically used as paylo

71 When conjugated with a tubulysin-based microtubule inhibitor, the biparatopic ADC demonstrates

72 BR1 is required by cells that are exposed to microtubule inhibitors to arrest in mitosis.

73 rget a potent, semisynthetic analogue of the microtubule inhibitor tubulysin B to FR-enriched tumors.

74 However, when continuously exposed to microtubule inhibitors, untransformed cells eventually s

75 Vinblastine and other microtubule inhibitors used as antimitotic cancer drugs

76 ization and function of c-Jun induced by the microtubule inhibitor vinblastine, which strongly induce

77 axons of neurons grown in the presence of a microtubule-inhibitor, vinblastine.

78 Novel triazine-based microtubule inhibitors were discovered by an efficient z

79 vivo stomatal aperture assays with different microtubule inhibitors were performed.

80 Microtubule inhibitors, widely used in cancer chemothera