ライフサイエンスコーパス: antimicrotubule

1 We present here a high-throughput assay for antimicrotubule activity in which fluorescence is used t

2 d critical structural elements necessary for antimicrotubule activity that correspond to comparable g

3 s with various mechanisms of action, such as antimicrotubule activity, histone deacetylase inhibition

4 tubulin fusion to observe the effects of the antimicrotubule agent benomyl.

5 mab to specifically deliver the maytansinoid antimicrotubule agent DM1 to HER2-positive cells.

6 njugate designed to deliver the maytansinoid antimicrotubule agent drug maytansinoid-1 directly to pr

7 benzamide, RH-4032, was found to be a potent antimicrotubule agent in tobacco (Nicotiana tabacum) cel

8 hetic derivative of Cryptophycin 1, a potent antimicrotubule agent isolated from cyanobacteria.

9 gate brentuximab vedotin delivers the potent antimicrotubule agent monomethylauristatin E to CD30-pos

10 Epothilone B is a novel nontaxane antimicrotubule agent that is active even against paclit

11 ) B derivative BMS 247550, a novel nontaxane antimicrotubule agent, as well as the death ligand Apo-2

12 -mercapto-1-oxopropyl)-maytansine), a potent antimicrotubule agent, covalently linked to the murine m

13 astuzumab with targeted delivery of a potent antimicrotubule agent, DM1, to human epidermal growth fa

14 ctively delivers monomethyl auristatin E, an antimicrotubule agent, into CD30-expressing cells.

15 PTX, an antimicrotubule agent, is a potent antitumor agent commo

16 Estramustine (EM), an antimicrotubule agent, is effective against hormone-refr

17 onjugated to the maytansinoid, DM1, a potent antimicrotubule agent, via the thioether linker, N-succi

18 ed a monoclonal antibody, and 6% received an antimicrotubule agent.

19 tinomycin D, doxorubicin, and etoposide) and antimicrotubule agents (i.e., vincristine and paclitaxel

20 pproach to improving the efficacy of certain antimicrotubule agents against breast cancer by regulati

21 only a selected subset of cytotoxic agents (antimicrotubule agents and a topoisomerase inhibitor).

22 2-MeOEMATE and 2-EtEMATE functioned as antimicrotubule agents and inhibited the ability of pacl

23 tubule disassembly and apoptosis elicited by antimicrotubule agents and knockdown of SIRT3 prevents t

24 Antimicrotubule agents are commonly used chemotherapy dr

25 of two alleles is strongly suppressed by the antimicrotubule agents benomyl and nocodazole and a thir

26 eening program aimed at the discovery of new antimicrotubule agents from natural products yielded lau

27 for IRF9 in the development of resistance to antimicrotubule agents in breast tumor cells and may lin

28 mitosis, this could increase sensitivity to antimicrotubule agents in human breast cancer cells over

29 Loss of p53 sensitizes to antimicrotubule agents in human tumor cells, but little

30 g a relatively low concentration of TRAIL to antimicrotubule agents markedly increases complete caspa

31 des a unique approach to studying effects of antimicrotubule agents on plant cells by allowing compet

32 Our results indicate that these antimicrotubule agents or okadaic acid can induce posttr

33 esistance that hampers the efficacy of other antimicrotubule agents such as paclitaxel and vincristin

34 revealed a correlation to clinically useful antimicrotubule agents such as paclitaxel and vincristin

35 2-MeOEMATE and 2-EtEMATE are novel antimicrotubule agents that have potent anticancer activ

36 er taxol nor nocodazole (30-100 microM), two antimicrotubule agents, enhanced K(ATP) channel activity

37 tathmin-mediated mechanisms of resistance to antimicrotubule agents, including altered drug binding a

38 protein (P-glycoprotein) than currently used antimicrotubule agents, including paclitaxel, docetaxel,

39 relationships with other classes of peptidic antimicrotubule agents, or for modeling studies of the t

40 Like other antimicrotubule agents, the sulfamoylated estrone deriva

41 The resulting hybrid compounds were potent antimicrotubule agents, thus establishing a structural r

42 t kill human cancer cells resistant to other antimicrotubule agents, vincas and taxanes, were screene

43 dard in vitro assay for evaluating potential antimicrotubule agents.

44 However, there is still a need for improved antimicrotubule agents.

45 crotubule polymerization and the efficacy of antimicrotubule agents.

46 high levels of stathmin may be resistant to antimicrotubule agents.

47 dent of IFN, corresponded with resistance to antimicrotubule agents.

48 in the cellular defense against EM and other antimicrotubule agents.

49 er focusing conferring greater resistance to antimicrotubule agents.

50 by pre-incubation of the cells with various antimicrotubule agents: Binding of [(3)H]RH-4032 was inh

51 The taxane class of antimicrotubule anticancer agents is perhaps the most im

52 Many antimicrotubule cancer drugs in clinic today, particular

53 ent study indicate that welwistatin is a new antimicrotubule compound that circumvents multiple drug

54 rtant targets for anticancer agents, and new antimicrotubule compounds are of continued interest in d

55 itrulline-para-aminobenzoate linker, and the antimicrotubule cytotoxin monomethyl auristatin E (MMAE)

56 homologue show increased sensitivity to the antimicrotubule drug benomyl, and the S. cerevisiae gene

57 ncourage further study of estramustine-based antimicrotubule drug combinations in HRPC.

58 MP may provide an advantage over oral EMP in antimicrotubule drug combinations.

59 well as neurons, which are common targets of antimicrotubule drug therapy.

60 nt chemotherapy resistance in patients after antimicrotubule drug treatment.

61 with a comparably cytotoxic exposure to the antimicrotubule drug vincristine (1.0x10(-6) cell(-1), P

62 mbly checkpoint in budding yeast (defined by antimicrotubule drug-induced arrest or delay) are also r

63 status of p53 determines the sensitivity to antimicrotubule drugs and that this is mediated through

64 nt: MAD2/mad2Delta cells respond normally to antimicrotubule drugs but cannot respond to chromosomes

65 These data suggest that the action of antimicrotubule drugs can be affected by stathmin in at

66 ree system was specifically inhibited by the antimicrotubule drugs Colcemid, podophyllotoxin, nocodaz

67 s betaI, betaII, betaIII, and betaIotaV with antimicrotubule drugs has been widely studied, but littl

68 The in vitro potency of antimicrotubule drugs may be evaluated by measuring the

69 arrest in the presence of damage induced by antimicrotubule drugs or catastrophic loss of spindle st

70 root skewing phenotype is suppressed by the antimicrotubule drugs propyzamide and oryzalin, and righ

71 Dinitroaniline herbicides are antimicrotubule drugs that bind to tubulins and inhibit

72 amaging agents can affect the sensitivity to antimicrotubule drugs through the regulation of MAP4 exp

73 During prolonged mitotic arrest induced by antimicrotubule drugs, cell fate decision is determined

74 eleased from chromosomes upon treatment with antimicrotubule drugs, including the reversible agent no

75 mily of drugs, but also myopathies caused by antimicrotubule drugs, mitochondrial toxins, foods, and

76 ssion of MAP4 and changes the sensitivity to antimicrotubule drugs, we assayed cell lines with wild-t

77 Mitotic cells are susceptible to antimicrotubule drugs.

78 ue for addressing the mechanism of action of antimicrotubule drugs.

79 rs that modulate the sensitivity of cells to antimicrotubule drugs.

80 e loss enhances or suppresses sensitivity to antimicrotubule drugs.

81 Our data suggest that the mechanism for the antimicrotubule effects of dilantin involves sequestrati

82 These results suggest that antimicrotubule effects, as mediated by rotenone, for ex

83 n-1-yl)benzenesulfonates (PAIB-SOs) that are antimicrotubule prodrugs activated by CYP1A1.