ライフサイエンスコーパス: antimitotic drug

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1 mitotic state of arrest generated by various antimitotic drugs.

2 diverse roles in mitosis and are targets for antimitotic drugs.

3 e organization, assembly, and sensitivity to antimitotic drugs.

4 uring mitosis, and determines sensitivity to antimitotic drugs.

5 in in microtubule assembly and resistance to antimitotic drugs.

6 cells maintain a high efflux capability for antimitotic drugs.

7 e cytotoxic and antineoplastic properties of antimitotic drugs.

8 tic signaling and the mechanism of action of antimitotic drugs.

9 interaction are distinct from those of other antimitotic drugs.

10 spases and CAD may be an important aspect of antimitotic drug action.

11 eful as a marker to define susceptibility to antimitotic drugs, and encourage a revision in the curre

12 ell proliferation by central delivery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunte

13 hydroxyurea; and inhibition of growth by the antimitotic drugs benomyl and thiabendazole.

14 Mitotic arrest induced by antimitotic drugs can cause apoptosis or p53-dependent c

15 n after depletion of mitotic cells using the antimitotic drug cytosine-beta-D-arabinofuranoside.

16 ins that have great potential as targets for antimitotic drug development.

17 s mutants that survive in the presence of an antimitotic drug, hemiasterlin, we identified eight stro

18 dynamics, conformation, and interaction with antimitotic drugs; however, very little is known about t

19 The antimitotic drug IKP104 [2-(4-fluorophenyl)-1-(2-chloro-

20 indings in terms of the variable efficacy of antimitotic drugs in cancer chemotherapy.

21 We conclude that variation in sensitivity to antimitotic drugs in drug-naive cell lines is governed m

22 o by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induced mitotic arrest and also in norm

23 ely, Tbr2+ IPCs were selectively depleted by antimitotic drugs, known to suppress neurogenesis.

24 binding site(s) for peptide and depsipeptide antimitotic drugs may consist of a series of overlapping

25 cells are depolymerized by cold, Ca(2+), or antimitotic drugs, neuronal microtubules are unusually s

26 of chemotherapy might be due to an action of antimitotic drugs on mitochondrial function and an inter

27 ined whether the single-cell response to the antimitotic drug paclitaxel (Ptx) was the same in tumors

28 We have characterized the effects of the antimitotic drug paclitaxel (Taxol(TM)) on the Ca(2+) si

29 lines, including cell lines resistant to the antimitotic drug paclitaxel and to other aurora kinase i

30 (doxorubicin, dacarbazine, temozolamide) or antimitotic drugs (paclitaxel and docetaxel) in a variet

31 t a phenotypic and molecular level for three antimitotic drugs: paclitaxel, nocodazole, and an inhibi

32 d in terms of the cellular mode of action of antimitotic drugs, particularly the importance of microt

33 timitotic kinesin-5 inhibitor and additional antimitotic drugs revealed strong induction of p53 after

34 Halichondrin B is an antimitotic drug that inhibits microtubule assembly.

35 regulation, as well as the mode of action of antimitotic drugs that disrupt normal microtubule behavi

36 Vinca alkaloids are antimitotic drugs that inhibit microtubule assembly and

37 otic arrest has proved clinically useful, as antimitotic drugs that interfere with proper chromosome-

38 The epothilones are naturally occurring antimitotic drugs that share with the taxanes a similar

39 This compound defines a novel class of antimitotic drugs that work through inhibition of src ki

40 totic arrest contributes to tumorigenesis or antimitotic drug toxicity is not well defined.

41 pite the common state of arrest, the various antimitotic drug treatments resulted in differences in t

42 nd thus how microtubule inhibitors and other antimitotic drugs ultimately elicit their lethal effects

43 Antimitotic drugs used in the chemotherapeutic treatment

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