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1 ld artificially in G2-phase by addition of a microtubule inhibitor.
2 ases a DNA cross-linking agent rather than a microtubule inhibitor.
3 s such, they represent downstream targets of microtubule inhibitors.
4 r than folate SMDCs constructed with various microtubule inhibitors.
5 tosis or in cells blocked at prometaphase by microtubule inhibitors.
6 arrest in the face of kinetochore defects or microtubule inhibitors.
7 c checkpoint function and chemoresistance to microtubule inhibitors.
8  were either sensitive or resistant to known microtubule inhibitors.
9  (PBMC) in their responses to treatment with microtubule inhibitors.
10 y that is activated by vinblastine and other microtubule inhibitors.
11 f sister chromatids in the presence of these microtubule inhibitors.
12 to reveal determinants of drug resistance to microtubule inhibitors.
13                                      Because microtubule inhibitors activate JNK, we sought to determ
14 evealed a compound with higher activity as a microtubule inhibitor and cytotoxic agent in comparison
15  its inviability after transient exposure to microtubule inhibitors and its precocious dissociation o
16  spindle checkpoint activation, and thus how microtubule inhibitors and other antimitotic drugs ultim
17                  Moreover, the data identify microtubule inhibitors and protein synthesis inhibitors
18                       Src kinase inhibitors, microtubule inhibitors, and PGE(2) prevented the T cell
19 s are identified, including glucocorticoids, microtubule inhibitors, and protein synthesis inhibitors
20 cells exhibit no motility in the presence of microtubule inhibitors, at concentrations that disassemb
21  metabolically stable, druglike colchicinoid microtubule inhibitors based on the styrylbenzothiazole
22 d that upon spindle checkpoint activation by microtubule inhibitors benomyl or nocodazole, wild-type
23 ed predominantly in G1 and to respond not to microtubule inhibitor but to mitogenic stimulus.
24  and Bcl-2 are phosphorylated in response to microtubule inhibitors, but the kinase(s) responsible an
25 s required for the M phase arrest induced by microtubule inhibitors, but the protein is not essential
26                   Paclitaxel (PTX) and other microtubule inhibitors cause mitotic arrest.
27  agents that induced Bcl-xL phosphorylation (microtubule inhibitors) caused loss of the 150-kDa form,
28                        Pretreatment with the microtubule inhibitor colchicine inhibited biliary excre
29         Increased expression of HSPB8 by the microtubule inhibitor Colchicine or by exogenous means s
30 tacks are unique in their sensitivity to the microtubule inhibitor colchicine, contrasted with their
31 -expressing tumor cells was augmented by the microtubule inhibitor, colchicine.
32 ication to the chemical structure of a known microtubule inhibitor, combretastatin A-4, Borowiak et a
33 ry for disease development and indicate that microtubule inhibitors could be used to suppress EMT and
34 ntified a mechanism of 2-methoxyestradiol, a microtubule inhibitor currently undergoing clinical tria
35 -treatment with ATM and vincristine (VCR), a microtubule inhibitor currently used in rhabdomyosarcoma
36 ation of ubiquitination at specific sites by microtubule inhibitors, demonstrating the effectiveness
37                                Nocodazole, a microtubule inhibitor, did not disperse aggregates.
38  filtration was generated for delivering the microtubule inhibitor DM1 to NMIBC with minimal nonspeci
39                                              Microtubule inhibitors do not reduce TACC3 and cKAP5/chT
40                   In contrast, the cytotoxic microtubule inhibitor docetaxel increased glycerophospho
41                                The nontaxane microtubule inhibitor eribulin is an approved therapeuti
42  together, our results show that these novel microtubule inhibitors have promising anticancer activit
43 on and that combination therapy with ATM and microtubule inhibitors holds promise for the treatment o
44   Eribulin (E7389), a mechanistically unique microtubule inhibitor in phase III clinical trials for c
45 inical efficacy data for vinflunine, a novel microtubule inhibitor, in MPM.
46           From this set we validate 14 novel microtubule inhibitors, including 3 with activity on res
47                                        These microtubule inhibitors increased osteoblast differentiat
48 rexate (antimetabolites), and vinblastine (a microtubule inhibitor) induced the same site-specific cl
49 cerning the role of Bcl-2 phosphorylation in microtubule inhibitor-induced apoptosis.
50 t the JNK pathway plays an essential role in microtubule inhibitor-induced apoptosis.
51 identify specific p53 residues necessary for microtubule inhibitor-induced phosphorylation.
52              Moreover, these cells underwent microtubule inhibitor-induced reduplication, leading to
53 ough MSC function, prototypically induced by microtubule inhibitors, is active selectively during mit
54 a cancer-selective cleavable linker, and the microtubule inhibitor monomethyl auristatin E (MMAE).
55           Covalent conjugation of the potent microtubule inhibitor monomethyl auristatin-F (MMAF) to
56 ery of cytotoxics, 1C1 was conjugated to the microtubule inhibitor monomethylauristatin phenylalanine
57 oint function would sensitize tumor cells to microtubule inhibitor (MTI)-induced apoptosis, we examin
58 orms in cells increased after treatment with microtubule inhibitors (MTIs) and that the pattern of p5
59 sented herein show that after treatment with microtubule inhibitors (MTIs), cells deficient in the Cd
60 sitivity to 31 compounds, including BCL2 and microtubule inhibitors (MTIs).
61   ER reorganisation is also prevented by the microtubule inhibitor nocodazole and by the inhibition o
62 missiveness was impaired upon treatment with microtubule inhibitor nocodazole, which was identified a
63 n, but is enhanced in cells treated with the microtubule inhibitor nocodazole.
64 elatively low concentration of nuclei or the microtubule inhibitor nocodazole.
65  after prolonged treatment of cells with the microtubule inhibitor nocodazole.
66                       Cells treated with the microtubule inhibitors nocodazole, colchicine, vincristi
67                             In contrast, the microtubule inhibitor, nocodazole, prevented development
68         Here we show that, unlike many other microtubule inhibitors, noscapine does not significantly
69 enzotrifluoride (chloralin) (2), an in vitro microtubule inhibitor of several Leishmania species, hav
70 ting these responses, we examined effects of microtubule inhibitors on the hedgehog (Hh) pathway, sin
71       Moreover, application of colchicine, a microtubule inhibitor, or paclitaxel, a microtubule stab
72 sis thaliana roots to moderate levels of the microtubule inhibitor, oryzalin.
73                                          For microtubule inhibitors, our approach implicated Notch an
74                                              Microtubule inhibitors paclitaxel and demecolcine inhibi
75 rethamine), anthracylines (doxorubicin), and microtubule inhibitors (paclitaxel).
76 ggest that Bcl-xL phosphorylation induced by microtubule inhibitors plays a key pro-apoptotic role at
77  perhaps other signaling pathways altered by microtubule inhibitors reflect perturbations of normal m
78    Cytochalasin D and vinblastine, actin and microtubule inhibitors, respectively, failed to complete
79  to aid in the design of effective parasitic microtubule inhibitors, several novel dinitroaniline ana
80                             Experiments with microtubule inhibitors show that the retracted microtubu
81                                              Microtubule inhibitors slowed but did not prevent membra
82                      Drug screening suggests microtubule inhibitors/stabilizers, DNA-damaging agents,
83 pathy; and, third, that structurally diverse microtubule inhibitors stimulate OXPHOS transcription wh
84 the antiangiogenic effects of 2-ME and other microtubule inhibitors such as Taxol, vincristine, and c
85 nically activated versions of their targets, microtubule inhibitors, such as eribulin, are deployed i
86 letion or interference with TNT formation by microtubule inhibitors, such as vincristine (VCR), preve
87 iclib, a CDK4/6 inhibitor, and paclitaxel, a microtubule inhibitor, synergize with the BET inhibitor
88 of Bcl-xL phosphorylation induced by several microtubule inhibitors tested.
89  analog of the natural product maytansine, a microtubule inhibitor that by itself has limited clinica
90 uct Dolastatin 10, are ultrapotent cytotoxic microtubule inhibitors that are clinically used as paylo
91       When conjugated with a tubulysin-based microtubule inhibitor, the biparatopic ADC demonstrates
92 BR1 is required by cells that are exposed to microtubule inhibitors to arrest in mitosis.
93 rget a potent, semisynthetic analogue of the microtubule inhibitor tubulysin B to FR-enriched tumors.
94        However, when continuously exposed to microtubule inhibitors, untransformed cells eventually s
95                        Vinblastine and other microtubule inhibitors used as antimitotic cancer drugs
96 ed efficacy in models that were resistant to microtubule inhibitors used as part of the current stand
97 ization and function of c-Jun induced by the microtubule inhibitor vinblastine, which strongly induce
98  axons of neurons grown in the presence of a microtubule-inhibitor, vinblastine.
99                         Novel triazine-based microtubule inhibitors were discovered by an efficient z
100 vivo stomatal aperture assays with different microtubule inhibitors were performed.
101                                              Microtubule inhibitors, widely used in cancer chemothera

 
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