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1 vented, because C/EBPalpha and PPARgamma are antimitotic.
2 perproliferation, indicating that ZA was not antimitotic.
3 sents a unique edge over the other available antimitotics.
5 a) promotes cellular differentiation and has antimitotic activities involving cell cycle arrest at G(
6 of 7,11-epi-thyrsiferol (4), (b) compare the antimitotic activities of thyrsiferol (2), Delta15,28-de
7 e benzimidazole series exhibited distinctive antimitotic activity as evidenced by blockade of bipolar
8 ptophycin 1 exerts its antiproliferative and antimitotic activity by binding reversibly and with high
9 High-content screening of this library for antimitotic activity followed by chemical modification i
12 ration and differentiation suggests that the antimitotic activity of NGF may be obligatory for differ
13 promising new tubulin-binding compound with antimitotic activity that has potential for treating neo
14 gen metabolite 2-methoxyestradiol has modest antimitotic activity that may result from a weak interac
20 Topical treatments of grafted HSE with the antimitotic agent colchicine select for keratinocyte pro
22 TI-286, a synthetic analogue of the peptidic antimitotic agent hemiasterlin, to tubulin is proposed.
24 neration synthesis of the exceedingly potent antimitotic agent N(14)-desacetoxytubulysin H (1) as wel
25 nblastine, or dolastatin 10 (another peptide antimitotic agent that depolymerizes microtubules) but w
31 Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
32 Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
33 B-II-5, compound 3), a new antikinetoplastid antimitotic agent, have been synthesized and evaluated.
37 was also inhibited by bullatacin and various antimitotic agents (podophyllotoxin, vinblastine, and co
39 agent in those tumors resistant to existing antimitotic agents and those dependent on Hedgehog pathw
41 nd-specific reversibility characteristics of antimitotic agents contribute to interactions between ce
43 inhibition was specifically synergistic with antimitotic agents in killing cancer cells that had unde
45 remarkably also reverse tumor resistance to antimitotic agents mediated via the P-glycoprotein efflu
46 D30 monoclonal antibody cAC10, linked to the antimitotic agents monomethyl auristatin E (MMAE) or F (
49 dentify putative biomarkers of resistance to antimitotic agents such as paclitaxel and monomethyl-aur
52 Compounds of this series are promising novel antimitotic agents that have the potential for treating
54 Paclitaxel (Taxol) and the epothilones are antimitotic agents that promote the assembly of mammalia
55 sulfonamides are a novel promising class of antimitotic agents with clinical development potential.
56 yins A and B and eleutherobin (coral-derived antimitotic agents) and of compound 1, an analogue of sa
57 lin binding of the Vinca alkaloids and other antimitotic agents, (2) proximity to stretches of amino
58 (TP53, best known as p53) in the presence of antimitotic agents, as determined by cytofluorometric an
59 and phomopsin A have been found to be potent antimitotic agents, causing cell death at picomolar or l
60 ctiveness of this drug exceeds that of other antimitotic agents, suggesting it may have an additional
73 estradiol, 2-Methoxyestradiol (2ME2), is an antimitotic and antiangiogenic cancer drug candidate tha
74 rolo[2,3-d]pyrimidin-2-amines, which possess antimitotic and antitumor activities against antimitotic
75 ese events is critical because C/EBPalpha is antimitotic and its expression prematurely would block t
81 nthetic member of the cryptophycin family of antimitotic antitumor agents that is currently undergoin
82 Treatment of ovarian carcinomas with the antimitotic antitumor drug paclitaxel is highly efficaci
83 e TCRP antimitotic cluster were confirmed as antimitotic based on independent assays, thus establishi
85 broad spectrum of activity of currently used antimitotics by significant toxicities in normal dividin
88 ine and other microtubule inhibitors used as antimitotic cancer drugs characteristically promote the
89 flow to quantify cell-cycle effects of three antimitotic cancer drugs over 8 d in HT-1080 fibrosarcom
90 CR leukemia cell line, which is resistant to antimitotic cancer drugs vincrisitine and paclitaxel thr
93 ta-tubulin isotypes, the primary targets for antimitotic chemotherapeutic drugs like taxanes, has imp
95 tion will facilitate rational improvement of antimitotic chemotherapy and perhaps cytotoxic chemother
98 ly, 113 of the 117 hit compounds in the TCRP antimitotic cluster were confirmed as antimitotic based
101 yl-6-phenyl-4(1H)-pyridinone (IKP-104) is an antimitotic compound which inhibits polymerization and i
102 raene lactone marine natural product, was an antimitotic compound, and we confirmed this prediction.
104 19 595 compound library and identified novel antimitotic compounds based on clustering analysis of th
106 s are a group of novel microtubule-targeted, antimitotic compounds that have a paclitaxel-like, assem
108 ich is located near the binding site of some antimitotic compounds, reduce microtubule dynamicity gre
110 otential interest to explore combinations of antimitotic coumarins with other chemotherapeutic agents
115 ell proliferation by central delivery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunte
116 n after depletion of mitotic cells using the antimitotic drug cytosine-beta-D-arabinofuranoside.
119 ined whether the single-cell response to the antimitotic drug paclitaxel (Ptx) was the same in tumors
120 We have characterized the effects of the antimitotic drug paclitaxel (Taxol(TM)) on the Ca(2+) si
121 lines, including cell lines resistant to the antimitotic drug paclitaxel and to other aurora kinase i
124 pite the common state of arrest, the various antimitotic drug treatments resulted in differences in t
125 s mutants that survive in the presence of an antimitotic drug, hemiasterlin, we identified eight stro
126 o by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induced mitotic arrest and also in norm
127 (doxorubicin, dacarbazine, temozolamide) or antimitotic drugs (paclitaxel and docetaxel) in a variet
131 We conclude that variation in sensitivity to antimitotic drugs in drug-naive cell lines is governed m
132 binding site(s) for peptide and depsipeptide antimitotic drugs may consist of a series of overlapping
133 of chemotherapy might be due to an action of antimitotic drugs on mitochondrial function and an inter
134 timitotic kinesin-5 inhibitor and additional antimitotic drugs revealed strong induction of p53 after
135 regulation, as well as the mode of action of antimitotic drugs that disrupt normal microtubule behavi
137 otic arrest has proved clinically useful, as antimitotic drugs that interfere with proper chromosome-
140 nd thus how microtubule inhibitors and other antimitotic drugs ultimately elicit their lethal effects
142 eful as a marker to define susceptibility to antimitotic drugs, and encourage a revision in the curre
144 cells are depolymerized by cold, Ca(2+), or antimitotic drugs, neuronal microtubules are unusually s
145 d in terms of the cellular mode of action of antimitotic drugs, particularly the importance of microt
155 t a phenotypic and molecular level for three antimitotic drugs: paclitaxel, nocodazole, and an inhibi
156 dynamics, conformation, and interaction with antimitotic drugs; however, very little is known about t
157 riant in cortical neuroblasts transforms the antimitotic effect of PACAP into a promitogenic signal.
158 significantly decreased the proapoptotic and antimitotic effect of transfected or secreted SEMA3B on
160 lts in an antagonistic antiproliferative and antimitotic effect, possibly due to the abrogation of Ta
163 in with an IC(50) of 6.9 microM and displays antimitotic effects in cultured T. brucei as assessed by
164 ne in rabbit eyelid, taking advantage of the antimitotic effects of doxorubicin on satellite cell div
166 n of calpains but did not interfere with the antimitotic effects of Taxol on microtubules, nor did it
172 subventricular zone quickly rebounds from an antimitotic insult by increasing proliferation and reple
173 aging in human cancer cells responding to an antimitotic kinesin-5 inhibitor and additional antimitot
175 combretastatin A-4 or with an analog of the antimitotic marine peptide diazonamide A (both the analo
176 e antitumor drugs vinblastine and taxol, the antimitotic mechanism of action of estramustine may be d
179 in vivo anticancer effects via tubulin-based antimitotic mechanisms, which are similar or identical t
180 tal radial glial disruption by delivering an antimitotic [methylazoxy methanol (MAM)] to pregnant fer
182 t inhibitors, an asymmetric synthesis of the antimitotic natural product, ustiloxin D, has been compl
183 activities comparable to those of the potent antimitotic natural products colchicine, podophyllotoxin
184 ies nearly comparable to those of the potent antimitotic natural products colchicine, podophyllotoxin
185 vity nearly comparable to that of the potent antimitotic natural products colchicine, podophyllotoxin
186 ad effects comparable to those of the potent antimitotic natural products podophyllotoxin and combret
189 ide cryptophycin 1 (CP1) was compared to the antimitotic peptide dolastatin 10 (D10) as an antiprolif
192 rated that hemiasterlin resembles most other antimitotic peptides in noncompetitively inhibiting the
196 t inactivates, specifically during M phase, "antimitotic" phosphatases directed against phosphorylati
198 c ring generally decreases antiparasitic and antimitotic potency, but placement of a dibutyl substitu
204 apy cooperates synergistically with existing antimitotic regimens, enabling efficacy of subtherapeuti
206 antimitotic and antitumor activities against antimitotic-sensitive as well as resistant tumor cells.
211 ecessary for spindle assembly, and potential antimitotic targets, we performed a proteomic and geneti
213 tives merit further examination as potential antimitotic therapeutics, specifically for brain cancers
217 ds (TTFields) are a locoregionally delivered antimitotic treatment that interferes with cell division
219 been strongly attenuated are given a similar antimitotic treatment, recovery is limited to the reduce
221 of immature precursors and neuroblasts by an antimitotic treatment, SVZ astrocytes divide to generate
224 se arrest and potentiates the effects of the antimitotics vincristine and vinblastine in cell culture
225 pindle assembly checkpoint proteins and that antimitotics with different mechanisms trigger very simi
226 thereby interference by C/EBPalpha (which is antimitotic) with mitotic clonal expansion, an essential
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