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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.
4          We hereby report that, unlike other antimitotics, AB-5 is extremely well tolerated by mice w
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
10 altering replication and possessing a strong antimitotic activity in human cancer cell lines.
11                                 The observed antimitotic activity is due to the binding of HTI-286 to
12 ration and differentiation suggests that the antimitotic activity of NGF may be obligatory for differ
13 estigated as anticancer agents; however, the antimitotic activity of these compounds does not always
14  promising new tubulin-binding compound with antimitotic activity that has potential for treating neo
15 gen metabolite 2-methoxyestradiol has modest antimitotic activity that may result from a weak interac
16 sues, C/EBP alpha is also associated with an antimitotic activity.
17 , and familial Mediterranean fever with high antimitotic activity.
18 enous mammalian catabolite of estradiol with antimitotic activity.
19 K substrates in Xenopus egg extracts and has antimitotic activity.
20 hesis of the potent microtubule-stabilizing, antimitotic agent (+)-discodermolide is described.
21 fanilamide (GB-II-5), is a potent, selective antimitotic agent against kinetoplastid parasites.
22   Topical treatments of grafted HSE with the antimitotic agent colchicine select for keratinocyte pro
23                       The interaction of the antimitotic agent estramustine with bovine microtubule p
24 TI-286, a synthetic analogue of the peptidic antimitotic agent hemiasterlin, to tubulin is proposed.
25 ocking proliferation of these cells with the antimitotic agent mitomycin C.
26 AP1 monoclonal antibody linked to the potent antimitotic agent monomethyl auristatin E.
27 neration synthesis of the exceedingly potent antimitotic agent N(14)-desacetoxytubulysin H (1) as wel
28 nblastine, or dolastatin 10 (another peptide antimitotic agent that depolymerizes microtubules) but w
29                            Vinblastine is an antimitotic agent that has been used extensively in canc
30  potency against GC3/c1, LYC5 cells, and the antimitotic agent vincristine.
31 lb/c mice, suggesting that 3c could be a new antimitotic agent with clinical potential.
32 model, suggesting that 3b is a promising new antimitotic agent with clinical potential.
33 model, suggesting that 4l is a promising new antimitotic agent with clinical potential.
34           Here, we identify DL78 as a potent antimitotic agent with selective anticancer activity thr
35    Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
36    Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
37 B-II-5, compound 3), a new antikinetoplastid antimitotic agent, have been synthesized and evaluated.
38 riety of stimuli, including the DNA-cleaving antimitotic agent, neocarzinostatin (NCS).
39 natural product hemiasterlin and is a potent antimitotic agent.
40 ed hydroxyphenstatin, a potent antitumor and antimitotic agent.
41 was also inhibited by bullatacin and various antimitotic agents (podophyllotoxin, vinblastine, and co
42                   By suppressing APC(Cdc20), antimitotic agents activate the spindle-assembly checkpo
43 ponents of the tubulysin family of picomolar antimitotic agents and previously led to a tubulysin tet
44  agent in those tumors resistant to existing antimitotic agents and those dependent on Hedgehog pathw
45                              Taxol and other antimitotic agents are frontline chemotherapy agents but
46 nd-specific reversibility characteristics of antimitotic agents contribute to interactions between ce
47 ifiable, compound-specific characteristic of antimitotic agents in general.
48 inhibition was specifically synergistic with antimitotic agents in killing cancer cells that had unde
49                   Alternatively, exposure to antimitotic agents just after neural tube closure could
50  remarkably also reverse tumor resistance to antimitotic agents mediated via the P-glycoprotein efflu
51 D30 monoclonal antibody cAC10, linked to the antimitotic agents monomethyl auristatin E (MMAE) or F (
52 one and in combination with DNA-damaging and antimitotic agents on human cancer cells.
53                Combinations of EM with other antimitotic agents such as docetaxel are synergistic in
54 dentify putative biomarkers of resistance to antimitotic agents such as paclitaxel and monomethyl-aur
55 ally distinct from those of well-established antimitotic agents such as taxol.
56         Chemotherapy of prostate cancer with antimitotic agents such as vinblastine and doxorubicin i
57 Compounds of this series are promising novel antimitotic agents that have the potential for treating
58                                              Antimitotic agents that interfere with microtubule forma
59   Paclitaxel (Taxol) and the epothilones are antimitotic agents that promote the assembly of mammalia
60  sulfonamides are a novel promising class of antimitotic agents with clinical development potential.
61 yins A and B and eleutherobin (coral-derived antimitotic agents) and of compound 1, an analogue of sa
62 lin binding of the Vinca alkaloids and other antimitotic agents, (2) proximity to stretches of amino
63 (TP53, best known as p53) in the presence of antimitotic agents, as determined by cytofluorometric an
64 and phomopsin A have been found to be potent antimitotic agents, causing cell death at picomolar or l
65   The induction of genetic variability using antimitotic agents, such as colchicine, has been widely
66 ctiveness of this drug exceeds that of other antimitotic agents, suggesting it may have an additional
67  continued to safely grow in the presence of antimitotic agents.
68 uld affect the sensitivity of tumor cells to antimitotic agents.
69 es with greater efficacy than currently used antimitotic agents.
70 agents that differed in this respect was the antimitotic agents.
71 poptosis in neuroblastoma cells treated with antimitotic agents.
72 r mitotic extension exhibited sensitivity to antimitotic agents.
73 ld enhance traditional and second-generation antimitotic agents.
74 ermeability relative to many clinically used antimitotic agents.
75 de a molecular marker to predict response to antimitotic agents.
76 ase in caspase-3/7 activation in response to antimitotic agents.
77 s and cancers that are resistant to standard antimitotic agents.
78 ch is not observed following treatments with antimitotic agents.
79 n of a series of triazole-based compounds as antimitotic agents.
80 d a great deal of interest as a new class of antimitotic agents.
81                        Several semisynthetic antimitotic alkaloids are emerging as possible candidate
82  estradiol, 2-Methoxyestradiol (2ME2), is an antimitotic and antiangiogenic cancer drug candidate tha
83 rolo[2,3-d]pyrimidin-2-amines, which possess antimitotic and antitumor activities against antimitotic
84  often considered to be a consequence of the antimitotic and apoptosis-promoting properties of chemot
85 ese events is critical because C/EBPalpha is antimitotic and its expression prematurely would block t
86  taxanes represent a combination of specific antimitotic and nonspecific antiangiogenic effects.
87 f promising antiproliferative compounds with antimitotic and potential VDA properties.
88                                     Both the antimitotic and the antiphenotypic effects are reversibl
89                                ABT-751 is an antimitotic and vascular disrupting agent with potent pr
90                                          The antimitotic anti-cancer drugs, including taxol, perturb
91 nthetic member of the cryptophycin family of antimitotic antitumor agents that is currently undergoin
92     Treatment of ovarian carcinomas with the antimitotic antitumor drug paclitaxel is highly efficaci
93 e TCRP antimitotic cluster were confirmed as antimitotic based on independent assays, thus establishi
94                         C/EBPalpha, which is antimitotic, becomes centromere-associated much later in
95 broad spectrum of activity of currently used antimitotics by significant toxicities in normal dividin
96 studied a naturally occurring small-molecule antimitotic called diazonamide A.
97 tosis is negligible and provide insight into antimitotic cancer chemotherapies.
98                                      Current antimitotic cancer chemotherapy based on vinca alkaloids
99 ine and other microtubule inhibitors used as antimitotic cancer drugs characteristically promote the
100 flow to quantify cell-cycle effects of three antimitotic cancer drugs over 8 d in HT-1080 fibrosarcom
101 CR leukemia cell line, which is resistant to antimitotic cancer drugs vincrisitine and paclitaxel thr
102  of mitosis are attractive targets for novel antimitotic cancer therapies.
103 potential targets for the discovery of novel antimitotic cancer therapies.
104 ta-tubulin isotypes, the primary targets for antimitotic chemotherapeutic drugs like taxanes, has imp
105                Vincristine, along with other antimitotic chemotherapeutic drugs, produces a periphera
106                 Interestingly, radiation and antimitotic chemotherapeutics did not increase overall t
107 t expected to cooperate with DNA-damaging or antimitotic chemotherapies as the former prevent cell-cy
108 tion will facilitate rational improvement of antimitotic chemotherapy and perhaps cytotoxic chemother
109 aploid cells and limits the effectiveness of antimitotic chemotherapy drugs.
110 ed targeting of cancer stem cells along with antimitotic chemotherapy yields effective tumor inhibiti
111 ovoking genome instability and resistance to antimitotic chemotherapy.
112 potential function for p53 in the outcome of antimitotic chemotherapy.
113 ly, 113 of the 117 hit compounds in the TCRP antimitotic cluster were confirmed as antimitotic based
114 in human cells, suggesting the potential for antimitotic combination therapy.
115 colchicinoids are analogues of the important antimitotic compound (-)-colchicine 1.
116 yl-6-phenyl-4(1H)-pyridinone (IKP-104) is an antimitotic compound which inhibits polymerization and i
117 raene lactone marine natural product, was an antimitotic compound, and we confirmed this prediction.
118                          (R,S)-1 is a potent antimitotic compound.
119 19 595 compound library and identified novel antimitotic compounds based on clustering analysis of th
120 agents (MTAs) that belong to the most potent antimitotic compounds known to date; however, their exac
121 asure and characterize cellular responses to antimitotic compounds or siRNAs.
122 s are a group of novel microtubule-targeted, antimitotic compounds that have a paclitaxel-like, assem
123                 Several structurally diverse antimitotic compounds, including the epothilones, compet
124 ich is located near the binding site of some antimitotic compounds, reduce microtubule dynamicity gre
125 pened the way to investigation and design of antimitotic compounds.
126 otential interest to explore combinations of antimitotic coumarins with other chemotherapeutic agents
127  prototypical PAIB-SO [(14)C]CEU-818 and its antimitotic counterpart [(14)C]CEU-602 are distributed i
128                                          The antimitotic depsipeptide cryptophycin 1 (CP1) was compar
129                                          The antimitotic depsipeptide dolastatin 15 was radiolabeled
130  clinical trials, is a peptide analog of the antimitotic depsipeptide dolastatin 15.
131 spases and CAD may be an important aspect of antimitotic drug action.
132 ell proliferation by central delivery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunte
133 n after depletion of mitotic cells using the antimitotic drug cytosine-beta-D-arabinofuranoside.
134 ins that have great potential as targets for antimitotic drug development.
135                                          The antimitotic drug IKP104 [2-(4-fluorophenyl)-1-(2-chloro-
136 ined whether the single-cell response to the antimitotic drug paclitaxel (Ptx) was the same in tumors
137     We have characterized the effects of the antimitotic drug paclitaxel (Taxol(TM)) on the Ca(2+) si
138 lines, including cell lines resistant to the antimitotic drug paclitaxel and to other aurora kinase i
139                         Halichondrin B is an antimitotic drug that inhibits microtubule assembly.
140 totic arrest contributes to tumorigenesis or antimitotic drug toxicity is not well defined.
141 pite the common state of arrest, the various antimitotic drug treatments resulted in differences in t
142 s mutants that survive in the presence of an antimitotic drug, hemiasterlin, we identified eight stro
143 o by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induced mitotic arrest and also in norm
144               We show that some slow-cycling antimitotic drug-resistant cancer cells, such as 5-fluor
145  (doxorubicin, dacarbazine, temozolamide) or antimitotic drugs (paclitaxel and docetaxel) in a variet
146 hydroxyurea; and inhibition of growth by the antimitotic drugs benomyl and thiabendazole.
147                    Mitotic arrest induced by antimitotic drugs can cause apoptosis or p53-dependent c
148 indings in terms of the variable efficacy of antimitotic drugs in cancer chemotherapy.
149 We conclude that variation in sensitivity to antimitotic drugs in drug-naive cell lines is governed m
150 binding site(s) for peptide and depsipeptide antimitotic drugs may consist of a series of overlapping
151 of chemotherapy might be due to an action of antimitotic drugs on mitochondrial function and an inter
152 timitotic kinesin-5 inhibitor and additional antimitotic drugs revealed strong induction of p53 after
153 regulation, as well as the mode of action of antimitotic drugs that disrupt normal microtubule behavi
154                          Vinca alkaloids are antimitotic drugs that inhibit microtubule assembly and
155 otic arrest has proved clinically useful, as antimitotic drugs that interfere with proper chromosome-
156      The epothilones are naturally occurring antimitotic drugs that share with the taxanes a similar
157       This compound defines a novel class of antimitotic drugs that work through inhibition of src ki
158                           We used a panel of antimitotic drugs to perturb mitosis in human fibroblast
159 nd thus how microtubule inhibitors and other antimitotic drugs ultimately elicit their lethal effects
160                                              Antimitotic drugs used in the chemotherapeutic treatment
161 eful as a marker to define susceptibility to antimitotic drugs, and encourage a revision in the curre
162 ely, Tbr2+ IPCs were selectively depleted by antimitotic drugs, known to suppress neurogenesis.
163  cells are depolymerized by cold, Ca(2+), or antimitotic drugs, neuronal microtubules are unusually s
164 d in terms of the cellular mode of action of antimitotic drugs, particularly the importance of microt
165 mitotic state of arrest generated by various antimitotic drugs.
166 e organization, assembly, and sensitivity to antimitotic drugs.
167 uring mitosis, and determines sensitivity to antimitotic drugs.
168 in in microtubule assembly and resistance to antimitotic drugs.
169 diverse roles in mitosis and are targets for antimitotic drugs.
170  cells maintain a high efflux capability for antimitotic drugs.
171 e cytotoxic and antineoplastic properties of antimitotic drugs.
172 tic signaling and the mechanism of action of antimitotic drugs.
173 interaction are distinct from those of other antimitotic drugs.
174 ble for resistance to these agents and other antimitotic drugs.
175 t a phenotypic and molecular level for three antimitotic drugs: paclitaxel, nocodazole, and an inhibi
176 dynamics, conformation, and interaction with antimitotic drugs; however, very little is known about t
177 riant in cortical neuroblasts transforms the antimitotic effect of PACAP into a promitogenic signal.
178 significantly decreased the proapoptotic and antimitotic effect of transfected or secreted SEMA3B on
179 d "tumor-treating fields (TTFields)," had an antimitotic effect on glioblastoma multiforme (GBM) cell
180                                          The antimitotic effect was found to be due to the inhibition
181 lts in an antagonistic antiproliferative and antimitotic effect, possibly due to the abrogation of Ta
182 letion of the polyaspartyl end abolished the antimitotic effect.
183 amides, the active compounds did not display antimitotic effects against Leishmania.
184 in with an IC(50) of 6.9 microM and displays antimitotic effects in cultured T. brucei as assessed by
185 ne in rabbit eyelid, taking advantage of the antimitotic effects of doxorubicin on satellite cell div
186 sion results in increased sensitivity to the antimitotic effects of okadaic acid.
187 y, resulted in profound sensitization to the antimitotic effects of Plk1 inhibition, leading to spind
188 n of calpains but did not interfere with the antimitotic effects of Taxol on microtubules, nor did it
189                                          The antimitotic effects of the widely used cancer chemothera
190                                        While antimitotic effects were the first recognized biological
191 mune signaling pathways independent of their antimitotic effects.
192 , which are the amino analogues of cytotoxic antimitotic flavonoids.
193                               Analogs of the antimitotic herbicide oryzalin (3,5-dinitro-N4,N4-di-n-p
194                           Ustiloxins A-F are antimitotic heterodetic cyclopeptides containing a 13-me
195 totic arrest and mitotic slippage induced by antimitotics in tumors.
196 subventricular zone quickly rebounds from an antimitotic insult by increasing proliferation and reple
197 aging in human cancer cells responding to an antimitotic kinesin-5 inhibitor and additional antimitot
198                        Leiodermatolide is an antimitotic macrolide isolated from the marine sponge Le
199                           Hemiasterlin is an antimitotic marine natural product with reported sub-nan
200  combretastatin A-4 or with an analog of the antimitotic marine peptide diazonamide A (both the analo
201 e antitumor drugs vinblastine and taxol, the antimitotic mechanism of action of estramustine may be d
202 though all clinically approved MTAs share an antimitotic mechanism of action, their distinct effects
203  spindles, consistent with the tubulin-based antimitotic mechanism of halichondrin B.
204                               Thus, like the antimitotic mechanisms of action of the antitumor drugs
205 in vivo anticancer effects via tubulin-based antimitotic mechanisms, which are similar or identical t
206 tal radial glial disruption by delivering an antimitotic [methylazoxy methanol (MAM)] to pregnant fer
207       This protein is a promising target for antimitotic monomethyl auristatin E (MMAE)-based antibod
208 t inhibitors, an asymmetric synthesis of the antimitotic natural product, ustiloxin D, has been compl
209 activities comparable to those of the potent antimitotic natural products colchicine, podophyllotoxin
210 ies nearly comparable to those of the potent antimitotic natural products colchicine, podophyllotoxin
211 vity nearly comparable to that of the potent antimitotic natural products colchicine, podophyllotoxin
212 ad effects comparable to those of the potent antimitotic natural products podophyllotoxin and combret
213 portant targets for the design of drugs with antimitotic or antineurodegenerative effects.
214 e innate immune signaling independent of its antimitotic or cytotoxic effects.
215  cancer, and demonstrate that TTP induces an antimitotic pathway that is diminished in cancer.
216 ide cryptophycin 1 (CP1) was compared to the antimitotic peptide dolastatin 10 (D10) as an antiprolif
217          Dolastatin 10 is a highly cytotoxic antimitotic peptide in phase II clinical trials.
218                     Hemiasterlin is a potent antimitotic peptide that interferes with microtubule dyn
219 rated that hemiasterlin resembles most other antimitotic peptides in noncompetitively inhibiting the
220               In addition, we speculate that antimitotic peptides mimic the interaction of stathmin w
221 for the synthesis of the tubulysin family of antimitotic peptides was developed.
222 structures observed with vinca alkaloids and antimitotic peptides.
223 t inactivates, specifically during M phase, "antimitotic" phosphatases directed against phosphorylati
224 ecific alliance to produce the highly potent antimitotic phytotoxin rhizoxin.
225 c ring generally decreases antiparasitic and antimitotic potency, but placement of a dibutyl substitu
226 enesulfonates (PAIB-SOs) are a new family of antimitotic prodrugs bioactivated in breast cancer cells
227              Both PM050489 and PM060184 show antimitotic properties in human tumor cells lines at sub
228                                    Given the antimitotic properties of cisplatin, we examined whether
229 s has functional significance related to the antimitotic properties of the compound.
230 nd determined that only Fatostatin possessed antimitotic properties.
231 hicine deactivates its anti-inflammatory and antimitotic properties.
232 mportant implications for the development of antimitotic regimens that target this process.
233 apy cooperates synergistically with existing antimitotic regimens, enabling efficacy of subtherapeuti
234 rol: the promitotic response to cAMP and the antimitotic response to the Nf1 tumor suppressor.
235 antimitotic and antitumor activities against antimitotic-sensitive as well as resistant tumor cells.
236                             TGF-beta-induced antimitotic signals are highly regulated during cell pro
237                                              Antimitotic spindle poisons are among the most important
238 after, we modified the lead sequences of the antimitotic stapled peptides with halo derivatives.
239  d without pre-degeneration, purification or antimitotic steps.
240  cross-links microtubules, is an established antimitotic target in other disease contexts, but its me
241  STARD9 is a mitotic kinesin and a potential antimitotic target.
242 ecessary for spindle assembly, and potential antimitotic targets, we performed a proteomic and geneti
243 ing the MAT2A clinical candidate AG-270 with antimitotic taxanes.
244                              Consistent with antimitotics that inhibit the dynamic instability of tub
245 tives merit further examination as potential antimitotic therapeutics, specifically for brain cancers
246 uired resistance to Ptx is common, and other antimitotic therapies can be similarly rendered ineffect
247  silencing and its potential as a target for antimitotic therapies.
248 if targeted, could enhance responsiveness to antimitotic therapy.
249 mitotic arrest may promote tumorigenesis and antimitotic toxicity by provoking DNA damage.
250 ds (TTFields) are a locoregionally delivered antimitotic treatment that interferes with cell division
251                      Here we show that after antimitotic treatment with cytosine-beta-D-arabinofurano
252 been strongly attenuated are given a similar antimitotic treatment, recovery is limited to the reduce
253                           After cessation of antimitotic treatment, recovery of neurogenesis was para
254 of immature precursors and neuroblasts by an antimitotic treatment, SVZ astrocytes divide to generate
255  activated stem cells that are eliminated by antimitotic treatment.
256                           The sponge-derived antimitotic tripeptide hemiasterlin was previously shown
257 se arrest and potentiates the effects of the antimitotics vincristine and vinblastine in cell culture
258 pindle assembly checkpoint proteins and that antimitotics with different mechanisms trigger very simi
259 thereby interference by C/EBPalpha (which is antimitotic) with mitotic clonal expansion, an essential

 
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