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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  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
15 sues, C/EBP alpha is also associated with an antimitotic activity.
16 enous mammalian catabolite of estradiol with antimitotic activity.
17 K substrates in Xenopus egg extracts and has antimitotic activity.
18 hesis of the potent microtubule-stabilizing, antimitotic agent (+)-discodermolide is described.
19 fanilamide (GB-II-5), is a potent, selective antimitotic agent against kinetoplastid parasites.
20   Topical treatments of grafted HSE with the antimitotic agent colchicine select for keratinocyte pro
21                       The interaction of the antimitotic agent estramustine with bovine microtubule p
22 TI-286, a synthetic analogue of the peptidic antimitotic agent hemiasterlin, to tubulin is proposed.
23 ocking proliferation of these cells with the antimitotic agent mitomycin C.
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
26                            Vinblastine is an antimitotic agent that has been used extensively in canc
27  potency against GC3/c1, LYC5 cells, and the antimitotic agent vincristine.
28 lb/c mice, suggesting that 3c could be a new antimitotic agent with clinical potential.
29 model, suggesting that 3b is a promising new antimitotic agent with clinical potential.
30 model, suggesting that 4l is a promising new antimitotic agent with clinical potential.
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.
34 riety of stimuli, including the DNA-cleaving antimitotic agent, neocarzinostatin (NCS).
35 natural product hemiasterlin and is a potent antimitotic agent.
36 ed hydroxyphenstatin, a potent antitumor and antimitotic agent.
37 was also inhibited by bullatacin and various antimitotic agents (podophyllotoxin, vinblastine, and co
38                   By suppressing APC(Cdc20), antimitotic agents activate the spindle-assembly checkpo
39  agent in those tumors resistant to existing antimitotic agents and those dependent on Hedgehog pathw
40                              Taxol and other antimitotic agents are frontline chemotherapy agents but
41 nd-specific reversibility characteristics of antimitotic agents contribute to interactions between ce
42 ifiable, compound-specific characteristic of antimitotic agents in general.
43 inhibition was specifically synergistic with antimitotic agents in killing cancer cells that had unde
44                   Alternatively, exposure to antimitotic agents just after neural tube closure could
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 (
47 one and in combination with DNA-damaging and antimitotic agents on human cancer cells.
48                Combinations of EM with other antimitotic agents such as docetaxel are synergistic in
49 dentify putative biomarkers of resistance to antimitotic agents such as paclitaxel and monomethyl-aur
50 ally distinct from those of well-established antimitotic agents such as taxol.
51         Chemotherapy of prostate cancer with antimitotic agents such as vinblastine and doxorubicin i
52 Compounds of this series are promising novel antimitotic agents that have the potential for treating
53                                              Antimitotic agents that interfere with microtubule forma
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
61 uld affect the sensitivity of tumor cells to antimitotic agents.
62 ld enhance traditional and second-generation antimitotic agents.
63 es with greater efficacy than currently used antimitotic agents.
64 agents that differed in this respect was the antimitotic agents.
65 poptosis in neuroblastoma cells treated with antimitotic agents.
66 ermeability relative to many clinically used antimitotic agents.
67 de a molecular marker to predict response to antimitotic agents.
68 ase in caspase-3/7 activation in response to antimitotic agents.
69 s and cancers that are resistant to standard antimitotic agents.
70 n of a series of triazole-based compounds as antimitotic agents.
71 d a great deal of interest as a new class of antimitotic agents.
72                        Several semisynthetic antimitotic alkaloids are emerging as possible candidate
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
76  taxanes represent a combination of specific antimitotic and nonspecific antiangiogenic effects.
77 f promising antiproliferative compounds with antimitotic and potential VDA properties.
78                                     Both the antimitotic and the antiphenotypic effects are reversibl
79                                ABT-751 is an antimitotic and vascular disrupting agent with potent pr
80                                          The antimitotic anti-cancer drugs, including taxol, perturb
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
84                         C/EBPalpha, which is antimitotic, becomes centromere-associated much later in
85 broad spectrum of activity of currently used antimitotics by significant toxicities in normal dividin
86 studied a naturally occurring small-molecule antimitotic called diazonamide A.
87                                      Current antimitotic cancer chemotherapy based on vinca alkaloids
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
91  of mitosis are attractive targets for novel antimitotic cancer therapies.
92 potential targets for the discovery of novel antimitotic cancer therapies.
93 ta-tubulin isotypes, the primary targets for antimitotic chemotherapeutic drugs like taxanes, has imp
94                Vincristine, along with other antimitotic chemotherapeutic drugs, produces a periphera
95 tion will facilitate rational improvement of antimitotic chemotherapy and perhaps cytotoxic chemother
96 aploid cells and limits the effectiveness of antimitotic chemotherapy drugs.
97 potential function for p53 in the outcome of antimitotic chemotherapy.
98 ly, 113 of the 117 hit compounds in the TCRP antimitotic cluster were confirmed as antimitotic based
99 in human cells, suggesting the potential for antimitotic combination therapy.
100 colchicinoids are analogues of the important antimitotic compound (-)-colchicine 1.
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.
103                          (R,S)-1 is a potent antimitotic compound.
104 19 595 compound library and identified novel antimitotic compounds based on clustering analysis of th
105 asure and characterize cellular responses to antimitotic compounds or siRNAs.
106 s are a group of novel microtubule-targeted, antimitotic compounds that have a paclitaxel-like, assem
107                 Several structurally diverse antimitotic compounds, including the epothilones, compet
108 ich is located near the binding site of some antimitotic compounds, reduce microtubule dynamicity gre
109 pened the way to investigation and design of antimitotic compounds.
110 otential interest to explore combinations of antimitotic coumarins with other chemotherapeutic agents
111                                          The antimitotic depsipeptide cryptophycin 1 (CP1) was compar
112                                          The antimitotic depsipeptide dolastatin 15 was radiolabeled
113  clinical trials, is a peptide analog of the antimitotic depsipeptide dolastatin 15.
114 spases and CAD may be an important aspect of antimitotic drug action.
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.
117 ins that have great potential as targets for antimitotic drug development.
118                                          The antimitotic drug IKP104 [2-(4-fluorophenyl)-1-(2-chloro-
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
122                         Halichondrin B is an antimitotic drug that inhibits microtubule assembly.
123 totic arrest contributes to tumorigenesis or antimitotic drug toxicity is not well defined.
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
128 hydroxyurea; and inhibition of growth by the antimitotic drugs benomyl and thiabendazole.
129                    Mitotic arrest induced by antimitotic drugs can cause apoptosis or p53-dependent c
130 indings in terms of the variable efficacy of antimitotic drugs in cancer chemotherapy.
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
136                          Vinca alkaloids are antimitotic drugs that inhibit microtubule assembly and
137 otic arrest has proved clinically useful, as antimitotic drugs that interfere with proper chromosome-
138      The epothilones are naturally occurring antimitotic drugs that share with the taxanes a similar
139       This compound defines a novel class of antimitotic drugs that work through inhibition of src ki
140 nd thus how microtubule inhibitors and other antimitotic drugs ultimately elicit their lethal effects
141                                              Antimitotic drugs used in the chemotherapeutic treatment
142 eful as a marker to define susceptibility to antimitotic drugs, and encourage a revision in the curre
143 ely, Tbr2+ IPCs were selectively depleted by antimitotic drugs, known to suppress neurogenesis.
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
146 in in microtubule assembly and resistance to antimitotic drugs.
147  cells maintain a high efflux capability for antimitotic drugs.
148 e cytotoxic and antineoplastic properties of antimitotic drugs.
149 tic signaling and the mechanism of action of antimitotic drugs.
150 diverse roles in mitosis and are targets for antimitotic drugs.
151 interaction are distinct from those of other antimitotic drugs.
152 mitotic state of arrest generated by various antimitotic drugs.
153 e organization, assembly, and sensitivity to antimitotic drugs.
154 uring mitosis, and determines sensitivity to antimitotic drugs.
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
159                                          The antimitotic effect was found to be due to the inhibition
160 lts in an antagonistic antiproliferative and antimitotic effect, possibly due to the abrogation of Ta
161 letion of the polyaspartyl end abolished the antimitotic effect.
162 amides, the active compounds did not display antimitotic effects against Leishmania.
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
165 sion results in increased sensitivity to the antimitotic effects of okadaic acid.
166 n of calpains but did not interfere with the antimitotic effects of Taxol on microtubules, nor did it
167                                          The antimitotic effects of the widely used cancer chemothera
168 , which are the amino analogues of cytotoxic antimitotic flavonoids.
169                               Analogs of the antimitotic herbicide oryzalin (3,5-dinitro-N4,N4-di-n-p
170                           Ustiloxins A-F are antimitotic heterodetic cyclopeptides containing a 13-me
171 totic arrest and mitotic slippage induced by antimitotics in tumors.
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
174                        Leiodermatolide is an antimitotic macrolide isolated from the marine sponge Le
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
177  spindles, consistent with the tubulin-based antimitotic mechanism of halichondrin B.
178                               Thus, like the antimitotic mechanisms of action of the antitumor drugs
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
181       This protein is a promising target for antimitotic monomethyl auristatin E (MMAE)-based antibod
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
187 portant targets for the design of drugs with antimitotic or antineurodegenerative effects.
188  cancer, and demonstrate that TTP induces an antimitotic pathway that is diminished in cancer.
189 ide cryptophycin 1 (CP1) was compared to the antimitotic peptide dolastatin 10 (D10) as an antiprolif
190          Dolastatin 10 is a highly cytotoxic antimitotic peptide in phase II clinical trials.
191                     Hemiasterlin is a potent antimitotic peptide that interferes with microtubule dyn
192 rated that hemiasterlin resembles most other antimitotic peptides in noncompetitively inhibiting the
193               In addition, we speculate that antimitotic peptides mimic the interaction of stathmin w
194 for the synthesis of the tubulysin family of antimitotic peptides was developed.
195 structures observed with vinca alkaloids and antimitotic peptides.
196 t inactivates, specifically during M phase, "antimitotic" phosphatases directed against phosphorylati
197 ecific alliance to produce the highly potent antimitotic phytotoxin rhizoxin.
198 c ring generally decreases antiparasitic and antimitotic potency, but placement of a dibutyl substitu
199              Both PM050489 and PM060184 show antimitotic properties in human tumor cells lines at sub
200                                    Given the antimitotic properties of cisplatin, we examined whether
201 s has functional significance related to the antimitotic properties of the compound.
202 nd determined that only Fatostatin possessed antimitotic properties.
203 mportant implications for the development of antimitotic regimens that target this process.
204 apy cooperates synergistically with existing antimitotic regimens, enabling efficacy of subtherapeuti
205 rol: the promitotic response to cAMP and the antimitotic response to the Nf1 tumor suppressor.
206 antimitotic and antitumor activities against antimitotic-sensitive as well as resistant tumor cells.
207                             TGF-beta-induced antimitotic signals are highly regulated during cell pro
208                                              Antimitotic spindle poisons are among the most important
209  d without pre-degeneration, purification or antimitotic steps.
210  STARD9 is a mitotic kinesin and a potential antimitotic target.
211 ecessary for spindle assembly, and potential antimitotic targets, we performed a proteomic and geneti
212                              Consistent with antimitotics that inhibit the dynamic instability of tub
213 tives merit further examination as potential antimitotic therapeutics, specifically for brain cancers
214  silencing and its potential as a target for antimitotic therapies.
215 if targeted, could enhance responsiveness to antimitotic therapy.
216 mitotic arrest may promote tumorigenesis and antimitotic toxicity by provoking DNA damage.
217 ds (TTFields) are a locoregionally delivered antimitotic treatment that interferes with cell division
218                      Here we show that after antimitotic treatment with cytosine-beta-D-arabinofurano
219 been strongly attenuated are given a similar antimitotic treatment, recovery is limited to the reduce
220                           After cessation of antimitotic treatment, recovery of neurogenesis was para
221 of immature precursors and neuroblasts by an antimitotic treatment, SVZ astrocytes divide to generate
222  activated stem cells that are eliminated by antimitotic treatment.
223                           The sponge-derived antimitotic tripeptide hemiasterlin was previously shown
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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