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1 withdrawal, nor did it modify sensitivity to jasplakinolide.
2  within 3 minutes of treatment with 1 microM jasplakinolide.
3 rption, we used the F-actin stabilizing drug jasplakinolide.
4 en demonstrated in a formal synthesis of (+)-jasplakinolide.
5 was blocked by the actin-polymerizing agent, jasplakinolide.
6 retreated with the actin filament stabilizer jasplakinolide.
7 MEK1/2 and ERK1/2 activation is nullified by jasplakinolide.
8 formation is inhibited by cytochalasin D and jasplakinolide.
9 dulation of skeletal protein architecture by jasplakinolide.
10 lly when actin filaments are stabilized with jasplakinolide.
11  be reversed by the actin-polymerizing agent jasplakinolide.
12 essentially identical to those obtained with jasplakinolide.
13 ith latrunculin B, C. difficile toxin B, and jasplakinolide.
14 ntrast, increasing actin polymerization with jasplakinolide (0.5 microm) increased SM22 and SM alpha-
15                 This led to the isolation of jasplakinolide (1) and eleven jasplakinolide analogues (
16 ied using cell-permeable actin polymerizing (jasplakinolide, 2 microm) or depolymerizing agents (latr
17 ids, and the former is a known source of (+)-jasplakinolide (7), which is inactive as a 15-HLO inhibi
18 king myofibrillar filamentous (F)-actin with jasplakinolide, a cell-permeant F-actin-binding toxin, b
19                                 In contrast, jasplakinolide, a drug that enhances actin polymerizatio
20                                              Jasplakinolide, a drug that prevents actin filament disa
21 tively depolymerizes actin and is blocked by jasplakinolide, a drug which stabilizes actin filaments.
22                                              Jasplakinolide, a membrane-permeable actin-polymerizing
23 ilized by culturing elongating bristles with jasplakinolide, a membrane-permeant inhibitor of actin f
24                                        Last, jasplakinolide, a pharmacological stabilizer of F-actin,
25 ent of an actin filament stabilizing regent, jasplakinolide, abrogated arsenic-induced NADPH oxidase
26       We found that latrunculin A (LatA) and jasplakinolide, actin drugs that release mDia1 from acti
27                                              Jasplakinolide also induced internalization of Trp3 and
28 ngly, however, stabilization of F-actin with jasplakinolide also resulted in a dose-dependent inhibit
29 tion of actin polymerization (latrunculin-A, jasplakinolide) also collapsed the actomyosin network.
30 alasin B, cytochalasin D, latrunculin A, and jasplakinolide, also inhibited Ebola virus GP-mediated e
31 e the actin cytoskeleton (cytochalasin D and jasplakinolide) altered the plasma membrane mobility of
32                                              Jasplakinolide, an actin polymerizing agent known to cau
33                                              Jasplakinolide, an actin polymerizing agent, mimics the
34                      Finally, treatment with jasplakinolide, an inhibitor of actin turnover, resulted
35 e isolation of jasplakinolide (1) and eleven jasplakinolide analogues (3-13) including seven new anal
36 is study was to isolate and study additional jasplakinolide analogues from two taxonomically distinct
37 eloped, dolastatin 11 was twice as active as jasplakinolide and 4-fold more active than phalloidin.
38 es of the actin-stabilizing natural products jasplakinolide and chondramide C.
39 ed optical tweezers to analyze the effect of jasplakinolide and cyclodextrin on the force exerted by
40 -permeant actin cytoskeleton-modifying drugs jasplakinolide and latrunculin A to investigate the acti
41                                              Jasplakinolide and latrunculin B did not prevent inhibit
42 somato/dendritic release was also blocked by jasplakinolide and latrunculin, suggesting that priming
43                      However, in contrast to jasplakinolide and phalloidin, dolastatin 11 did not inh
44 as demonstrated by stiffening in response to jasplakinolide and the abrogation of spreading.
45 statin 11 was qualitatively more active than jasplakinolide and, in a quantitative assay we developed
46 cific actin ligands such as latrunculin B or jasplakinolide, antibody to the actin regulatory protein
47 emia are blocked by actin stabilization with jasplakinolide, as well as proteasome inhibition with MG
48                                              Jasplakinolide B (11) exhibited potent cytotoxicity (GI(
49 ith a greatly reduced ability to bind actin, jasplakinolide B, did not enhance apoptosis.
50  Here, we introduce SiR-XActin, a simplified jasplakinolide-based, far-red fluorescent probe that ena
51 ally consistent with the localization of the jasplakinolide-binding site at an interface of three act
52                                      Because jasplakinolide both decreases the amount of sequestered
53 Ouabain, an Na(+)-K(+)-ATPase inhibitor, and jasplakinolide both prevent approximately 50% of the ATP
54  to but fails to depolymerize phalloidin- or jasplakinolide-bound actin filaments.
55  underlying force generation were reduced by jasplakinolide but not by cyclodextrin.
56  to those of the sponge-derived depsipeptide jasplakinolide, but dolastatin 11 was about 3-fold more
57  the F-actin-stabilizing marine depsipeptide jasplakinolide by functionalizing them with azobenzene p
58                Treatment of these cells with jasplakinolide caused rapid and dramatic effects on the
59 tent, whereas polymerization of F-actin with jasplakinolide causes VSM contraction and decreased G-ac
60                               This effect of jasplakinolide correlated with its ability to stabilize
61 inolide were found to be separable; 1 microM jasplakinolide could permeate cells, bind cellular filam
62            Experiments with mycalolide B and jasplakinolide demonstrate that neuropeptidergic DCV mot
63         Blocking actin dynamic turnover with jasplakinolide demonstrates that dynamic actin is requir
64 s and G-actin depletion, by the marine toxin jasplakinolide, destabilised the endogenous PPP1R15A-PP1
65           Actin modulation by latrunculin or jasplakinolide did not affect AQP4-M23 diffusion, but de
66                In live, permeabilised cells, jasplakinolide did not inhibit filament assembly from su
67 We also demonstrate that an actin inhibitor, jasplakinolide, diminishes spin-mediated enhancement.
68                                         Like jasplakinolide, dolastatin 11 induced the hyperassembly
69                                         Like jasplakinolide, (-)-doliculide caused the hyperassembly
70  experiments inducing actin stabilisation by Jasplakinolide, emphasising that the actin cytoskeleton
71 tin stabilization by the cell permeant agent jasplakinolide enhanced cell death upon interleukin (IL)
72 is, the actin modifying drugs phalloidin and jasplakinolide enhanced secretion, while latrunculin-A i
73                     Expected consequences of jasplakinolide function are consistent with the experime
74                                              Jasplakinolide had no effect on HCO3- absorption in tubu
75 ore, the stabilization of actin network with jasplakinolide had no effect on virus yields.
76 did not change the rate of mean disassembly, Jasplakinolide halted it completely, indicating that the
77 ed unchanged when applying Latrunculin A and Jasplakinolide in low doses, except that additional freq
78 atin 11 was about 3-fold more cytotoxic than jasplakinolide in the cells studied.
79              Treatment of CTLL-20 cells with jasplakinolide, in the presence or absence of recombinan
80 itive stimulation, whereas actin polymerizer jasplakinolide increases the number of active boutons in
81                                              Jasplakinolide-induced actin polymerization synergizes w
82                                        These jasplakinolide-induced filaments decorated with myosin s
83 broblasts, there was a delay in the onset of jasplakinolide-induced inhibition of lamellipodium protr
84  ends of actin filaments by model fitting of jasplakinolide-induced temporal changes in G-actin conce
85 t assembly/disassembly with latrunculin-A or jasplakinolide induces an approximately twofold increase
86 eters in vitro define the mechanism by which jasplakinolide induces polymerization of monomeric actin
87 nsulin secretion, whereas stabilization with jasplakinolide inhibited secretion, consistent with the
88      Latrunculin significantly enhanced, and jasplakinolide inhibited, high-K(+)-evoked somato/dendri
89                                              Jasplakinolide inhibits actin disassembly, and latruncul
90 eation, the enhancement of polymerization by jasplakinolide is amplified in the presence of actin-mon
91                                              Jasplakinolide is the only readily available drug that s
92                          The natural product jasplakinolide is widely used to stabilize F-actin.
93 parasites with the filament-stabilizing drug jasplakinolide (JAS) and monitored the distribution of a
94 Here, we report the near-atomic structure of jasplakinolide (JAS)-stabilized PfAct1 filaments determi
95 e actin-stabilizing and depolymerizing drugs jasplakinolide (Jasp) and latrunculin B, we demonstrate
96                                      We used jasplakinolide (jasp), a cell-permeable macrocyclic pept
97         Treatment of murine ovaries with muM Jasplakinolide (JASP), an actin polymerization-promoting
98 ly mimicked by the actin filament stabilizer Jasplakinolide (JASP).
99 when actin depolymerization was inhibited by jasplakinolide, LPL peptide-induced adhesion was inhibit
100 tion-phase synthesis of des-bromo-des-methyl-jasplakinolide-lysine opens a way to better fluorescent
101                         Des-bromo-des-methyl-jasplakinolide-lysine was coupled with red-emitting fluo
102 tion-phase synthesis of des-bromo-des-methyl-jasplakinolide-lysine, used as the "recognition unit" (l
103 y, enriching the cortical cytoskeleton using jasplakinolide maintained raft probe co-clustering, CD45
104                                              Jasplakinolide markedly enhances the rate of actin filam
105 with cytochalasin D or stabilizing them with jasplakinolide negates the effects of suppressing or act
106                                      Neither jasplakinolide nor cyclodextrin affected force or veloci
107        A detailed analysis of the effects of jasplakinolide on the kinetics of actin polymerization s
108 e anti-CD3 antibodies, treatment with either jasplakinolide or latrunculin A abolished granule exocyt
109      Disrupting actin filament dynamics with jasplakinolide or latrunculin A arrested fusion at a lat
110  50% by slowing actin filament turnover with jasplakinolide or latrunculin A.
111 armacological treatments (Cytochalasin D and Jasplakinolide) or genetic disruption (zyxin gene deleti
112                                              Jasplakinolide paradoxically stabilizes actin filaments
113 or analysis, we compared (-)-doliculide with jasplakinolide, phalloidin, and chondramide C to gain in
114                                              Jasplakinolide prevented amiloride-induced actin remodel
115 y contrast, stabilizing actin filaments with jasplakinolide prevented cytochalasin D-, latrunculin A-
116                                              Jasplakinolide prevents the carbachol inhibition of ilea
117  a membrane-permeable stabilizer of F-actin, jasplakinolide, prevents antigen-stimulated changes in D
118 trunculin B and the actin stabilization drug jasplakinolide rapidly disrupted transport of secretory
119            In addition, (-)-doliculide, like jasplakinolide, readily displaced a fluorescent phalloid
120  genes have been deleted, rendering normally jasplakinolide-resistant yeast cells sensitive to its ef
121 clear ERK, whereas actin polymerization with jasplakinolide restored nuclear translocation of activat
122  and disassembly cycle with latrunculin A or jasplakinolide results in near complete cessation of all
123 le inhibition of microfilament dynamics with jasplakinolide results in reduced numbers of viral antig
124                  Stabilization of F-actin by jasplakinolide significantly reduced the ability of glut
125                                              Jasplakinolide stabilization of the actin cytoskeleton i
126                        Cryo-EM structures of jasplakinolide-stabilized and native (i.e. unstabilized)
127                             Like phalloidin, jasplakinolide stabilizes F-actin and promotes actin pol
128 L, and stabilization of polymerized actin by jasplakinolide suppressed the morphological conversion.
129 eveloped a new generation of photoswitchable jasplakinolides that feature rationally designed red-shi
130                    Conversely, treating with jasplakinolide to enhance actin polymerization increased
131                     Using cytochalasin D and jasplakinolide to selectively inhibit actin retrograde f
132 ted cells compared with control and 1 microM jasplakinolide-treated cells.
133                                              Jasplakinolide-treated tachyzoites were unable to invade
134  Inhibition of actin polymerization alone by jasplakinolide treatment failed to reproduce the inhibit
135 to treatment with the actin-binding compound jasplakinolide upon IL-2 deprivation.
136 tion induced by the actin polymerizing agent jasplakinolide was not altered by deletion of Dicer, sug
137                                              Jasplakinolide was not toxic to CTLL-20 cells, nor was a
138                                         When jasplakinolide was used to overcome the severing action
139               In cells the two activities of jasplakinolide were found to be separable; 1 microM jasp
140  these biochemical assays (-)-doliculide and jasplakinolide were quantitatively virtually identical i
141 formation is unaffected by cytochalasin D or jasplakinolide, whereas its ability to inhibit MEK1/2 an
142 d, and is assessed here using the actin drug jasplakinolide, which has two known activities - inhibit
143                       We found that 25 nM of jasplakinolide, which is known to inhibit actin filament
144 n B was partially blocked by the addition of jasplakinolide, which promotes actin assembly.
145            Unlike store-mediated Ca2+ entry, jasplakinolide, which reorganises actin filaments into a
146                                              Jasplakinolide, which stabilizes F-actin, or latrunculin
147 tin, as treatment with a synthetic analog of jasplakinolide with a greatly reduced ability to bind ac
148 ithin 1-5 minutes of treatment with 1 microM jasplakinolide, without any perturbation of actin organi

 
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