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

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