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1  collisions are twice as likely to result in microtubule depolymerization.
2 compromised NDC80 function was restored upon microtubule depolymerization.
3 n mutant overides the checkpoint response to microtubule depolymerization.
4 at the shmoo tip increased during periods of microtubule depolymerization.
5 e molecules in the pSMAC was not affected by microtubule depolymerization.
6 ments could facilitate tracking during rapid microtubule depolymerization.
7 ontractile dysfunction that is normalized by microtubule depolymerization.
8 covalently binds to beta-tubulin and induces microtubule depolymerization.
9 e incipient bud site or bud tip, followed by microtubule depolymerization.
10 1/ XKIF2-tubulin dimer complex released upon microtubule depolymerization.
11 verloaded myocardium, which is normalized by microtubule depolymerization.
12  this overlapping expression is disrupted by microtubule depolymerization.
13 nsitivity to Vinca alkaloids, which promotes microtubule depolymerization.
14 ttering of Golgi transferases in response to microtubule depolymerization.
15 nical defects are normalized in each case by microtubule depolymerization.
16 Vs was quite depressed but was normalized by microtubule depolymerization.
17 ere suppressed in the absence of significant microtubule depolymerization.
18 f stathmin by RSK2 reduced stathmin-mediated microtubule depolymerization.
19 s as ERGIC-53 underlies Golgi Dispersal upon microtubule depolymerization.
20 ssessed by measuring sarcomere motion during microtubule depolymerization.
21 concerted mechanism involving Kif24-mediated microtubule depolymerization.
22 d maintenance of the mitotic checkpoint upon microtubule depolymerization.
23 dle elongation, and initiation of interpolar microtubule depolymerization.
24 t a single frequency are greatly enhanced by microtubule depolymerization.
25 sease mice also showed altered survival upon microtubule depolymerization.
26 , the Dam1 complex couples kinetochores with microtubule depolymerization.
27 t to reduce MAP kinase activation induced by microtubule depolymerization.
28 the effect of 5-HT(1A) on NMDAR currents and microtubule depolymerization.
29 al defects observed in wild-type cells after microtubule depolymerization.
30  2-fold reduction in energy dissipation upon microtubule depolymerization.
31 results reveal a novel mechanism to regulate microtubule depolymerization.
32  significantly attenuated colchicine-induced microtubule depolymerization.
33 ely active XLfc recapitulates the effects of microtubule depolymerization.
34 laser-induced severing or nocodazole-induced microtubule depolymerization.
35                                              Microtubule depolymerization abolished uptake of complem
36 nes 192 and 111 preferentially regulates its microtubule depolymerization activity and localization t
37 ifferent MCAK domains contribute to in vitro microtubule depolymerization activity and physiological
38                                         MCAK microtubule depolymerization activity is inhibited by Au
39 ork provides a mechanism by which the robust microtubule depolymerization activity of kinesin-13s can
40                   These data reveal that the microtubule depolymerization activity of kinesin-8 origi
41 he C-terminal domain is necessary for robust microtubule depolymerization activity, limiting spindle
42 196 in the neck region of MCAK inhibited its microtubule depolymerization activity.
43 o interact with microtubules and reduces its microtubule depolymerization activity.
44 nal domain are necessary for robust in vitro microtubule depolymerization activity.
45 eoplasia after treatment with vincristine, a microtubule depolymerization agent.
46                                              Microtubule depolymerization also resulted in activation
47                        Uncaging n-CA4 causes microtubule depolymerization and an accompanying reducti
48     Treatment with nocodazole, which induced microtubule depolymerization and cell shape changes with
49                          Moreover, actin and microtubule depolymerization and changing chromatin cond
50 also reduced rotenone- or colchicine-induced microtubule depolymerization and death of TH(+) through
51 y attenuated rotenone- or colchicine-induced microtubule depolymerization and ensuing accumulation of
52      Antibodies against a p22 peptide induce microtubule depolymerization and ER fragmentation; this
53 XKCM1 is a kinesin-like protein that induces microtubule depolymerization and is required for mitotic
54                                              Microtubule depolymerization and kinesin-related motors
55 gi membrane underlies Golgi dispersal during microtubule depolymerization and mitosis.
56 eptide isolated from marine sponges, induces microtubule depolymerization and mitotic arrest in cells
57 otubule ends for force generation coupled to microtubule depolymerization and polymerization.
58 d, thereby creating a boundary that prevents microtubule depolymerization and rescues microtubule pol
59 e activity of molecular motors important for microtubule depolymerization and sliding and the cell cy
60 ences the stringency of cellular response to microtubule depolymerization and spindle damage.
61                                  We identify microtubule depolymerization and the accumulation of cyt
62                     The ability to attenuate microtubule depolymerization and the ensuing MAP kinase
63 l ionic currents to define the route between microtubule depolymerization and the increase in the rat
64                 Muscarinic agonists promoted microtubule depolymerization and translocation of tubuli
65 bulin shape-induced alternations between pro-microtubule-depolymerization and pro-motility kinesin st
66 es of inducing tubulin conformation changes, microtubule depolymerization, and eventual cell cycle ar
67  mitotic spindle disruption, mitotic arrest, microtubule depolymerization, and inhibition of the asse
68 ty of MCAK to recycle for multiple rounds of microtubule depolymerization, and preventing MCAK from b
69  Its mechanism of action is determined to be microtubule depolymerization, and the compound is shown
70 otocatalyst and the fluorescent reporter for microtubule depolymerization, and with confocal microsco
71  treatments with either lower temperature or microtubule depolymerization are known to decrease axona
72       Here, by establishing colcemid-induced microtubule depolymerization as a sensitive assay, we ex
73 multiple kinesin-like proteins important for microtubule depolymerization, as well as kinesin-5, cont
74        We used steady-state ATPase kinetics, microtubule depolymerization assays, and microtubule.MCA
75 nlike the situation for vertebrate spindles, microtubule depolymerization at poles and polewards flux
76 kinetochore fibers occurred by inhibition of microtubule depolymerization at poles, with no change in
77 at dynein and Xklp2 regulate flux-associated microtubule depolymerization at spindle poles.
78 ts impotence at minus ends permits continued microtubule depolymerization at the spindle poles.
79                                              Microtubule depolymerization blocks lysosome and Golgi e
80 s with mutations in SGO1 respond normally to microtubule depolymerization but not to lack of tension
81           Actin depolymerization can trigger microtubule depolymerization but not vice versa.
82  endothelial cells, CA-4-P is known to cause microtubule depolymerization, but little is known about
83                                              Microtubule depolymerization by colchicine normalizes co
84  viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine was found to
85                                Consistently, microtubule depolymerization by nocodazole blocks granul
86                                              Microtubule depolymerization by nocodazole inhibits lame
87                       Arrest of mitosis upon microtubule depolymerization by nocodazole is also condi
88 ernative, tubulin curvature-sensing model of microtubule depolymerization by the budding yeast kinesi
89      Furthermore, both the dynein mutant and microtubule depolymerization cause lateral Cad99C secret
90                                              Microtubule depolymerization caused by colchicine, demec
91 RP1-EGFP expression protected cells from the microtubule depolymerization caused by vincristine and c
92                                              Microtubule depolymerization causes APC to relocalize fr
93 n of cortical ER, whereas locally increasing microtubule depolymerization causes exaggerated asymmetr
94 e poles by a Pacman-flux mechanism linked to microtubule depolymerization: chromosomes actively depol
95 d transition to end-on attachment, whereupon microtubule depolymerization commences.
96 e dominant mechanism, kinetochore-associated microtubule depolymerization contributes to anaphase A.
97 nge of functional assays, we have shown that microtubule depolymerization correlates with the activat
98 omolar concentrations, in the absence of net microtubule depolymerization, cryptophycin 1 potently st
99                                The nature of microtubule depolymerization dictates the type of shape
100                                              Microtubule depolymerization disrupted vesicular transpo
101                    Spatiotemporal control of microtubule depolymerization during cell division underl
102 oscillations in contractility are induced by microtubule depolymerization during cell spreading.
103 y for a kinesin-related protein by promoting microtubule depolymerization during mitotic spindle asse
104                                      Because microtubule depolymerization elicits striking effects on
105 ntial for ciliary length control through its microtubule depolymerization function.
106                                              Microtubule depolymerization gives rise to FH-B cell com
107                                        After microtubule depolymerization, Golgi membrane components
108                             MAP20 suppresses microtubule depolymerization; however, unlike the animal
109 d fast tubulin washout experiments to induce microtubule depolymerization in a controlled manner at d
110  changes in tubulin conformation act against microtubule depolymerization in a precise directional wa
111 y attenuated rotenone- or colchicine-induced microtubule depolymerization in an MEK-dependent manner.
112  density and that colchicine caused complete microtubule depolymerization in both control and PAB pap
113 rm of the complex for energy coupling during microtubule depolymerization in budding yeast.
114  of MCAK is necessary but not sufficient for microtubule depolymerization in cells or in vitro.
115 ensitivity can be separated from the others; microtubule depolymerization in mature TRNs causes touch
116 I-induced PCD by taxol implicates a role for microtubule depolymerization in mediating PCD.
117                                 In contrast, microtubule depolymerization in midgastrula embryos, aft
118 tine, crocin, or colchicine; and 6) leads to microtubule depolymerization in PC3 cells.
119 cal microscopy, it was possible to visualize microtubule depolymerization in real time as the result
120 ment of A-10 cells with paclitaxel prevented microtubule depolymerization in response to welwistatin.
121 ation in developing cortical neurons induces microtubule depolymerization in the growth cone peripher
122 ment with vincristine did not cause profound microtubule depolymerization in the unmyelinated axons o
123 cies of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inh
124 e function was equivalent, and unaffected by microtubule depolymerization, in cells from control LVs
125                                              Microtubule depolymerization, in contrast, does not affe
126 o the duration of a growth pause just before microtubule depolymerization, indicating an important ro
127 lar microtubule network that is resistant to microtubule depolymerization induced by alkaloids, cold
128               Thus, our results suggest that microtubule depolymerization induced by PD toxins such a
129        Transcription profiling revealed that microtubule depolymerization induced the autocrine growt
130                    The results indicate that microtubule depolymerization induces distinct cell death
131                                      Second, microtubule depolymerization induces expansion of the ki
132                               Docetaxel is a microtubule depolymerization inhibitor with unique physi
133 uction is suppressed in PtK1 cells, and that microtubule depolymerization inhibits this process.
134 these behaviors: active interfaces transduce microtubule depolymerization into mechanical work, and p
135 ce that can translate the force generated by microtubule depolymerization into movement along the lat
136 y encircle a single microtubule, can convert microtubule depolymerization into the poleward kinetocho
137                                              Microtubule depolymerization is controlled in part by mi
138 n to involve Kar3p, is markedly delayed when microtubule depolymerization is inhibited by the tub2-15
139 ubules, decreasing their density; such local microtubule depolymerization is necessary for GSIS, like
140                      These data suggest that microtubule depolymerization is not required for neocent
141  these two components of flux indicates that microtubule depolymerization is not required for the mic
142                                              Microtubule depolymerization is rapid and results in the
143 crotubule polymerization and 'curved' during microtubule depolymerization) is an essential requiremen
144 lified by that occurring during drug-induced microtubule depolymerization, is accompanied by the sepa
145 F-kappaB is activated rapidly in response to microtubule depolymerization, its cell survival function
146                                 In contrast, microtubule depolymerization lead to decreased mean spee
147                   Mutations in unc-104, like microtubule depolymerization, lead to a reduced level of
148               During the mitotic cell cycle, microtubule depolymerization leads to a cell cycle arres
149 we confirm and extend previous findings that microtubule depolymerization leads to the rapid activati
150 ition of Arp2/3 function in combination with microtubule depolymerization led to a virtual block in H
151 )AR transcripts is microtubule-dependent, as microtubule depolymerization markedly reduces the number
152                                              Microtubule depolymerization may also be the mechanism b
153 lts show that subcellular domains along with microtubule depolymerization may influence the actin cyt
154 l cell-based assay for the quantification of microtubule depolymerization, measured through fluoresce
155 a "Pacman" kinetochore mechanism, coupled to microtubule depolymerization near the kinetochore, predo
156 s that poleward microtubule flux, coupled to microtubule depolymerization near the spindle poles, is
157                                              Microtubule depolymerization normalized myocardial contr
158 etermine whether the ameliorative effects of microtubule depolymerization on cellular contractile dys
159 rophase NE invaginations (PNEIs), similar to microtubule depolymerization or down-regulation of the d
160 ome repositioning was impaired by inhibiting microtubule depolymerization or dynein.
161                              First, inducing microtubule depolymerization or stabilization before the
162          S. typhi invasion was unaffected by microtubule depolymerization or stabilization.
163 erature and to agents that cause DNA damage, microtubule depolymerization, or cell wall stress (likel
164 ), was unaffected by actin depolymerization, microtubule depolymerization, or detergent extraction.
165 ased catastrophes accompanied SUN1 loss, and microtubule depolymerization phenocopied effects on junc
166        Both the active site and mechanism of microtubule depolymerization predictions are in good agr
167 ative model that proposes a coupling between microtubule depolymerization rates and microtubule slidi
168  These microtubule bundles were resistant to microtubule depolymerization reagents and enriched in ac
169               In myocardial tissue, we found microtubule depolymerization reduced myocardial viscoela
170                            Kar3Cik1-promoted microtubule depolymerization requires ATP turnover, and
171                                              Microtubule depolymerization restored LV contractile fun
172 ment of HeLa cells with nocodazole to induce microtubule depolymerization results in Rho-dependent ac
173 mergence of abnormal satellites, as complete microtubule depolymerization results in the disappearanc
174      Such redirected flow was accelerated by microtubule depolymerization, showing that the suppressi
175 DA-mediated induction of HIF-1alpha required microtubule depolymerization, since HIF-1alpha levels we
176 ce must act on a single motor to achieve the microtubule depolymerization speed of a motor ensemble.
177     Furthermore, FTI and agents that prevent microtubule depolymerization, such as taxol or epothilon
178                                       During microtubule depolymerization, the central, juxtanuclear
179 n retinas treated with lower temperature and microtubule depolymerization, the time constants increas
180 go cycles of conformational change to couple microtubule depolymerization to chromosome movement.
181 e Dam1 kinetochore complex is able to couple microtubule depolymerization to poleward movement.
182 d identities of coupling proteins that allow microtubule depolymerization to pull chromosomes to pole
183 0.1 microM and 1.2 microM, respectively) and microtubule depolymerization was not affected, indicatin
184                      More than 50 years ago, microtubule depolymerization was proposed as the force r
185 hmin, an 18-kDa phosphoprotein that promotes microtubule depolymerization, was found to be frequently
186 dehyde-fixed retina, and retina treated with microtubule depolymerization were used.
187 nished the ability of tau to protect against microtubule depolymerization, whereas with T4C3 only pse
188 spindles and misaligned chromosomes, reduced microtubule depolymerization, which led to significant p
189 which locally stabilize microtubules and, on microtubule depolymerization with nocodazole, activate t
190                                    Following microtubule depolymerization with nocodazole, Arl3 reloc
191 rin was maintained at 15 degrees C and after microtubule depolymerization with nocodazole.
192          In migrating dendritic cells, local microtubule depolymerization within protrusions remote f

 
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