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1 ments could facilitate tracking during rapid microtubule depolymerization.
2 n mutant overides the checkpoint response to microtubule depolymerization.
3 at the shmoo tip increased during periods of microtubule depolymerization.
4 e molecules in the pSMAC was not affected by microtubule depolymerization.
5 ontractile dysfunction that is normalized by microtubule depolymerization.
6 covalently binds to beta-tubulin and induces microtubule depolymerization.
7 e incipient bud site or bud tip, followed by microtubule depolymerization.
8 1/ XKIF2-tubulin dimer complex released upon microtubule depolymerization.
9 verloaded myocardium, which is normalized by microtubule depolymerization.
10 this overlapping expression is disrupted by microtubule depolymerization.
11 nsitivity to Vinca alkaloids, which promotes microtubule depolymerization.
12 ttering of Golgi transferases in response to microtubule depolymerization.
13 nical defects are normalized in each case by microtubule depolymerization.
14 Vs was quite depressed but was normalized by microtubule depolymerization.
15 ere suppressed in the absence of significant microtubule depolymerization.
16 d maintenance of the mitotic checkpoint upon microtubule depolymerization.
17 s as ERGIC-53 underlies Golgi Dispersal upon microtubule depolymerization.
18 ssessed by measuring sarcomere motion during microtubule depolymerization.
19 dle elongation, and initiation of interpolar microtubule depolymerization.
20 t a single frequency are greatly enhanced by microtubule depolymerization.
21 sease mice also showed altered survival upon microtubule depolymerization.
22 , the Dam1 complex couples kinetochores with microtubule depolymerization.
23 t to reduce MAP kinase activation induced by microtubule depolymerization.
24 the effect of 5-HT(1A) on NMDAR currents and microtubule depolymerization.
25 f stathmin by RSK2 reduced stathmin-mediated microtubule depolymerization.
26 al defects observed in wild-type cells after microtubule depolymerization.
27 results reveal a novel mechanism to regulate microtubule depolymerization.
28 significantly attenuated colchicine-induced microtubule depolymerization.
29 ely active XLfc recapitulates the effects of microtubule depolymerization.
30 concerted mechanism involving Kif24-mediated microtubule depolymerization.
31 collisions are twice as likely to result in microtubule depolymerization.
32 compromised NDC80 function was restored upon microtubule depolymerization.
34 nes 192 and 111 preferentially regulates its microtubule depolymerization activity and localization t
35 ifferent MCAK domains contribute to in vitro microtubule depolymerization activity and physiological
37 ork provides a mechanism by which the robust microtubule depolymerization activity of kinesin-13s can
38 he C-terminal domain is necessary for robust microtubule depolymerization activity, limiting spindle
44 Treatment with nocodazole, which induced microtubule depolymerization and cell shape changes with
45 also reduced rotenone- or colchicine-induced microtubule depolymerization and death of TH(+) through
46 y attenuated rotenone- or colchicine-induced microtubule depolymerization and ensuing accumulation of
48 XKCM1 is a kinesin-like protein that induces microtubule depolymerization and is required for mitotic
51 eptide isolated from marine sponges, induces microtubule depolymerization and mitotic arrest in cells
56 l ionic currents to define the route between microtubule depolymerization and the increase in the rat
58 es of inducing tubulin conformation changes, microtubule depolymerization, and eventual cell cycle ar
59 mitotic spindle disruption, mitotic arrest, microtubule depolymerization, and inhibition of the asse
60 ty of MCAK to recycle for multiple rounds of microtubule depolymerization, and preventing MCAK from b
61 Its mechanism of action is determined to be microtubule depolymerization, and the compound is shown
62 treatments with either lower temperature or microtubule depolymerization are known to decrease axona
65 nlike the situation for vertebrate spindles, microtubule depolymerization at poles and polewards flux
66 kinetochore fibers occurred by inhibition of microtubule depolymerization at poles, with no change in
70 s with mutations in SGO1 respond normally to microtubule depolymerization but not to lack of tension
72 endothelial cells, CA-4-P is known to cause microtubule depolymerization, but little is known about
74 viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine was found to
78 ernative, tubulin curvature-sensing model of microtubule depolymerization by the budding yeast kinesi
80 RP1-EGFP expression protected cells from the microtubule depolymerization caused by vincristine and c
82 n of cortical ER, whereas locally increasing microtubule depolymerization causes exaggerated asymmetr
83 e poles by a Pacman-flux mechanism linked to microtubule depolymerization: chromosomes actively depol
84 e dominant mechanism, kinetochore-associated microtubule depolymerization contributes to anaphase A.
85 nge of functional assays, we have shown that microtubule depolymerization correlates with the activat
86 omolar concentrations, in the absence of net microtubule depolymerization, cryptophycin 1 potently st
90 y for a kinesin-related protein by promoting microtubule depolymerization during mitotic spindle asse
93 d fast tubulin washout experiments to induce microtubule depolymerization in a controlled manner at d
94 changes in tubulin conformation act against microtubule depolymerization in a precise directional wa
95 y attenuated rotenone- or colchicine-induced microtubule depolymerization in an MEK-dependent manner.
96 density and that colchicine caused complete microtubule depolymerization in both control and PAB pap
99 ensitivity can be separated from the others; microtubule depolymerization in mature TRNs causes touch
102 ment of A-10 cells with paclitaxel prevented microtubule depolymerization in response to welwistatin.
103 ment with vincristine did not cause profound microtubule depolymerization in the unmyelinated axons o
104 cies of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inh
105 e function was equivalent, and unaffected by microtubule depolymerization, in cells from control LVs
107 o the duration of a growth pause just before microtubule depolymerization, indicating an important ro
108 lar microtubule network that is resistant to microtubule depolymerization induced by alkaloids, cold
113 uction is suppressed in PtK1 cells, and that microtubule depolymerization inhibits this process.
114 these behaviors: active interfaces transduce microtubule depolymerization into mechanical work, and p
115 ce that can translate the force generated by microtubule depolymerization into movement along the lat
116 y encircle a single microtubule, can convert microtubule depolymerization into the poleward kinetocho
118 n to involve Kar3p, is markedly delayed when microtubule depolymerization is inhibited by the tub2-15
119 ubules, decreasing their density; such local microtubule depolymerization is necessary for GSIS, like
121 these two components of flux indicates that microtubule depolymerization is not required for the mic
123 crotubule polymerization and 'curved' during microtubule depolymerization) is an essential requiremen
124 lified by that occurring during drug-induced microtubule depolymerization, is accompanied by the sepa
125 F-kappaB is activated rapidly in response to microtubule depolymerization, its cell survival function
129 we confirm and extend previous findings that microtubule depolymerization leads to the rapid activati
130 ition of Arp2/3 function in combination with microtubule depolymerization led to a virtual block in H
132 lts show that subcellular domains along with microtubule depolymerization may influence the actin cyt
133 a "Pacman" kinetochore mechanism, coupled to microtubule depolymerization near the kinetochore, predo
134 s that poleward microtubule flux, coupled to microtubule depolymerization near the spindle poles, is
136 etermine whether the ameliorative effects of microtubule depolymerization on cellular contractile dys
137 rophase NE invaginations (PNEIs), similar to microtubule depolymerization or down-regulation of the d
141 erature and to agents that cause DNA damage, microtubule depolymerization, or cell wall stress (likel
142 ), was unaffected by actin depolymerization, microtubule depolymerization, or detergent extraction.
144 ative model that proposes a coupling between microtubule depolymerization rates and microtubule slidi
145 These microtubule bundles were resistant to microtubule depolymerization reagents and enriched in ac
148 ment of HeLa cells with nocodazole to induce microtubule depolymerization results in Rho-dependent ac
149 mergence of abnormal satellites, as complete microtubule depolymerization results in the disappearanc
150 Such redirected flow was accelerated by microtubule depolymerization, showing that the suppressi
151 DA-mediated induction of HIF-1alpha required microtubule depolymerization, since HIF-1alpha levels we
152 Furthermore, FTI and agents that prevent microtubule depolymerization, such as taxol or epothilon
154 n retinas treated with lower temperature and microtubule depolymerization, the time constants increas
156 d identities of coupling proteins that allow microtubule depolymerization to pull chromosomes to pole
157 0.1 microM and 1.2 microM, respectively) and microtubule depolymerization was not affected, indicatin
159 hmin, an 18-kDa phosphoprotein that promotes microtubule depolymerization, was found to be frequently
161 nished the ability of tau to protect against microtubule depolymerization, whereas with T4C3 only pse
162 spindles and misaligned chromosomes, reduced microtubule depolymerization, which led to significant p
163 which locally stabilize microtubules and, on microtubule depolymerization with nocodazole, activate t
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