ライフサイエンスコーパス: kinetochore microtubule

1 r mechanically amplifying damage at a single kinetochore microtubule.

2 partial ring-shaped structures girding their kinetochore microtubules.

3 ubulin for fluorescent speckle microscopy on kinetochore microtubules.

4 which reduces phosphorylation and stabilizes kinetochore microtubules.

5 lity of parallel microtubules, including the kinetochore microtubules.

6 terminus in controlling dynamic behavior of kinetochore microtubules.

7 sister chromatids and decreased stability of kinetochore microtubules.

8 ng MCAK to depolymerize incorrectly oriented kinetochore microtubules.

9 se A occurs exclusively at the minus ends of kinetochore microtubules.

10 indle equator, a process mediated by dynamic kinetochore microtubules.

11 oteins, such as the Ndc80 complex, that bind kinetochore microtubules.

12 ints, and associated with the centrosome and kinetochore/ microtubules.

13 per human kinetochore ( approximately 14 per kinetochore microtubule), 215 CENP-C, 72 CENP-T and only

14 ion between chromosomal kinetochores and the kinetochore microtubules activates the spindle assembly

15 id) are stretched between the ends of sister-kinetochore microtubules along the spindle axis.

16 s of different spindle types illustrates how kinetochore microtubules amplify spindle microtubule den

17 ubulin subunits are added to the plus end of kinetochore microtubules and are removed from their minu

18 dle has two classes of nuclear microtubules: kinetochore microtubules and interpolar microtubules.

19 ion of NuSAP to the polar force generated at kinetochore microtubules and to the regulation of the po

20 and Borealin/DASRA, localizes to chromatin, kinetochores, microtubules, and the cell cortex in a cel

21 w in symmetrically dividing human cells that kinetochore-microtubules associated to old centrosomes a

22 es, where it is required to establish proper kinetochore-microtubule associations and regulate the sp

23 oximately 0.7 microm/min for speckles within kinetochore microtubules at metaphase increased during a

24 One kinetochore microtubule attaches to a single centromere

25 netochore fibers shorten from spindle poles, kinetochore microtubule attachment errors increase, and

26 When stable kinetochore microtubule attachment is prevented by Nuf2

27 oint proteins are closely linked to the core kinetochore microtubule attachment site comprised of the

28 Budding yeast is unique in having only one kinetochore microtubule attachment site per centromere.

29 B phosphorylation in achieving proper stable kinetochore microtubule attachment.

30 ying anaphase onset in response to errors in kinetochore microtubule attachment.

31 nd EB1, providing a potential link in stable kinetochore microtubule attachment.

32 tly regulate APC function involved in stable kinetochore microtubule attachment.

33 The Ndc80 complex is a key site of regulated kinetochore-microtubule attachment (a process required f

34 icrotubule assembly (nocodazole), eliminated kinetochore-microtubule attachment (loss of Nuf2), or st

35 le microtubule-binding elements and promotes kinetochore-microtubule attachment [8-11].

36 gest that in addition to a role in fostering kinetochore-microtubule attachment and chromosome alignm

37 ora B-dependent mitotic processes, including kinetochore-microtubule attachment and chromosome congre

38 ents of the NDC80 complex, are essential for kinetochore-microtubule attachment and chromosome segreg

39 This checkpoint monitors the status of kinetochore-microtubule attachment and delays the metaph

40 The mitotic checkpoint monitors kinetochore-microtubule attachment and prevents anaphase

41 master spindle checkpoint kinase Mps1 senses kinetochore-microtubule attachment and promotes checkpoi

42 t the 3D protein architecture of a metaphase kinetochore-microtubule attachment and provide new funct

43 ins a template-copy relationship crucial for kinetochore-microtubule attachment and SAC signaling.

44 al passenger complex is essential for proper kinetochore-microtubule attachment and spindle stability

45 P-F is important for the formation of proper kinetochore-microtubule attachment and, similar to CENP-

46 ochore kinases, including Aurora B, regulate kinetochore-microtubule attachment and/or SAC activation

47 it anaphase signal but also actively correct kinetochore-microtubule attachment defects.

48 r isolates requires BUB1B to suppress lethal kinetochore-microtubule attachment defects.

49 find that the Aurora B kinase Ipl1 regulates kinetochore-microtubule attachment during both meiotic d

50 embly checkpoint (SAC) monitors and promotes kinetochore-microtubule attachment during mitosis.

51 es in anaphase are symptomatic of defects in kinetochore-microtubule attachment dynamics that cause c

52 checkpoint function, centrosome copy number, kinetochore-microtubule attachment dynamics, and cell-cy

53 eveal that both Aurora A and B contribute to kinetochore-microtubule attachment dynamics, and they un

54 lar spindle intermediate' in which merotelic kinetochore-microtubule attachment errors accumulate bef

55 The spindle checkpoint that monitors kinetochore-microtubule attachment has been implicated i

56 0 complex is essential for persistent end-on kinetochore-microtubule attachment in cells [1, 2], but

57 Nuf2, and the Hec1 tail each contributes to kinetochore-microtubule attachment in distinct ways.

58 trate this remarkable change in the plane of kinetochore-microtubule attachment in human cells are no

59 sequently ensuring proper spindle length and kinetochore-microtubule attachment in meiotic oocytes.

60 ity and requires the proper establishment of kinetochore-microtubule attachment in mitosis.

61 ho-deficient dam1-3A mutants show stabilized kinetochore-microtubule attachment in vivo.

62 netochore but is unable to correct errors in kinetochore-microtubule attachment in Xenopus egg extrac

63 Stable kinetochore-microtubule attachment is essential for cell

64 the Dam1 complex as a processivity factor in kinetochore-microtubule attachment is regulated by conse

65 opy number of each of these complexes at one kinetochore-microtubule attachment site is necessary to

66 contributes uniquely to the building of the kinetochore-microtubule attachment site.

67 emonstrate a mechanism for Plk1 in promoting kinetochore-microtubule attachment to ensure chromosome

68 of structural protein complexes in a single kinetochore-microtubule attachment using quantitative fl

69 The most severe defects in kinetochore-microtubule attachment were observed in cell

70 rylation of the Ndc80 complex prevent stable kinetochore-microtubule attachment, and mutations that b

71 elicit Aurora B-dependent destabilization of kinetochore-microtubule attachment, and would activate t

72 In addition to proteins necessary for the kinetochore-microtubule attachment, bi-orientation requi

73 hat central kinetochore components influence kinetochore-microtubule attachment, but the mechanism re

74 some duplication, bipolar spindle formation, kinetochore-microtubule attachment, chromatid cohesion,

75 Moreover, Shp2 deficiency caused defective kinetochore-microtubule attachment, chromosome misalignm

76 obrevins also prevent spindle pole focusing, kinetochore-microtubule attachment, melanosome aggregati

77 ts with Blinkin and is essential for correct kinetochore-microtubule attachment, mitotic/spindle-asse

78 a B is regarded as the "master regulator" of kinetochore-microtubule attachment, other mitotic kinase

79 hosphorylatable MCAK mutant prevents correct kinetochore-microtubule attachment, resulting in abnorma

80 kinetochore complex plays a critical role in kinetochore-microtubule attachment, yet our understandin

81 checkpoint highly responsive to Mps1 and to kinetochore-microtubule attachment.

82 recapitulates much of the functionality of a kinetochore-microtubule attachment.

83 raphy to identify the structure of the human kinetochore-microtubule attachment.

84 on of functional mitotic spindles and proper kinetochore-microtubule attachment.

85 us to visualize the overall arrangement of a kinetochore-microtubule attachment.

86 ate chromosome segregation depends on proper kinetochore-microtubule attachment.

87 of anaphase to the establishment of bipolar kinetochore-microtubule attachment.

88 KAP complex in ensuring the correct plane of kinetochore-microtubule attachment.

89 of centromeric regions that prevented proper kinetochore-microtubule attachment.

90 in (MCAK) is a key regulator for an accurate kinetochore-microtubule attachment.

91 ccurate chromosome segregation by monitoring kinetochore-microtubule attachment.

92 n, function, and sensory capabilities of the kinetochore-microtubule attachment.

93 anaphase onset in the presence of defective kinetochore-microtubule attachment.

94 tid cohesion and the establishment of proper kinetochore-microtubule attachment.

95 saccharomyces pombe, which has more than one kinetochore-microtubule attachment/centromere, and co-or

96 e a diminished capacity to correct erroneous kinetochore microtubule attachments and account for the

97 romatin of bioriented chromosomes stabilizes kinetochore microtubule attachments and turns off SAC ac

98 Here we show that kinetochore microtubule attachments in cancer cells with

99 Furthermore, increasing the stability of kinetochore microtubule attachments in normal diploid RP

100 Kinetochore microtubule attachments that are too stable

101 on during metaphase and generation of stable kinetochore microtubule attachments.

102 lled by the spindle checkpoint, which senses kinetochore- microtubule attachments and tension across

103 Aurora B functions to correct improper kinetochore-microtubule attachments and alert the spindl

104 esults in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to an

105 es not prevent the formation of load-bearing kinetochore-microtubule attachments and reduces the fide

106 ic processes: initially establishing correct kinetochore-microtubule attachments and subsequently sil

107 ents within the Ska complex to ensure robust kinetochore-microtubule attachments and timely progressi

108 of sister chromatid disjunction destabilizes kinetochore-microtubule attachments and triggers the eng

109 Strong kinetochore-microtubule attachments are essential for fa

110 We found that kinetochore-microtubule attachments are established even

111 A key outstanding question is how kinetochore-microtubule attachments are modulated to ens

112 Differential stability of kinetochore-microtubule attachments at low versus high t

113 CH domain mutants, however, generated stable kinetochore-microtubule attachments but failed to genera

114 PP2A-B56 regulates the stability of kinetochore-microtubule attachments by dephosphorylating

115 Dephosphorylation is proposed to stabilize kinetochore-microtubule attachments by strengthening ele

116 m causing CIN is the persistence of improper kinetochore-microtubule attachments called merotely.

117 rophase arrest, chromosome condensation, and kinetochore-microtubule attachments during early prometa

118 e role of tension requires reconstitution of kinetochore-microtubule attachments for biochemical and

119 nopolin complex regulates different types of kinetochore-microtubule attachments in fungi, ensuring s

120 s this, we induced formation of hyper-stable kinetochore-microtubule attachments in human cells using

121 Kinase and contributes to the generation of kinetochore-microtubule attachments in mitosis.

122 -170 are involved in the timely formation of kinetochore-microtubule attachments in mitosis.

123 vitro microtubule binding, has no effect on kinetochore-microtubule attachments in the Caenorhabditi

124 e that tension selectively stabilizes proper kinetochore-microtubule attachments in vivo through a co

125 nstrate that CENP-A NAC/CAD and KMN regulate kinetochore-microtubule attachments independently, even

126 at these centromeres reflects the number of kinetochore-microtubule attachments instead of their len

127 Precise regulation of kinetochore-microtubule attachments is essential for suc

128 During anaphase, however, kinetochore-microtubule attachments must be maintained d

129 The checkpoint responds to unstable kinetochore-microtubule attachments resulting from an im

130 regation requires selective stabilization of kinetochore-microtubule attachments that come under tens

131 s by the aurora B kinase, which destabilizes kinetochore-microtubule attachments that lack tension.

132 CLIP-170 is implicated in the formation of kinetochore-microtubule attachments through direct inter

133 PP2A(B56) also stabilizes kinetochore-microtubule attachments to shut off the spin

134 of sister chromatids, indicating failure of kinetochore-microtubule attachments under tension.

135 dephosphorylation promotes stabilization of kinetochore-microtubule attachments via the Ska complex

136 nt appeared intact in HDAC3-deficient cells, kinetochore-microtubule attachments were impaired becaus

137 The Aurora B kinase coordinates kinetochore-microtubule attachments with spindle checkpo

138 In the absence of stable kinetochore-microtubule attachments, a cell surveillance

139 met) arrest in metaphase with mature bipolar kinetochore-microtubule attachments, a satisfied checkpo

140 mplex (CPC) controls chromosome congression, kinetochore-microtubule attachments, and spindle checkpo

141 osomes in Kif2b-deficient cells show typical kinetochore-microtubule attachments, but the velocity of

142 Plk1 is also implicated in stabilizing kinetochore-microtubule attachments, but these attachmen

143 ctive stabilization of correct 'bi-oriented' kinetochore-microtubule attachments, which come under te

144 y intrinsic spindle instability and abnormal kinetochore-microtubule attachments, which favor chromos

145 segregation of chromosomes depends on proper kinetochore-microtubule attachments.

146 g protein NDC80, and the formation of stable kinetochore-microtubule attachments.

147 c80 complex (KMN) network, the key player in kinetochore-microtubule attachments.

148 could regulate the stability of load-bearing kinetochore-microtubule attachments.

149 mechanism by which aurora B resets aberrant kinetochore-microtubule attachments.

150 rrest, chromatids separate but retain robust kinetochore-microtubule attachments.

151 l" of Hec1 is required for generating stable kinetochore-microtubule attachments.

152 , it is unclear whether it directly mediates kinetochore-microtubule attachments.

153 ister kinetochores, or establish cold-stable kinetochore-microtubule attachments.

154 ino acid tail domain fail to generate stable kinetochore-microtubule attachments.

155 o 5 Mb in length, and typically support many kinetochore-microtubule attachments.

156 in mitosis, ensuring proper biorientation of kinetochore-microtubule attachments.

157 ghest levels of association in cells lacking kinetochore-microtubule attachments.

158 alignment and missegregation due to improper kinetochore-microtubule attachments.

159 ays that promote formation of stable bipolar kinetochore-microtubule attachments.

160 motes chromosome biorientation by regulating kinetochore-microtubule attachments.

161 ein imparts intrinsic tension selectivity to kinetochore-microtubule attachments.

162 ential and direct role in generating dynamic kinetochore-microtubule attachments.

163 spindle and increased the risk of merotelic kinetochore-microtubule attachments.

164 omosome biorientation by detaching incorrect kinetochore-microtubule attachments.

165 On kinetochore microtubules, Bik1 and Bim1 are redundant fo

166 It requires recruitment of outer kinetochore microtubule binders by centromere proteins C

167 he N-terminal tail of Ndc80 is essential for kinetochore-microtubule binding in human cells but is no

168 ion on isolated mitotic chromosomes inhibits kinetochore-microtubule binding in vitro.

169 dy proposes a novel mechanism for regulating kinetochore-microtubule binding involving NDC80 complex

170 These results demonstrate that kinetochore-microtubule binding is dependent on electros

171 d for the efficient and accurate assembly of kinetochore-microtubule binding sites.

172 at this signal dissipates automatically upon kinetochore-microtubule binding, but it has been shown t

173 cate that in addition to Aurora B regulating kinetochore-microtubule binding, the kinetochore also co

174 e metaphase spindle in animal somatic cells, kinetochore microtubule bundles (K fibers) are often dis

175 Further, kinetochore microtubule bundles are severely destabilize

176 ed reduced centromere stretch and diminished kinetochore microtubule bundles.

177 tubule copy number from one to more than one kinetochore-microtubule/centromere does not alter the re

178 ylation by Aurora B, which corrects improper kinetochore-microtubule connections in vivo, reduces the

179 s paper, we develop a mathematical model for kinetochore-microtubule connections that directly incorp

180 Of note, changing kinetochore-microtubule copy number from one to more tha

181 eration between these two complexes enhances kinetochore-microtubule coupling and is regulated by Aur

182 member, Stu2, makes a major contribution to kinetochore-microtubule coupling.

183 regional centromeres that each attach to 3-5 kinetochore microtubules, Dam1 complex homologs are not

184 monopolar and bipolar cells with or without kinetochore microtubule depletion.

185 Tight regulation of kinetochore microtubule dynamics is required to generate

186 a molecular model in which Kif18A regulates kinetochore microtubule dynamics to control mitotic chro

187 e demonstrate that Aurora A kinase regulates kinetochore-microtubule dynamics of metaphase chromosome

188 paper, we show that Plk1 activity suppresses kinetochore-microtubule dynamics to stabilize initial at

189 centromere alignment via spatial control of kinetochore-microtubule dynamics.

190 sts; all lacked dense outer plates, and most kinetochore microtubule ends flared into curved protofil

191 p67A) involved in regulating the dynamics of kinetochore microtubule ends.

192 osphomimetic mDia3 mutant do not form stable kinetochore microtubule fibers; despite they are able to

193 ered kinetochore oscillations, and decreased kinetochore microtubule flux.

194 and movement of mono-oriented chromosomes on kinetochore microtubules for proper alignment at metapha

195 First, it protects kinetochore microtubules from depolymerization by MCAK.

196 ic chromatin through cohesin, condensin, and kinetochore microtubules functions to coordinate dynamic

197 of the spindle poles and/or the activity of kinetochore microtubules generate mechanical forces that

198 Interestingly, non-kinetochore microtubules have been observed between sist

199 Kif18A accumulates as a gradient on kinetochore microtubules in a manner dependent on its mo

200 Pa ESP associated with kinetochore microtubules in metaphase and then with anap

201 s I, we speculate that late establishment of kinetochore microtubules in oocytes reduces the likeliho

202 centromeres, implicating hyperstabilized non-kinetochore microtubules in spindle collapse.

203 ecome essential for the establishment of the kinetochore-microtubule interaction after treatment with

204 he Ndc80/Hec1 (Ndc80) kinetochore complex in kinetochore-microtubule interaction and spindle checkpoi

205 erved signaling axis that integrates dynamic kinetochore-microtubule interaction and spindle orientat

206 e bipolar attachment after the disruption of kinetochore-microtubule interaction by a microtubule dep

207 polar attachment after the disruption of the kinetochore-microtubule interaction by nocodazole, which

208 entify more genes required for the efficient kinetochore-microtubule interaction under stressful DNA

209 Furthermore, confocal scanning showed that kinetochore-microtubule interaction, an important mechan

210 coordination between cohesion resolution and kinetochore-microtubule interactions (K-fibers), a proce

211 ylates kinetochore substrates to destabilize kinetochore-microtubule interactions and eliminate incor

212 tly demonstrated that Cenp-F is required for kinetochore-microtubule interactions and spindle checkpo

213 t metaphase, pulling forces originating from kinetochore-microtubule interactions can, with time, rup

214 thetic or natural kinetochores, showing that kinetochore-microtubule interactions generate an inward

215 ubule rescue ensures efficient and sustained kinetochore-microtubule interactions in early mitosis.

216 together to contribute to the regulation of kinetochore-microtubule interactions in early mitosis.

217 Here we visualized individual kinetochore-microtubule interactions in Saccharomyces ce

218 omplex (KMN) network, which is essential for kinetochore-microtubule interactions in vivo.

219 hich incorporates a molecular scale model of kinetochore-microtubule interactions into a negative fee

220 gulate microtubule dynamics to ensure proper kinetochore-microtubule interactions is unknown.

221 o describe metaphase chromosome dynamics via kinetochore-microtubule interactions mediated by nonmoto

222 Erroneous kinetochore-microtubule interactions must be detected an

223 However, the molecular basis for robust kinetochore-microtubule interactions remains poorly unde

224 division and regulates spindle assembly and kinetochore-microtubule interactions.

225 ism for the tension-dependent fine-tuning of kinetochore-microtubule interactions.

226 dulating the activity of aurora B kinase and kinetochore-microtubule interactions.

227 pl1/Aurora B protein kinase to ensure proper kinetochore-microtubule interactions.

228 n identified, none have proven essential for kinetochore-microtubule interactions.

229 Ndc80 complex to stabilize correctly formed kinetochore-microtubule interactions.

230 may play significant roles in the nature of kinetochore-microtubule interactions.

231 including Bub3, onto kinetochores to promote kinetochore-microtubule interactions.

232 ia at least two mechanisms: by weakening the kinetochore-microtubule interface and also by destabiliz

233 This work defines an integrated kinetochore-microtubule interface formed by the Ska1 and

234 In budding yeast, the kinetochore-microtubule interface is formed by the plus

235 led kinetochores, and force generated at the kinetochore-microtubule interface is the main driver of

236 ra B transiently interacts with HDAC3 at the kinetochore-microtubule interface of congressing chromos

237 Ska complex as a key effector of Mps1 at the kinetochore-microtubule interface, as mutations that mim

238 , the Ndc80 complex, a central player in the kinetochore-microtubule interface, binds only to the str

239 play a corresponding role at the vertebrate kinetochore-microtubule interface, we isolated a three s

240 The Ndc80 complex is a key component of the kinetochore-microtubule interface.

241 hospho-aurora B, and force generation at the kinetochore-microtubule interface.

242 Mif2p, to 16 for the DAM-DASH complex at the kinetochore-microtubule interface.

243 protein network plays a central role at the kinetochore-microtubule interface.

244 and regulation of the core components of the kinetochore-microtubule interface.

245 Distinct kinetochore-microtubule interfaces mediate these behavio

246 Incorrect attachment of kinetochore microtubules is the leading cause of chromos

247 rotein flexibility inforce generation at the kinetochore-microtubule junctions.

248 is safeguarded by the precise regulation of kinetochore microtubule (k-MT) attachment stability.

249 We have probed single kinetochore microtubule (k-MT) dynamics in budding yeast

250 Notably, numerous kinetochore-microtubule (k-MT) attachment errors are pre

251 c checkpoint and the machinery that corrects kinetochore-microtubule (k-MT) attachment errors.

252 CAKs act at kinetochores to correct improper kinetochore-microtubule (k-MT) attachments, and depletio

253 cause of CIN is the persistence of aberrant kinetochore-microtubule (k-MT) attachments, which manife

254 Mitotic spindle formation and kinetochore-microtubule (K-MT) capture typically occur w

255 quently segregated via attachment to dynamic kinetochore microtubule (kMT) plus ends.

256 ter they are captured in an end-on manner by kinetochore microtubules (KMT) emanating from the spindl

257 Ipl1 was found to release kinetochore-microtubule (kMT) associations after meiotic

258 s chromosome alignment, maturation of proper kinetochore-microtubule (kMT) attachments, correction of

259 east, the mitotic spindle is comprised of 32 kinetochore microtubules (kMTs) and approximately 8 inte

260 pindles, which have roughly equal amounts of kinetochore microtubules (kMTs) and nonkinetochore micro

261 Kinetochores bound to kinetochore microtubules (kMTs) exhibit directional inst

262 movements while being end-on attached to the kinetochore microtubules (KMTs) from spindle poles.

263 eukaryotes, mature K-fibers consist of 10-30 kinetochore microtubules (kMTs) whose plus ends are embe

264 Chromosomes attach to kinetochore microtubules (kMTs), which extend from the s

265 mosome is attached to one or more of its own kinetochore microtubules (kMTs).

266 t couples chromosomes to the dynamic ends of kinetochore microtubules (kMTs).

267 ir intervening chromatin, by singly attached kinetochore microtubules (kMTs).

268 congression by promoting catastrophe of long kinetochore microtubules (kMTs).

269 Defects in kinetochore-microtubule (KT-MT) attachment and the spind

270 ess mainly relies on the forces generated by kinetochore-microtubule (KT-MT) attachment.

271 iven that the kinase is thought to stabilize kinetochore-microtubule (kt-MT) attachments.

272 curate segregation rely on the plasticity of kinetochore-microtubule (KT-MT) attachments.

273 nfiguration produces tension that stabilizes kinetochore-microtubule (kt-MT) attachments.

274 ession and generates tension that stabilizes kinetochore-microtubule (kt-MT) interactions.

275 ome segregation in mitosis relies on correct kinetochore-microtubule (KT-MT) interactions.

276 protein kinase Aurora B, which destabilizes kinetochore microtubules (ktMTs) in the absence of tensi

277 er at a slower time scale, increases average kinetochore microtubule length approximately 14%, and de

278 Thus, kinetochore microtubules maintain a constant net length,

279 ed spindles and misaligned chromosomes, with kinetochore-microtubule misattachments, on specific depl

280 er of CENP-A molecules exceeds the number of kinetochore-microtubule (MT) attachment sites on each ch

281 some segregation in cell division, erroneous kinetochore-microtubule (MT) attachments are recognized

282 re proteins during early mitosis, increasing kinetochore-microtubule (MT) turnover and preventing pre

283 hromosomes produce a steady poleward flux of kinetochore microtubules (MTs [kMTs]) in higher eukaryot

284 mber of eight kinetochore proteins that link kinetochore microtubules (MTs [kMTs]) to centromeric DNA

285 rgy released through the depolymerization of kinetochore microtubules (MTs).

286 y displaced from Cse4 at the kinetochore and kinetochore microtubule plus ends.

287 ism through which the regulatory networks at kinetochore microtubule plus- and minus-ends could commu

288 here that Ndc80/Hec1 functions in regulating kinetochore microtubule plus-end dynamics and attachment

289 twork of regulatory proteins for controlling kinetochore microtubule plus-end dynamics, which was com

290 curs during metaphase when polymerization of kinetochore microtubule plus-ends is balanced by depolym

291 At kinetochore-microtubule plus ends, the kinesin-8 family

292 and have implications for how Kif18A affects kinetochore-microtubule plus-end dynamics during mitosis

293 nerate poleward forces for anaphase A and 2) kinetochore microtubules shorten at their plus ends.

294 y are segregated to the spindle poles as the kinetochore microtubules shorten during anaphase A of mi

295 ch kinetochores are anchored to plus ends of kinetochore microtubules that shorten exclusively at the

296 ding to the model, requires equal numbers of kinetochore microtubules to both poles.

297 ientations that had at least four times more kinetochore microtubules to one pole than to the other p

298 issipation after photoactivation showed that kinetochore-microtubule turnover in prometaphase is subs

299 Curved protofilaments on anaphase kinetochore microtubules were no more flared than their

300 in HeLa and PtK1 cells that a bundle of non-kinetochore microtubules, which we term 'bridging fibre'