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

3 partial ring-shaped structures girding their kinetochore microtubules.

4 ubulin for fluorescent speckle microscopy on kinetochore microtubules.

5 which reduces phosphorylation and stabilizes kinetochore microtubules.

6 lity of parallel microtubules, including the kinetochore microtubules.

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

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

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

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

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

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

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

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

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

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

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

18 One kinetochore microtubule attaches to a single centromere

19 When stable kinetochore microtubule attachment is prevented by Nuf2

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

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

22 B phosphorylation in achieving proper stable kinetochore microtubule attachment.

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

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

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

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

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

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

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

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

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

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

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

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

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

36 cesses, including sister chromatid cohesion, kinetochore-microtubule attachment and the spindle assem

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

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

39 sion, for components of the highly conserved kinetochore-microtubule attachment complex.

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

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

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

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

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

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

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

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

48 0 complex is essential for persistent end-on kinetochore-microtubule attachment in cells [1, 2], but

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

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

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

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

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

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

55 Stable kinetochore-microtubule attachment is essential for cell

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

57 indle length fluctuations can occur when the kinetochore-microtubule attachment lifetime is long.

58 ate that Hec1 tail phosphorylation regulates kinetochore-microtubule attachment stability independent

59 ure of chromosome congression independent of kinetochore-microtubule attachment stability.

60 s residence time on microtubules and enhance kinetochore-microtubule attachment strength.

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

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

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

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

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

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

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

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

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

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

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

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

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

74 ccurate chromosome segregation by monitoring kinetochore-microtubule attachment.

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

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

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

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

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

80 hase I is also prolonged, due to late stable kinetochore-microtubule attachment.

81 which is believed primarily due to unstable kinetochore-microtubule attachment.

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

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

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

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

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

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

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

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

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

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

92 Kinetochore microtubule attachments that are too stable

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

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

95 microtubules to establish force-transducing kinetochore-microtubule attachments and 2) regulating th

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

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

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

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

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

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

102 ation of prometaphase kinetochores, improper kinetochore-microtubule attachments and weakened spindle

103 Strong kinetochore-microtubule attachments are essential for fa

104 Kinetochore-microtubule attachments are essential to dir

105 We found that kinetochore-microtubule attachments are established even

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

107 Further analyses uncovered that kinetochore-microtubule attachments are severely comprom

108 romotes Dam1c oligomerization to ensure that kinetochore-microtubule attachments are stabilized as ki

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

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

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

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

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

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

115 Incorrect kinetochore-microtubule attachments during mitosis can l

116 complex Ndc80 is essential to ensure correct kinetochore-microtubule attachments during mitosis.

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

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

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

120 itment to kinetochores and for generation of kinetochore-microtubule attachments in human cells.

121 fer to reveal the architecture of individual kinetochore-microtubule attachments in human cells.

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

123 -170 are involved in the timely formation of kinetochore-microtubule attachments in mitosis.

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

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

126 o protect centromeric cohesion and stabilise kinetochore-microtubule attachments in yeast and mouse m

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

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

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

130 The stability of kinetochore-microtubule attachments is fine-tuned to pre

131 occur at mitotic entry, the establishment of kinetochore-microtubule attachments leads to spatial chr

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

133 o and evicted from these regions to regulate kinetochore-microtubule attachments remains unclear.

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

135 crotubule dynamics but accumulates erroneous kinetochore-microtubule attachments that are not destabi

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

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

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

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

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

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

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

143 efective chromosome congression and aberrant kinetochore-microtubule attachments which in turn promot

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

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

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

147 on destabilizes astral microtubules, but not kinetochore-microtubule attachments, and chromosome alig

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

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

150 (PP1), which silences the SAC and stabilizes kinetochore-microtubule attachments, how these distinct

151 c MCAK to discriminate correct vs. incorrect kinetochore-microtubule attachments, thereby promoting m

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

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

154 icated in both stabilizing and destabilizing kinetochore-microtubule attachments.

155 tubulin accumulates on correct, more stable, kinetochore-microtubule attachments.

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

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

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

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

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

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

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

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

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

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

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

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

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

169 ection mechanism that destabilizes incorrect kinetochore-microtubule attachments.

170 omosome biorientation by detaching incorrect kinetochore-microtubule attachments.

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

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

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

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

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

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

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

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

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

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

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

182 Further, kinetochore microtubule bundles are severely destabilize

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

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

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

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

187 e, we report that the evolutionarily ancient kinetochore-microtubule coupling machine, the KMN (Knl1/

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

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

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

191 Tight regulation of kinetochore microtubule dynamics is required to generate

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

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

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

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

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

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

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

199 ered kinetochore oscillations, and decreased kinetochore microtubule flux.

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

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

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

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

204 Each kinetochore microtubule has one (rarely, two) Dam1C/DASH

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

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

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

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

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

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

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

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

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

214 important insight into how Aurora B disrupts kinetochore-microtubule interaction in a tension-depende

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

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

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

218 ientation, Aurora B kinase disrupts aberrant kinetochore-microtubule interactions [3-6].

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

220 The spindle checkpoint monitors kinetochore-microtubule interactions and generates a "wa

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

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

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

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

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

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

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

228 Erroneous kinetochore-microtubule interactions must be detected an

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

230 tochore components and so releasing aberrant kinetochore-microtubule interactions.

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

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

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

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

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

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

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

238 n motors provide the molecular forces at the kinetochore-microtubule interface and along the spindle

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

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

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

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

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

244 les is strongly influenced by factors at the kinetochore-microtubule interface such as Fin1 and Dam1,

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

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

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

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

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

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

251 Distinct kinetochore-microtubule interfaces mediate these behavio

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

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

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

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

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

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

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

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

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

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

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

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

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

265 In small spindles, kinetochore microtubules (KMTs) connect directly with th

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

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

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

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

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

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

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

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

274 s kinetochore substrates to correct improper kinetochore-microtubule (KT-MT) attachments, whereas ten

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

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

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

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

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

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

281 of PP1 near the C-terminus of Ndc80, a core kinetochore-microtubule linker.

282 Thus, kinetochore microtubules maintain a constant net length,

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

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

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

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

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

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

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

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

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

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

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

294 atocyte anaphase A does not stem solely from kinetochore microtubule shortening.

295 error correction, without affecting overall kinetochore microtubule stability.

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

297 focused on the dynamics and organization of kinetochore microtubules, that is, on the region between

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

299 mains tethered to centrosomes by lengthening kinetochore microtubules, which are under tension, sugge

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