ライフサイエンスコーパス: prometaphase

1 ocortical progenitors, transiently arrest at prometaphase.

2 ed with a "Bell" shaped profile and peaks at prometaphase.

3 tely maintain chromosome architecture during prometaphase.

4 ired to arrest cell growth after a prolonged prometaphase.

5 st, but rather is a component of an extended prometaphase.

6 ement when cells progressed from prophase to prometaphase.

7 rphase and in the vicinity of the spindle in prometaphase.

8 particular, the number of cells in prophase/prometaphase.

9 isk from less uniform distributions early in prometaphase.

10 reaccumulates in G2 and is degraded again in prometaphase.

11 e frequently bent, and have splayed poles by prometaphase.

12 need for poleward chromosome movement during prometaphase.

13 t prophase and that ZW10 joins them later at prometaphase.

14 ar, microtubule-based protein machine during prometaphase.

15 to explain the typical observed duration of prometaphase.

16 estricted and can occur in both G1 phase and prometaphase.

17 ative cells in duo2 enter PMII but arrest at prometaphase.

18 ly after the nuclear envelope breaks down in prometaphase.

19 m after nuclear envelope breakdown (NEBD) at prometaphase.

20 otein required for chromosome congression at prometaphase.

21 e and have reduced spindle bipolarity during prometaphase.

22 ossibly functions in spindle assembly during prometaphase.

23 xtracts and localizes to the kinetochores at prometaphase.

24 showed that E6 cells may die at prophase or prometaphase.

25 r nuclear envelope breakdown (NEBD) in early prometaphase.

26 fter fenestration of the nuclear envelope in prometaphase.

27 re loading of Bub3, BubR1, and CENP-E during prometaphase.

28 uring late prophase do not impede entry into prometaphase.

29 an increased proportion of cells present in prometaphase.

30 n of motor proteins with kinetochores during prometaphase.

31 locity of oscillatory chromosome movement in prometaphase.

32 y suppresses directed chromosome movement in prometaphase.

33 lope breakdown, which occurs at the onset of prometaphase.

34 s time, existing prophase cells do not enter prometaphase.

35 e within 2 to 10 min and leads the cell into prometaphase.

36 y position spindle poles specifically during prometaphase.

37 n unusual stage of mitosis defined as pseudo-prometaphase.

38 ed initial interactions with microtubules in prometaphase.

39 g of forces acting on the chromosomes during prometaphase.

40 orylation in nocodazole or unperturbed early prometaphase.

41 teasome-dependent destruction of cyclin A in prometaphase.

42 or to disassembly of the preprophase band in prometaphase.

43 to identify 156 Cyclin A/Cdk1 substrates in prometaphase.

44 ed kinetochores for activation of the SAC in prometaphase.

45 eation from DNA and aberrant spindles during prometaphase.

46 interface of congressing chromosomes during prometaphase.

47 s, which lack microtubule attachments during prometaphase.

48 sphorylated dynein in these functions during prometaphase.

49 nduced defects in chromosome movement during prometaphase.

50 ed cells resistant to AurB inhibition during prometaphase.

51 otic spindle and causes cell-cycle arrest at prometaphase.

52 hores and microtubules dominate during early prometaphase.

53 s occur between cohered sister chromatids at prometaphase.

54 easingly focused at inner centromeres during prometaphase [1, 2], but little is known about how its l

55 bly associated with the meiotic spindle from prometaphase-1 through to anaphase-2, but also exhibited

56 n), as compared with control injected cells (prometaphase, 21.5 +/- 3.3 min; metaphase, 18.9 +/- 4.5

57 to survivin exhibited delayed progression in prometaphase (31.5 +/- 6.9 min) and metaphase (126.8 +/-

58 t protein Mad2 (mitotic arrest deficient) in prometaphase abrogates the spindle checkpoint, producing

59 proteasome that, when inhibited, results in prometaphase accumulation and the subsequent death of Ra

60 Serine 331 phosphorylation contributed to prometaphase accumulation in nocodazole after partial Mp

61 unable to establish a proper orientation at prometaphase, allowing individual kinetochores to be cap

62 dynamics in mitosis, chromosome movement in prometaphase and anaphase, signaling of the spindle chec

63 otein abundance remodeling between prophase, prometaphase and anaphase.

64 chromosome vicinity to the cytoplasm during prometaphase and back to the chromatin in telophase.

65 It localizes specifically to centromeres in prometaphase and delocalizes at the metaphase-anaphase t

66 1-depleted cells transit more slowly through prometaphase and display increased chromosome congressio

67 hat Clp1p/Flp1p localizes to kinetochores in prometaphase and functions in chromosome segregation, si

68 The meiotic central spindle appears during prometaphase and includes passenger complex proteins suc

69 kpoint senses unattached kinetochores during prometaphase and inhibits the anaphase-promoting complex

70 that localizes to centromeric regions during prometaphase and is required for the maintenance of sist

71 ystallin follows disassembly of the Golgi at prometaphase and its reassembly at the completion of cyt

72 fragmented and dispersed Golgi membranes in prometaphase and later stages of mitosis do not contain

73 S31 phosphorylation is observed only in late prometaphase and metaphase and is absent in anaphase.

74 ep55 localizes to the mitotic spindle during prometaphase and metaphase and to the spindle midzone an

75 ine oscillation and breathing speeds in late prometaphase and metaphase are set by microtubule depoly

76 Cytological studies of prometaphase and metaphase I in mtrm hemizygotes demonst

77 ts frequently orient toward only one pole in prometaphase and metaphase I.

78 activity, which gradually increases through prometaphase and metaphase I.

79 omposition to provide distinct activities to prometaphase and metaphase kinetochores.

80 tion, causing its rapid accumulation between prometaphase and metaphase of Cdc20 hypomorphic cells.

81 ble spindle configurations, mitotic delay at prometaphase and metaphase, and elevated aneuploidy.

82 th a subset of attached kinetochores in late prometaphase and metaphase, and rarely in anaphase.

83 veals that spindle angles vary widely during prometaphase and metaphase, and therefore do not reliabl

84 During prometaphase and metaphase, depletion of KLP59D, which t

85 ibit mitotic defects that include protracted prometaphase and misalignment of chromosomes.

86 urora B kinase), a pronounced attenuation at prometaphase and multipolar spindles.

87 cleus in prophase, on the mitotic spindle in prometaphase and on the microtubules that overlap in the

88 ts, defining the transition from prophase to prometaphase and resulting in complete mixing of cyto- a

89 n of load-bearing attachments during most of prometaphase and results in extensive chromosome missegr

90 Mitotic Golgi fragments, seen in prometaphase and telophase, were found to localize adjac

91 1 is phosphorylated by AIR-2 during prophase/prometaphase and that phosphorylation increases TLK-1 ki

92 kinase is associated with centromeres during prometaphase and with midzone microtubules during anapha

93 achment errors are present in early mitosis (prometaphase), and the persistence of those errors is th

94 e in the kinetochore localization of MAD1 in prometaphase, and a defect in the SAC.

95 erphase, spreads throughout the cytoplasm in prometaphase, and is condensed in the midbody during cyt

96 , and HCT116 cells was high during prophase, prometaphase, and metaphase, whereas H3K9 monomethylatio

97 ochore localization and activity of Kif2b in prometaphase, and phosphorylation of T125 is required fo

98 dynamics to stabilize initial attachments in prometaphase, and Plk1 removal from kinetochores is nece

99 and bipolar spindle assembly during prophase/prometaphase, and subsequently generating interkinetocho

100 colocalize with RED at the spindle poles in prometaphase, and their expression can abrogate the SAC.

101 32 is first detectable on chromosomes during prometaphase, and this localization is independent of mi

102 localize to centrosomes during prophase and prometaphase, and Tiam1, acting through Rac, ordinarily

103 s, global inhibition of SUMOylation caused a prometaphase arrest due to defects in targeting the micr

104 Proteasome inhibitors did not affect the prometaphase arrest induced by Cdc34 injection.

105 In Ptk2 cells the outcome is prometaphase arrest or aberrant chromosome segregation a

106 ntibodies leads to spindle abnormalities and prometaphase arrest or chromosome missegregation.

107 enotype for cells treated with GSK461364A is prometaphase arrest with characteristic collapsed polar

108 ted in a G(2) delay, followed by a prominent prometaphase arrest, as a consequence of defective spind

109 ion results in altered microtubule dynamics, prometaphase arrest, tetraploidy, and mitotic cell death

110 nd accumulation at the kinetochores, causing prometaphase arrest, whereas a phospho-mimetic Ser338D C

111 s from accumulating cyclin B and securin and prometaphase arrest.

112 ivity to nocodazole, and cannot recover from prometaphase arrest.

113 cific phosphorylation of HP1alpha leading to prometaphase arrest.

114 zed by defective chromosome condensation and prometaphase arrest.

115 lA depletion causes spindle abnormalities in prometaphase associated with abnormal centromeric accumu

116 omosome segregation: (a) moving plateward at prometaphase; (b) participating in spindle checkpoint co

117 ced the onset of anaphase prematurely during prometaphase, before the chromosomes had assembled at th

118 tested the classical hypothesis that astral, prometaphase bipolar mitotic spindles are maintained by

119 RNA interference (RNAi) results in a strong prometaphase block with an active spindle checkpoint, wh

120 ted by 5-fold or more over the course of the prometaphase block, which is Mad2 dependent.

121 leading to mitotic spindle abnormalities and prometaphase block.

122 Unattached kinetochores in prometaphase bound on average only a small fraction (est

123 trate at kinetochores in late prophase/early prometaphase but become depleted by 5-fold or more over

124 sister chromatids gradually biorient during prometaphase, but current models of mitosis in S. cerevi

125 tion of HSET alone increases the duration of prometaphase, but does not alter the velocity of chromos

126 hosphorylation of 3F3/2 epitopes at prophase/prometaphase, but is needed for 3F3/2 dephosphorylation

127 itive for spindle checkpoint proteins during prometaphase, but lose their staining as tension is appl

128 DYNLT3 is present on kinetochores at prometaphase, but not later mitotic stages, demonstratin

129 ciated with kinetochores during prophase and prometaphase, but not metaphase, anaphase and telophase.

130 hBubR1 also localizes to kinetochores during prometaphase, but only when hBub3 is overexpressed.

131 destruction and allowing progression beyond prometaphase, but the kinases directing this phosphoryla

132 the correction of k-MT attachment errors in prometaphase, but the mechanism restricting this activit

133 The mitotic spindle self-assembles in prometaphase by a combination of centrosomal pathway, in

134 S81-EME1 endonuclease, which is activated at prometaphase by formation of the SMX tri-nuclease contai

135 ylated during mitosis or in cells blocked at prometaphase by microtubule inhibitors.

136 ghout G1 and S, but not in cells arrested in prometaphase by nocodazole.

137 es the establishment of kt-MT attachments in prometaphase by stabilizing microtubules and that reduct

138 We conclude that a short delay in the prometaphase caused by the absence of centrioles activat

139 Thus, in prometaphase Cdc20 positively regulates Cdk1 by mediatin

140 Here we show that k-MT attachments in prometaphase cells are considerably less stable than in

141 Direct observation of prometaphase cells expressing GFP-alpha-tubulin shows th

142 w reduced PNEI, and the ratio of prophase to prometaphase cells is increased, suggesting an NEBD dela

143 dk1, and inhibited Cdk1 activity in p21(+/+) prometaphase cells, but not in p21(-/-) cells.

144 ound that at bi-oriented chromosomes in late prometaphase cells, CENP-T is stretched approximately 16

145 crotubules were disassembled in prophase and prometaphase cells, the cells were then injected with an

146 Ablation of aurora B causes defects in both prometaphase chromosomal congression and the spindle che

147 INCENP1-405 interferes with both prometaphase chromosome alignment and the completion of

148 complex plays a critical role in maintaining prometaphase chromosome architecture.

149 me loss and improve our understanding of how prometaphase chromosome congression relates to anaphase

150 on forces" (PEFs) are hypothesized to direct prometaphase chromosome movements by pushing chromosome

151 en the two sister kinetochores on bioriented prometaphase chromosomes to produce two chromosome fragm

152 rganization of microtubules, the movement of prometaphase chromosomes, and the release of the spindle

153 s and accumulate both at the kinetochores of prometaphase chromosomes.

154 In prophase and prometaphase, cohesin release from chromosome arms occur

155 es the levels of Mad1 at kinetochores during prometaphase, correlating with the inability of Mad1 to

156 k-MT attachment errors form during prometaphase due to stochastic interactions between kine

157 ere we characterize the relationship between prometaphase duration and the proliferative capacity of

158 ughter cells would proliferate regardless of prometaphase duration.

159 eal the existence of a mechanism that senses prometaphase duration; if prometaphase lasts >1.5 hr, th

160 se like [Mastl] in mammals) is essential for prometaphase entry or progression by suppressing protein

161 on of defects in chromosome alignment during prometaphase even in cells with normal centrosome number

162 teins, begin to act as early as prophase and prometaphase, even before the spindle forms and shifts t

163 During prometaphase, forces exerted at kinetochores, in combina

164 The exclusion of YY1 from DNA in prometaphase HeLa cells correlated with an increase in t

165 dCAP-G for condensation during prophase and prometaphase; however, we find that alternate mechanisms

166 ture associated with the X-Y bivalent during prometaphase I and metaphase I.

167 ocyte maturation caused a permanent block at prometaphase I and spindle elongation.

168 We found that cyclin A2 decreases in prometaphase I but recovers after the first meiotic divi

169 ere we report that haspin inhibition in late prometaphase I causes acceleration of MI, bypass of the

170 hat MEI-S332 localizes to the centromeres of prometaphase I chromosomes in oocytes, remaining there u

171 cortically located filamentous structures in prometaphase I upon oocyte maturation.

172 separation of sister kinetochores occurs in prometaphase I, and a complete separation occurs in prom

173 mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientat

174 e of the APC/C, is degraded prematurely, and prometaphase I/metaphase I is accelerated.

175 monstrate that the GSC cell cycle arrests at prometaphase if centrosomes are misoriented.

176 phase I, and a complete separation occurs in prometaphase II.

177 ovements and rotations is needed to complete prometaphase in 10-20 min while keeping erroneous merote

178 removed from chromosome arms in prophase and prometaphase in a manner that depends on Wapl and phosph

179 nhances its loading onto kinetochores during prometaphase in a microtubule-dependent manner to promot

180 actin and to localize to kinetochores during prometaphase, indicating that the CK2 phosphorylation of

181 back-and-forth centromere oscillation during prometaphase is abolished.

182 Ska3 protein accumulation at kinetochores in prometaphase is dependent on Sgo1 protein.

183 od of spindle elongation during prophase and prometaphase is prolonged in atk5-1 cells.

184 ead, live imaging shows that the duration of prometaphase is prolonged in the mutants while two acent

185 wed that kinetochore-microtubule turnover in prometaphase is substantially suppressed by partial Auro

186 whereas in CFPAC-1 cells prolonged arrest in prometaphase is the usual response.

187 hat MAD2 localizes to an outer domain of the prometaphase kinetochore.

188 ein immunofluorescence staining is bright at prometaphase kinetochores and dimmer at metaphase kineto

189 Plk1 localizes to prometaphase kinetochores and is reduced at metaphase ki

190 tion of dynein and its cofactor dynactin, to prometaphase kinetochores and that Spindly kinetochore r

191 ut retain Cdc20 and was absent at unattached prometaphase kinetochores for the Cdc20 derivative GFP-C

192 Prometaphase kinetochores interact with spindle microtub

193 ntains a robust spindle checkpoint signal at prometaphase kinetochores until they attain mature attac

194 First, prometaphase kinetochores with few or no kinetochore mic

195 hree- to sixfold in comparison to unattached prometaphase kinetochores, but remain detectable.

196 bset of spindle microtubules that exist near prometaphase kinetochores, known as preformed K-fibers (

197 Unpaired prometaphase kinetochores, which occurred in a mutant en

198 of Plk1 and the Kinesin-7 motor CENP-E from prometaphase kinetochores.

199 h checkpoint proteins more characteristic of prometaphase kinetochores.

200 in CENP-E, BubR1, and Mad2 in comparison to prometaphase kinetochores.

201 dephosphorylated forms of dynein coexist at prometaphase kinetochores.

202 sociated with increased Mad1/Mad2 signals at prometaphase kinetochores.

203 hanism that senses prometaphase duration; if prometaphase lasts >1.5 hr, this mechanism triggers a du

204 HeLa cells causes transient accumulation of prometaphase-like cells with chromosomes that display po

205 es were disorganized, the majority showing a prometaphase-like configuration.

206 from the microtubule-organizing centers in a prometaphase-like pattern rather than achieving a bipola

207 ral and monopolar spindles, as well as small prometaphase-like spindles with improper chromosomal att

208 assembly checkpoint, leading to arrest in a prometaphase-like state.

209 Most injected cells arrested in a prometaphase-like state.

210 proximal spindle fibers, mirroring the dual prometaphase localization of the spindle checkpoint prot

211 In prometaphase, MAD2L2 sequestered free CDH1 away from the

212 late prophase, the kinetochore fibers during prometaphase, metaphase, and anaphase, the interzone spi

213 th bipolar mitotic spindles progress to late prometaphase-metaphase at normal rates.

214 hosphorylation of MDC1 causes a delay of the prometaphase-metaphase transition.

215 rophase/diplotene, increases to a maximum at prometaphase-metaphase, and drops during anaphase.

216 omosomes align at the spindle equator during prometaphase/metaphase II, whereas acentric fragments, a

217 y, and size to the fragments observed in the prometaphase/metaphase stage of the cell cycle in vivo.

218 stablishment of normal spindle length during prometaphase/metaphase.

219 h with 3-BAABU resulted in mitotic arrest at prometaphase/metaphase/anaphase, with separation and dis

220 s aberrant poleward chromosome motion during prometaphase, misalignment of holocentric kinetochores,

221 the active, but not inactive, centromeres of prometaphase multicentric chromosomes using antibodies t

222 lay defects in centromere positioning during prometaphase of meiosis I.

223 tochore-microtubule attachments during early prometaphase of MI.

224 MEI-S332 localizes onto centromeres in prometaphase of mitosis or meiosis I, remaining until si

225 nucleus in interphase and the centromeres in prometaphase of mitosis).

226 , mutant generative nuclei in duo2 arrest in prometaphase of PMII with a 2C DNA content.

227 lated de novo synthesis of this cyclin after prometaphase onset.

228 alter the velocity of chromosome movement in prometaphase or anaphase.

229 Cells injected with phosphatase at prometaphase or metaphase exited mitosis in the presence

230 Cells with stabilized prometaphase or metaphase microtubule arrays were able t

231 Microinjection of C3 into prometaphase or metaphase normal rat kidney epithelial c

232 that lacked attached microtubules; i.e., at prometaphase or when the microtubules were depolymerized

233 mosome congression to the spindle equator in prometaphase, or segregation to the poles in anaphase wh

234 inetochore microtubules in prophase or early prometaphase, or upon nocodazole treatment.

235 f HKIF4A in human cells results in defective prometaphase organization, chromosome mis-alignment at m

236 ng mitosis, occurs via distinct prophase and prometaphase pathways.

237 During prophase and prometaphase, preceding kinetochore-microtubule attachme

238 function centered on M phase entry and early prometaphase progression and challenge the view that cyc

239 y mitotic events, such as PIP(3) generation, prometaphase progression, and spindle orientation.

240 When microinjected into living prophase or prometaphase PtK1 cells, anti-Mad2 antibody induced the

241 Throughout prometaphase, puncta of both motors aligned on interpola

242 e-chromosome associations established during prometaphase remain intact during anaphase to facilitate

243 t the mechanism restricting this activity to prometaphase remains unknown.

244 espect to each other on the mitotic rings of prometaphase rosettes and anaphase cells.

245 sembling lamin-B envelope that surrounds the prometaphase spindle and augments the finely tuned, anta

246 KLP61F activity maintains the prometaphase spindle by antagonizing Ncd and another unk

247 of pole-pole separation and could maintain a prometaphase spindle displaying small fluctuations in it

248 ibody stained not only kinetochores but also prometaphase spindle poles and proximal spindle fibers,

249 tic kinesin force balance to maintain robust prometaphase spindles as MTs assemble and chromosomes ar

250 Inhibition of KCM1 during mitosis led to prometaphase spindles with excessively long MTs and spin

251 to a new stochastic force-balance model for prometaphase spindles, providing a good fit to data from

252 nning during prophase and lasting until late prometaphase, spindles of atk5-1 plants become abnormall

253 ysis of the condensation pattern (CP) at the prometaphase stage of somatic chromosomes.

254 kinetochore labeling first appeared at early prometaphase, started to fade during chromosome congress

255 Analogies with eukaryotic prometaphase suggest that this could be a primordial seg

256 rientation of these univalent chromosomes at prometaphase suggests that they are unable to establish

257 n on pole-kinetochore connections throughout prometaphase, tension that compels sister kinetochores t

258 During prometaphase, the KT initially interacts with a single M

259 At the end of prometaphase, the nonexchange chromosomes retract into t

260 complex/cyclosome (APC/C) activity early in prometaphase, thereby allowing accumulation of APC/C sub

261 eds, and direction of motion associated with prometaphase through anaphase chromosome movements can b

262 t associates with the outer kinetochore from prometaphase through anaphase.

263 A is required for its proper degradation in prometaphase through competing with BUBR1 for the same s

264 ive role in bipolar spindle formation during prometaphase through producing spindle dynamism.

265 to achieve efficient kinetochore capture at prometaphase, timely chromosome congression to the metap

266 imaging demonstrated a delay in mitosis from prometaphase to anaphase and confirmed that multinucleat

267 tinct features of chromosome motilities from prometaphase to anaphase in a coherent manner.

268 model can recreate chromosome movement from prometaphase to anaphase in good agreement with experime

269 during late S phase and G2, and maximal from prometaphase to anaphase.

270 microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and fa

271 How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknow

272 otic spindles and the proper transition from prometaphase to metaphase during mitosis.

273 Plk1) at kinetochores as cells progress from prometaphase to metaphase is surprising given that the k

274 -1 protein localizes to the kinetochore from prometaphase to metaphase, and this depends on KNL-1, a

275 lel positions while MDCK cells progress from prometaphase to metaphase.

276 among all chromosomes as cells transit from prometaphase to metaphase.

277 ubstitution, unambiguously showing that from prometaphase to telophase of mammalian cells, most of th

278 m their origins as nascent K-fibers in early prometaphase to their fully matured form at metaphase, j

279 impose sufficient tension on sisters during prometaphase to transiently separate centromeric chromat

280 ibutes to spindle pole separation during the prometaphase-to-metaphase transition (when it antagonize

281 sister individualization at the prophase to prometaphase transition of the eukaryotic cell cycle.

282 the time the nuclear membrane breaks down in prometaphase until early G1, when it is actively exporte

283 ase; however, centromeric association during prometaphase was unaffected.

284 t not CYCLIN B, begins to be degraded in the prometaphase when APC/C is inactivated by the spindle as

285 nt in maintaining the checkpoint toward late prometaphase when the cell contains only a few or a sing

286 nhibiting Cdk chemically, we showed that, in prometaphase, when Cdk1 substrates approach the peak of

287 tochore displays analogous rearrangements at prometaphase, when microtubule/chromosome interactions a

288 omerase-II accumulates at centromeres during prometaphase, where it resolves the DNA catenations that

289 overexpression prolongs cell cycle arrest in prometaphase, whereas LMW-E overexpression reduces the l

290 Opposing centromeres separate in prometaphase, whereas the phH3-Ser28-marked pericentrome

291 phosphorylated substrates at kinetochores in prometaphase, which correlates with aberrant kinetochore

292 tudy implicates FZR1 as a major regulator of prometaphase whose activity helps to prevent chromosome

293 f the PyST expressing cells were arrested in prometaphase with almost no cells progressing beyond met

294 s to spindle microtubules and cells block in prometaphase with an active spindle checkpoint.

295 res is apparent by early prophase and during prometaphase with decreased staining on chromosomes alig

296 these analogs, Plk1(as) cells accumulate in prometaphase with defects that parallel those found in P

297 that most cells deficient in HBXIP arrest in prometaphase with monopolar spindles whereas HBXIP overe

298 ynein/dynactin activity by microinjection in prometaphase with purified p50 "dynamitin" protein or co

299 in HeLa S3 cells after they were arrested in prometaphase with taxol, nocodazole, vincristine, or mon

300 entry into mitosis and is then destroyed in prometaphase within minutes of nuclear envelope breakdow