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1 sphorylated dynein in these functions during prometaphase.
2 nduced defects in chromosome movement during prometaphase.
3 ed cells resistant to AurB inhibition during prometaphase.
4 otic spindle and causes cell-cycle arrest at prometaphase.
5 hores and microtubules dominate during early prometaphase.
6 ora B kinase activity via PP2A inhibition in prometaphase.
7 tely maintain chromosome architecture during prometaphase.
8 ly detected in interphase, but absent during prometaphase.
9 st, but rather is a component of an extended prometaphase.
10 ement when cells progressed from prophase to prometaphase.
11 rphase and in the vicinity of the spindle in prometaphase.
12 particular, the number of cells in prophase/prometaphase.
13 reaccumulates in G2 and is degraded again in prometaphase.
14 e frequently bent, and have splayed poles by prometaphase.
15 need for poleward chromosome movement during prometaphase.
16 t prophase and that ZW10 joins them later at prometaphase.
17 ar, microtubule-based protein machine during prometaphase.
18 to explain the typical observed duration of prometaphase.
19 estricted and can occur in both G1 phase and prometaphase.
20 ative cells in duo2 enter PMII but arrest at prometaphase.
21 almost all CTCF chromatin binding is lost in prometaphase.
22 ly after the nuclear envelope breaks down in prometaphase.
23 otein required for chromosome congression at prometaphase.
24 e and have reduced spindle bipolarity during prometaphase.
25 ossibly functions in spindle assembly during prometaphase.
26 xtracts and localizes to the kinetochores at prometaphase.
27 showed that E6 cells may die at prophase or prometaphase.
28 r nuclear envelope breakdown (NEBD) in early prometaphase.
29 fter fenestration of the nuclear envelope in prometaphase.
30 uring late prophase do not impede entry into prometaphase.
31 an increased proportion of cells present in prometaphase.
32 ocortical progenitors, transiently arrest at prometaphase.
33 n of motor proteins with kinetochores during prometaphase.
34 locity of oscillatory chromosome movement in prometaphase.
35 y suppresses directed chromosome movement in prometaphase.
36 lope breakdown, which occurs at the onset of prometaphase.
37 s time, existing prophase cells do not enter prometaphase.
38 m after nuclear envelope breakdown (NEBD) at prometaphase.
39 e within 2 to 10 min and leads the cell into prometaphase.
40 y position spindle poles specifically during prometaphase.
41 to identify 156 Cyclin A/Cdk1 substrates in prometaphase.
42 s occur between cohered sister chromatids at prometaphase.
43 ed with a "Bell" shaped profile and peaks at prometaphase.
44 ired to arrest cell growth after a prolonged prometaphase.
45 isk from less uniform distributions early in prometaphase.
46 arrest of leukemia and other cancer cells in prometaphase.
47 re loading of Bub3, BubR1, and CENP-E during prometaphase.
48 ed initial interactions with microtubules in prometaphase.
49 orylation in nocodazole or unperturbed early prometaphase.
50 teasome-dependent destruction of cyclin A in prometaphase.
51 or to disassembly of the preprophase band in prometaphase.
52 ed kinetochores for activation of the SAC in prometaphase.
53 eation from DNA and aberrant spindles during prometaphase.
54 interface of congressing chromosomes during prometaphase.
55 s, which lack microtubule attachments during prometaphase.
56 easingly focused at inner centromeres during prometaphase [1, 2], but little is known about how its l
57 bly associated with the meiotic spindle from prometaphase-1 through to anaphase-2, but also exhibited
58 n), as compared with control injected cells (prometaphase, 21.5 +/- 3.3 min; metaphase, 18.9 +/- 4.5
59 to survivin exhibited delayed progression in prometaphase (31.5 +/- 6.9 min) and metaphase (126.8 +/-
60 t protein Mad2 (mitotic arrest deficient) in prometaphase abrogates the spindle checkpoint, producing
61 proteasome that, when inhibited, results in prometaphase accumulation and the subsequent death of Ra
62 Serine 331 phosphorylation contributed to prometaphase accumulation in nocodazole after partial Mp
63 unable to establish a proper orientation at prometaphase, allowing individual kinetochores to be cap
64 anscription start sites remain accessible in prometaphase, although adjacent nucleosomes can also bec
65 dynamics in mitosis, chromosome movement in prometaphase and anaphase, signaling of the spindle chec
66 rylation gradients within the spindle during prometaphase and anaphase, thereby locally regulating fa
69 It localizes specifically to centromeres in prometaphase and delocalizes at the metaphase-anaphase t
70 1-depleted cells transit more slowly through prometaphase and display increased chromosome congressio
71 hat Clp1p/Flp1p localizes to kinetochores in prometaphase and functions in chromosome segregation, si
72 The meiotic central spindle appears during prometaphase and includes passenger complex proteins suc
73 kpoint senses unattached kinetochores during prometaphase and inhibits the anaphase-promoting complex
74 ystallin follows disassembly of the Golgi at prometaphase and its reassembly at the completion of cyt
75 fragmented and dispersed Golgi membranes in prometaphase and later stages of mitosis do not contain
76 S31 phosphorylation is observed only in late prometaphase and metaphase and is absent in anaphase.
77 ep55 localizes to the mitotic spindle during prometaphase and metaphase and to the spindle midzone an
78 ine oscillation and breathing speeds in late prometaphase and metaphase are set by microtubule depoly
80 s and to central spindle microtubules during prometaphase and metaphase I of female meiosis [9, 10].
84 tion, causing its rapid accumulation between prometaphase and metaphase of Cdc20 hypomorphic cells.
85 ble spindle configurations, mitotic delay at prometaphase and metaphase, and elevated aneuploidy.
87 veals that spindle angles vary widely during prometaphase and metaphase, and therefore do not reliabl
91 te loss of CTCF binding to CTCF sites during prometaphase and rearrangement of the chromatin landscap
92 ts, defining the transition from prophase to prometaphase and resulting in complete mixing of cyto- a
93 n of load-bearing attachments during most of prometaphase and results in extensive chromosome missegr
95 1 is phosphorylated by AIR-2 during prophase/prometaphase and that phosphorylation increases TLK-1 ki
96 kinase is associated with centromeres during prometaphase and with midzone microtubules during anapha
97 achment errors are present in early mitosis (prometaphase), and the persistence of those errors is th
99 , and HCT116 cells was high during prophase, prometaphase, and metaphase, whereas H3K9 monomethylatio
100 ochore localization and activity of Kif2b in prometaphase, and phosphorylation of T125 is required fo
101 dynamics to stabilize initial attachments in prometaphase, and Plk1 removal from kinetochores is nece
102 and bipolar spindle assembly during prophase/prometaphase, and subsequently generating interkinetocho
103 colocalize with RED at the spindle poles in prometaphase, and their expression can abrogate the SAC.
104 localize to centrosomes during prophase and prometaphase, and Tiam1, acting through Rac, ordinarily
105 ation in prometaphase, extends the length of prometaphase, and ultimately causes cells to exit mitosi
106 s, global inhibition of SUMOylation caused a prometaphase arrest due to defects in targeting the micr
110 enotype for cells treated with GSK461364A is prometaphase arrest with characteristic collapsed polar
111 ted in a G(2) delay, followed by a prominent prometaphase arrest, as a consequence of defective spind
112 ion results in altered microtubule dynamics, prometaphase arrest, tetraploidy, and mitotic cell death
113 nd accumulation at the kinetochores, causing prometaphase arrest, whereas a phospho-mimetic Ser338D C
118 lA depletion causes spindle abnormalities in prometaphase associated with abnormal centromeric accumu
119 erative and show a delay in early mitosis at prometaphase, associated with chromosome-alignment defec
120 omosome segregation: (a) moving plateward at prometaphase; (b) participating in spindle checkpoint co
121 tested the classical hypothesis that astral, prometaphase bipolar mitotic spindles are maintained by
122 RNA interference (RNAi) results in a strong prometaphase block with an active spindle checkpoint, wh
126 trate at kinetochores in late prophase/early prometaphase but become depleted by 5-fold or more over
127 sister chromatids gradually biorient during prometaphase, but current models of mitosis in S. cerevi
128 tion of HSET alone increases the duration of prometaphase, but does not alter the velocity of chromos
129 itive for spindle checkpoint proteins during prometaphase, but lose their staining as tension is appl
131 ciated with kinetochores during prophase and prometaphase, but not metaphase, anaphase and telophase.
132 destruction and allowing progression beyond prometaphase, but the kinases directing this phosphoryla
133 the correction of k-MT attachment errors in prometaphase, but the mechanism restricting this activit
135 S81-EME1 endonuclease, which is activated at prometaphase by formation of the SMX tri-nuclease contai
138 es the establishment of kt-MT attachments in prometaphase by stabilizing microtubules and that reduct
143 w reduced PNEI, and the ratio of prophase to prometaphase cells is increased, suggesting an NEBD dela
145 ound that at bi-oriented chromosomes in late prometaphase cells, CENP-T is stretched approximately 16
146 crotubules were disassembled in prophase and prometaphase cells, the cells were then injected with an
147 Ablation of aurora B causes defects in both prometaphase chromosomal congression and the spindle che
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 rganization of microtubules, the movement of prometaphase chromosomes, and the release of the spindle
154 es the levels of Mad1 at kinetochores during prometaphase, correlating with the inability of Mad1 to
156 ere we characterize the relationship between prometaphase duration and the proliferative capacity of
158 eal the existence of a mechanism that senses prometaphase duration; if prometaphase lasts >1.5 hr, th
159 the CDK1-bound fraction from destruction in prometaphase, ensuring a period of prolonged CDK1 activi
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 stead, it prevents chromatin condensation in prometaphase, extends the length of prometaphase, and ul
165 in which histone methylations occur first in prometaphase, histone acetylation, and CTCF in anaphase/
166 dCAP-G for condensation during prophase and prometaphase; however, we find that alternate mechanisms
171 ere we report that haspin inhibition in late prometaphase I causes acceleration of MI, bypass of the
174 separation of sister kinetochores occurs in prometaphase I, and a complete separation occurs in prom
175 mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientat
181 ovements and rotations is needed to complete prometaphase in 10-20 min while keeping erroneous merote
182 removed from chromosome arms in prophase and prometaphase in a manner that depends on Wapl and phosph
183 nhances its loading onto kinetochores during prometaphase in a microtubule-dependent manner to promot
184 actin and to localize to kinetochores during prometaphase, indicating that the CK2 phosphorylation of
188 ead, live imaging shows that the duration of prometaphase is prolonged in the mutants while two acent
189 wed that kinetochore-microtubule turnover in prometaphase is substantially suppressed by partial Auro
191 ein immunofluorescence staining is bright at prometaphase kinetochores and dimmer at metaphase kineto
193 tion of dynein and its cofactor dynactin, to prometaphase kinetochores and that Spindly kinetochore r
194 ut retain Cdc20 and was absent at unattached prometaphase kinetochores for the Cdc20 derivative GFP-C
196 ntains a robust spindle checkpoint signal at prometaphase kinetochores until they attain mature attac
199 actions generates reduced phosphorylation of prometaphase kinetochores, improper kinetochore-microtub
200 bset of spindle microtubules that exist near prometaphase kinetochores, known as preformed K-fibers (
207 hanism that senses prometaphase duration; if prometaphase lasts >1.5 hr, this mechanism triggers a du
208 HeLa cells causes transient accumulation of prometaphase-like cells with chromosomes that display po
210 from the microtubule-organizing centers in a prometaphase-like pattern rather than achieving a bipola
211 ral and monopolar spindles, as well as small prometaphase-like spindles with improper chromosomal att
214 proximal spindle fibers, mirroring the dual prometaphase localization of the spindle checkpoint prot
216 late prophase, the kinetochore fibers during prometaphase, metaphase, and anaphase, the interzone spi
220 s its molecular architecture during the long prometaphase/metaphase I in Drosophila melanogaster oocy
221 omosomes align at the spindle equator during prometaphase/metaphase II, whereas acentric fragments, a
222 y, and size to the fragments observed in the prometaphase/metaphase stage of the cell cycle in vivo.
224 s aberrant poleward chromosome motion during prometaphase, misalignment of holocentric kinetochores,
231 that removal of TOP2A from cells arrested in prometaphase or metaphase cause dramatic loss of compact
233 mosome congression to the spindle equator in prometaphase, or segregation to the poles in anaphase wh
235 f HKIF4A in human cells results in defective prometaphase organization, chromosome mis-alignment at m
237 function centered on M phase entry and early prometaphase progression and challenge the view that cyc
239 -seq and Hi-C analyses, we found that during prometaphase, promoters, enhancers, and insulators retai
241 e-chromosome associations established during prometaphase remain intact during anaphase to facilitate
243 sembling lamin-B envelope that surrounds the prometaphase spindle and augments the finely tuned, anta
245 of pole-pole separation and could maintain a prometaphase spindle displaying small fluctuations in it
246 ibody stained not only kinetochores but also prometaphase spindle poles and proximal spindle fibers,
247 tic kinesin force balance to maintain robust prometaphase spindles as MTs assemble and chromosomes ar
248 Inhibition of KCM1 during mitosis led to prometaphase spindles with excessively long MTs and spin
249 to a new stochastic force-balance model for prometaphase spindles, providing a good fit to data from
250 nning during prophase and lasting until late prometaphase, spindles of atk5-1 plants become abnormall
252 accessibility and lose the CTCF footprint in prometaphase, suggesting loss of CTCF binding and rearra
253 n on pole-kinetochore connections throughout prometaphase, tension that compels sister kinetochores t
256 complex/cyclosome (APC/C) activity early in prometaphase, thereby allowing accumulation of APC/C sub
257 eds, and direction of motion associated with prometaphase through anaphase chromosome movements can b
259 A is required for its proper degradation in prometaphase through competing with BUBR1 for the same s
261 to achieve efficient kinetochore capture at prometaphase, timely chromosome congression to the metap
262 f membranes and chromatin is critical during prometaphase to allow for proper chromosome compaction a
263 imaging demonstrated a delay in mitosis from prometaphase to anaphase and confirmed that multinucleat
265 model can recreate chromosome movement from prometaphase to anaphase in good agreement with experime
267 microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and fa
268 How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknow
269 d G1 phases and a continuous transition from prometaphase to G1, we reveal an interlocking dephosphor
271 Plk1) at kinetochores as cells progress from prometaphase to metaphase is surprising given that the k
272 -1 protein localizes to the kinetochore from prometaphase to metaphase, and this depends on KNL-1, a
275 ubstitution, unambiguously showing that from prometaphase to telophase of mammalian cells, most of th
276 m their origins as nascent K-fibers in early prometaphase to their fully matured form at metaphase, j
277 impose sufficient tension on sisters during prometaphase to transiently separate centromeric chromat
278 ibutes to spindle pole separation during the prometaphase-to-metaphase transition (when it antagonize
279 in DNA replication exhibited a delay in the prometaphase-to-metaphase transition and anaphase defect
280 lt, limb progenitor cells experience delayed prometaphase-to-metaphase transition and prolonged S-pha
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
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
291 phosphorylated substrates at kinetochores in prometaphase, which correlates with aberrant kinetochore
292 n excess of non-CDK1-bound cyclin B1 in late prometaphase, while CDK1-bound cyclin B1 is destroyed on
293 tudy implicates FZR1 as a major regulator of prometaphase whose activity helps to prevent chromosome
294 f the PyST expressing cells were arrested in prometaphase with almost no cells progressing beyond met
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