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1 nment of chromosomes at the metaphase plate (chromosome congression).
2 and this recruitment is important for proper chromosome congression.
3 ncreased their stability and interfered with chromosome congression.
4 etochore Mad2 became undetectable soon after chromosome congression.
5 mosome oscillation, but is not essential for chromosome congression.
6 romosomes towards the metaphase plate during chromosome congression.
7 , and cell lines, which is due to defects in chromosome congression.
8 otor EG5 for proper spindle architecture and chromosome congression.
9  robust bipolar spindle capable of efficient chromosome congression.
10 P-E farnesylation are required for efficient chromosome congression.
11 d force transduction but are dispensable for chromosome congression.
12  mitotic spindle equator, a process known as chromosome congression.
13 aration in early mitosis promoting efficient chromosome congression.
14 nesins that may be important for its role in chromosome congression.
15  with pharmacological agents and for mitotic chromosome congression.
16 uding kinetochore-microtubule attachment and chromosome congression.
17 ed defects in spindle assembly and metaphase chromosome congression.
18 eparation in prophase facilitates subsequent chromosome congression.
19 taneously promoting checkpoint signaling and chromosome congression.
20 d assembly is spatially regulated to achieve chromosome congression.
21 ple and stable self-organizing mechanism for chromosome congression.
22 s in a manner that is required for efficient chromosome congression.
23 e separation, spindle pole organization, and chromosome congression.
24  tension-responsive signal transduction, and chromosome congression.
25 ulator of Plk1 at the kinetochore to promote chromosome congression.
26  localization at the kinetochore and rescued chromosome congression.
27 protein E may contribute to Xorbit's role in chromosome congression.
28 ntial for checkpoint control and for correct chromosome congression.
29 ession in the cell, and correlates with slow chromosome congression.
30 s with unattached kinetochores to facilitate chromosome congression,(11)(,)(12)(,)(13)(,)(14)(,)(15)(
31 K led to reduced centromere stretch, delayed chromosome congression, alignment defects, and severe mi
32 phase alignment is an indicator of defective chromosome congression and aberrant kinetochore-microtub
33 he mitotic spindle is required for efficient chromosome congression and accurate chromosome segregati
34                    Errors in the fidelity of chromosome congression and alignment can lead to imprope
35           This was accompanied by defects in chromosome congression and alignment of the maternal and
36  generates forces that contribute to mitotic chromosome congression and alignment.
37 ein (HURP) as a protein that is required for chromosome congression and alignment.
38 r of the kinesin-10 family) are required for chromosome congression and alignment; Kif4A and Kif4B (m
39 erotelic attachment, resulting in failure of chromosome congression and an increased propensity for l
40 thout functional centrosomes have a delay in chromosome congression and anaphase onset, which can be
41 ntraction reduces CSV and facilitates timely chromosome congression and correct segregation.
42 xchange factors implicating small GTPases in chromosome congression and cytokinesis.
43 e function of two sister kinetochores during chromosome congression and imply that vertebrate kinetoc
44 assembly of the bipolar spindle and promotes chromosome congression and interkinetochore tension duri
45 hrough mitosis during metaphase, even though chromosome congression and metaphase alignment do not ap
46  the first zygotic division, PLK-1-dependent chromosome congression and metaphase plate alignment are
47 r envelope detachment, and impairs metaphase chromosome congression and mitotic Golgi fragmentation,
48  as a crucial component that monitors proper chromosome congression and mitotic timing during cell di
49 ith abnormally condensed chromosomes, failed chromosome congression and multiple centrosomes.
50      Subtle losses in Plk1 activity impaired chromosome congression and produced severe anaphase dysf
51 ent motor activity of CENP-E serves to power chromosome congression and provides a flexible, motile t
52     Genome stability relies upon efficacious chromosome congression and regulation by the spindle ass
53                    In the absence of Nup358, chromosome congression and segregation are severely pert
54 isrupts centrosome maturation and results in chromosome congression and segregation defects during mi
55                                              Chromosome congression and segregation have been widely
56 newly developed system for observing meiotic chromosome congression and segregation in living maize c
57  amplification and is required for efficient chromosome congression and segregation in mammalian cell
58 rnover of the spindle is a driving force for chromosome congression and segregation in mitosis.
59             Coordination of cytokinesis with chromosome congression and segregation is critical for p
60                                              Chromosome congression and segregation require the prope
61    Constitutive Astrin:PP1-delivery disrupts chromosome congression and segregation, revealing a dyna
62 dynamic spindle microtubules and drives both chromosome congression and segregation.
63 her effectors to coordinate cytokinesis with chromosome congression and segregation.
64 ins CENP-E and CENP-F, which are involved in chromosome congression and spindle assembly checkpoint s
65 -1 down-regulation significantly compromises chromosome congression and the deposition of HJURP-CENP-
66 fs (SLiMs), they control distinct aspects of chromosome congression and the SAC.
67 g regulation of microtubule dynamics, proper chromosome congression, and correction of improper kinet
68 abnormal chromosome arm orientation, delayed chromosome congression, and sensitized cells to nocodazo
69 has conserved roles in kinetochore assembly, chromosome congression, and spindle checkpoint signaling
70 the conserved NDC80 complex are required for chromosome congression, and their disruption results in
71 t early prometaphase, started to fade during chromosome congression, and then disappeared at midanaph
72 g microtubule dynamics, spindle assembly and chromosome congression, and thus cell cycle progression
73 nstrating that spindle length regulation and chromosome congression are intrinsic to the spindle and
74 is a kinesin-like motor protein required for chromosome congression at prometaphase.
75 s at kinetochores and resulted in defects in chromosome congression at the metaphase plate.
76          After stable attachment, throughout chromosome congression, at metaphase, and throughout ana
77 e interactions with microtubules, and direct chromosome congression, biorientation, error correction,
78 the spindle assembly checkpoint (SAC) and in chromosome congression, but the role of its catalytic ac
79                         Kinetochores mediate chromosome congression by either sliding along the latti
80                                   Perturbing chromosome congression by other means also resulted in f
81 ccharomyces cerevisiae) was shown to mediate chromosome congression by promoting catastrophe of long
82 ing motor proteins, Cin8p and Kip1p, mediate chromosome congression by suppressing kMT plus-end assem
83 ochore associations, however, this effect on chromosome congression could be phenocopied.
84  p-T78-dependent Plk1 localization induced a chromosome congression defect and compromised the spindl
85 gical defects, disoriented mitotic spindles, chromosome congression defects and delayed mitotic progr
86 T-based Aurora B kinase activity, and lethal chromosome congression defects in cancer cells.
87 er KT components, impaired KT-MT attachment, chromosome congression defects, and whole-chromosome ins
88 vents binding of Class I proteins and causes chromosome congression defects, but does not perturb spi
89                   Loss of Shot also leads to chromosome congression defects, cell cycle progression d
90 ion across the mitotic spindle, resulting in chromosome congression defects, mitotic cell accumulatio
91 RH leads to loss of CENP-E and consequently, chromosome congression defects.
92 excluded the CPC from chromosomes and caused chromosome congression defects.
93 th multiple disorganized spindles and severe chromosome congression defects.
94 nonkinetochore fiber microtubules to support chromosome congression, defining for the first time a re
95 al for recruiting a pool of PP2A involved in chromosome congression during meiosis I.
96                         Net1 is required for chromosome congression during metaphase and generation o
97 -related protein that has been implicated in chromosome congression during mitosis, and we found that
98  provide the polar ejection force needed for chromosome congression during mitosis.
99 rotubule motor protein that is essential for chromosome congression during mitosis.
100 ion of multipolar spindles, causing abnormal chromosomes congression during metaphase and separation
101 creased centrosome separation but also their chromosome congression errors and mitotic delay.
102 y through prometaphase and display increased chromosome congression errors.
103                    Strong mitotic arrest and chromosome congression failure occurred after Pp1-87B do
104  results in perturbing spindle formation and chromosome congression following maturation.
105 -E motor activity as an essential feature of chromosome congression from poles and localized PP1 deli
106 ent pool of KIF4A and thus actively promotes chromosome congression from the spindle poles to the met
107 functions required to establish and maintain chromosome congression have distinguishable requirements
108                                              Chromosome congression in cells also requires positive c
109  has evolved to facilitate Bub3 activity and chromosome congression in higher eukaryotes.
110 dly growing cell lines and were required for chromosome congression in mitotic HeLa cells, the gradie
111 stem also affects spindle pole formation and chromosome congression in vivo.
112 the DYNLT3 light chain, may be important for chromosome congression, in addition to having a role in
113 me alignment defects are due to a failure of chromosome congression independent of kinetochore-microt
114 tor to anaphase A but is not responsible for chromosome congression, interkinetochore tension, or the
115 sion on the kinetochore, and in its absence, chromosome congression is defective.
116                          Thus, CENP-E-driven chromosome congression is guided by microtubule detyrosi
117 nally, KLP61F activity contributes to normal chromosome congression, kinetochore spacing, and anaphas
118  chromosome passenger complex (CPC) controls chromosome congression, kinetochore-microtubule attachme
119 emature exit from mitosis without detectable chromosome congression or anaphase movements.
120 in spindle pole organization and separation, chromosome congression or segregation, and anaphase spin
121 I was recently revised by the discovery that chromosome congression precedes metaphase I arrest.
122 mprove our understanding of how prometaphase chromosome congression relates to anaphase chromosome se
123                                              Chromosome congression requires the stable attachment of
124 the kinetochore is critical for facilitating chromosome congression, segregation, and checkpoint sign
125 ), with a concomitant increase in defects in chromosome congression, separation, and segregation.
126 O-specific isopeptidases, causes a defect in chromosome congression that depends on its precise kinet
127 ile knockdown of DUSP7 also led to defective chromosome congression that resulted in a prolonged mito
128 zed between homologous chromosomes, promotes chromosome congression through the action of the chromok
129 ation of the centrosome/nucleus complex, for chromosome congression to a well ordered metaphase plate
130  fission yeast kinesin-8 contributes both to chromosome congression to the metaphase plate and to the
131 4 into mammalian cells at prophase inhibited chromosome congression to the metaphase plate with many
132  kinetochore capture at prometaphase, timely chromosome congression to the metaphase plate, and prope
133 ryonic fibroblasts (MEFs) display defects in chromosome congression to the metaphase plate, severe ch
134                        During cell division, chromosome congression to the spindle center, their orie
135     Dynein/dynactin inhibition did not block chromosome congression to the spindle equator in prometa
136  attachments in Nnf1R-depleted cells prevent chromosome congression, whereas those in Mcm21R-depleted

 
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