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1 yed in akir-1 mutants and are accompanied by lagging chromosomes.
2 ls overexpressing Mad2 display high rates of lagging chromosomes.
3 micronuclei form when mitotic errors produce lagging chromosomes.
4 defects such as centrosome amplification and lagging chromosomes.
5  metaphase plate and an increase in anaphase lagging chromosomes.
6 indles and asymmetric, bipolar spindles with lagging chromosomes.
7 utations cause chromosome missegregation and lagging chromosomes.
8 ore defects within the regions of misaligned/lagging chromosomes.
9 n early mitosis, but few anaphase cells show lagging chromosomes.
10 events merotelic kinetochores from producing lagging chromosomes.
11 rora B through Chk1, preventing formation of lagging chromosomes.
12 of poleward movements in anaphase to prevent lagging chromosomes.
13 ather than just one and can produce anaphase lagging chromosomes, a major source of aneuploidy.
14                   As micronuclei formed from lagging chromosomes also activate this pathway, recognit
15 he presence of supernumerary centrosomes and lagging chromosomes among mitotic NPCs.
16 luding premature chromatid separation (PCS), lagging chromosomes, anaphase bridges, micronuclei, cent
17                    Furthermore, they exhibit lagging chromosomes and a dramatic left-handed twist at
18              These disruptions contribute to lagging chromosomes and aberrant microtubule bridges dur
19 it from MII, there is a dramatic increase in lagging chromosomes and an inhibition of cytokinesis.
20      These cells often entered anaphase with lagging chromosomes and elicited increased segregation e
21 ore anaphase onset, but ZW10 mutants exhibit lagging chromosomes and irregular chromosome segregation
22 inely tuned poleward flux safeguards against lagging chromosomes and micronuclei at mitotic exit by p
23 OE leads to its mislocalization and CIN with lagging chromosomes and micronuclei in pseudodiploid DLD
24      Real-time imaging of live NPCs revealed lagging chromosomes and multipolar divisions.
25 AN components at the centromere and leads to lagging chromosomes and spindle pole defects.
26 g the number of abnormal anaphase cells with lagging chromosomes and/or acentric fragments.
27  errors in chromosome segregation (including lagging chromosomes), and abnormalities in spindle morph
28 sruptions, including those which result from lagging chromosomes, and achieve stereotypic outputs, su
29  induces premature separation of chromatids, lagging chromosomes, and anaphase bridges.
30 ed in vitro, showed chromosome misalignment, lagging chromosomes, and aneuploidy with premature separ
31 rotelic microtubule-kinetochore attachments, lagging chromosomes, and aneuploidy.
32 in B by the APC/C, supernumerary centrioles, lagging chromosomes, and aneuploidy.
33 salignment, chromosomal congression defects, lagging chromosomes, and chromosome missegregation.
34 indle morphology, increased the frequency of lagging chromosomes, and inhibited the proliferation of
35 wn of the Twins B subunit led to bridged and lagging chromosomes, and knockdown of the B' Widerborst
36 equency of CA, multipolar spindles, anaphase-lagging chromosomes, and micronuclei.
37 late, premature sister chromatid separation, lagging chromosomes, and multipolar spindles.
38                                         Most lagging chromosomes are passively inherited rather than
39 tion and aberrant mitosis with misaligned or lagging chromosomes are significantly increased in Ptpn1
40 festing disorganized spindle, misaligned and lagging chromosomes as well as micronucleated cells.
41 ypes associated with zw10 and rod mutations: lagging chromosomes at anaphase and precocious sister ch
42 rmation of stable attachments and eventually lagging chromosomes at anaphase I.
43  misalignment at metaphase plates as well as lagging chromosomes at anaphase.
44 ing division, these cells frequently exhibit lagging chromosomes at both metaphase and anaphase, sugg
45 1.16% of untreated anaphase cells exhibiting lagging chromosomes at the spindle equator, and this per
46 uploidy phenotype involved the occurrence of lagging chromosomes but not chromosome bridges, indicati
47  High levels of mBub3 remain associated with lagging chromosomes but not with correctly aligned chrom
48 clei arise from cells entering anaphase with lagging chromosomes, cellular mechanisms allowing late-s
49 splay a significantly increased frequency of lagging chromosomes during anaphase.
50 umerary centrosomes, multipolar spindles and lagging chromosomes during anaphase.
51                                              Lagging chromosomes during cancer cell divisions frequen
52 rebral cortical neuroblasts in situ detected lagging chromosomes during mitosis, suggesting the norma
53  shown to cause centrosome amplification and lagging chromosomes during mitosis.
54 ic checkpoint, and an increased frequency of lagging chromosomes during mitosis.
55 -deficient zygotes, followed by mitosis with lagging chromosomes, elongated spindles, micronuclei, an
56 ing chromosomes in anaphase, suggesting that lagging chromosomes fail to segregate properly.
57  congression and an increased propensity for lagging chromosomes following mitotic delay.
58                                        Thus, lagging chromosomes in anaphase are symptomatic of defec
59          We discovered that the frequency of lagging chromosomes in anaphase is very sensitive to par
60 d during mitosis, we show that a majority of lagging chromosomes in anaphase segregate to the correct
61                   The single kinetochores of lagging chromosomes in anaphase were stretched laterally
62                Cells depleted of KBP exhibit lagging chromosomes in anaphase, an effect that is recap
63 tly show alignment defects during metaphase, lagging chromosomes in anaphase, and chromatin bridges d
64 efects in chromosome alignment in metaphase, lagging chromosomes in anaphase, failure of cytokinesis
65  damage and consequent chromatin bridges and lagging chromosomes in anaphase, frequently leading to c
66 ith merotelic kinetochores often manifest as lagging chromosomes in anaphase, suggesting that lagging
67 tubule (k-MT) attachments, which manifest as lagging chromosomes in anaphase.
68 ected by the mitotic checkpoint, and induces lagging chromosomes in anaphase.
69 e, vulnerability to DNA damage and increased lagging chromosomes in mitosis.
70     Kif2a-depleted animal caps have anaphase lagging chromosomes in stage 9 and 10 embryos and subseq
71 s allows the correction and reintegration of lagging chromosomes in the main nuclei before completion
72                      Errors can manifest as "lagging chromosomes" in anaphase, although their mechani
73  most missegregated chromosomes consisted of lagging chromosomes involving both sister chromatids.
74                      We speculate that these lagging chromosomes might be linked to developmental def
75 ion, including multipolar spindle formation, lagging chromosomes, misalignment and mitotic slippage.
76 bit mitotic defects including misaligned and lagging chromosomes, multipolar spindles, and increased
77 nd thereby, delays abscission in response to lagging chromosomes, nuclear pore defects, and tension f
78      However, it remains unknown whether the lagging chromosomes observed in anaphase segregate to th
79  show chromosome segregation defects such as lagging chromosomes on the spindle during anaphase and h
80 patocytes of differing ploidies, we found no lagging chromosomes or micronuclei in mitotic polyploid
81 t mitoses, including misaligned chromosomes, lagging chromosomes, polylobed nuclei, and delayed passa
82 ly inactive Smurf2 results in misaligned and lagging chromosomes, premature anaphase onset, and defec
83 rd various forms of mitotic errors including lagging chromosomes producing micronuclei, multipolar sp
84 increase in anaphase-lagging cells, with the lagging chromosomes showing reduced centromere protein C
85 luded multipolar chromosome segregations and lagging chromosomes that lead to formation of micronucle
86 -MT attachments and leading to high rates of lagging chromosomes that missegregate.
87 uently enter anaphase in a timely manner but lagging chromosomes then manifest.
88                                              Lagging chromosomes were also positioned closer to the m
89  Extended anaphases, chromosome bridges, and lagging chromosomes were frequent during these polyploid
90 tly, these cells exhibit a high frequency of lagging chromosomes when they enter anaphase.
91                  Intriguingly, the number of lagging chromosomes with high Bub3 staining increases dr
92 rized by chromosomal bridges in anaphase and lagging chromosomes, without affecting spindle checkpoin