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1 lation ensures mitotic fidelity after genome reduplication.
2 sible to SAS-6, correlating with a block for reduplication.
3 calizes to centrosomes and blocks centrosome reduplication.
4 CDK2 kinase inhibition also allow centrosome reduplication.
5 specifically blocks modified centrioles from reduplication.
6  mother centrioles, which prevents centriole reduplication.
7 e number and ensuring the block to centriole reduplication.
8 lecule inhibitor SU9516 suppressed centriole reduplication.
9  Mps1 mediates cyclin A-dependent centrosome reduplication.
10 roduces extra centrosomes, called centrosome reduplication.
11  to mitotic divisions without impairing endo-reduplication.
12 of Aurora A activation to prevent centrosome reduplication.
13 n, perivascular edema, and basement membrane reduplication.
14 ulatory mislocation (56%), followed by place reduplication (19%), and chimeric assimilation (13%).
15 nabling continued proliferation after genome reduplication, a finding with implications for cancer pr
16       Inhibition of Cdk2 prevents centrosome reduplication and destabilizes mMps1p, causing its subse
17 that myeloid alpha-defensin genes evolved by reduplication and divergence from Paneth cell defensin g
18 lls correlates with the onset of endomitotic reduplication and is associated with the loss of the abi
19                  Our studies show centrosome reduplication and mitotic catastrophe in osteosarcoma ce
20 escued p27K-expressing cells from centrosome reduplication and mitotic catastrophe.
21 d a second S phase resulting in whole-genome reduplication and tetraploidy.
22                    Chromosome loss, loss and reduplication, and deletions are the majority events tha
23         Mechanisms responsible for centriole reduplication are poorly understood.
24  but the mechanisms underlying this block to reduplication are unclear.
25 n, whereas AtSPO11-3 is involved in DNA endo-reduplication as a part of the topo VI complex.
26 1 is a regulator of centriole and centrosome reduplication as well as the initiation of DNA replicati
27  was dispensable in the mouse liver for endo-reduplication, but this could be explained by the ORC1 h
28  stabilizing Mps1 mutations cause centrosome reduplication, bypassing cyclin A.
29 ently showed that naturally occurring genome reduplication does not alter mitotic chromosome structur
30 nhibitory role for the protein in centrosome reduplication during S-phase delay.
31 oles undergo multiple rounds of duplication (reduplication) during prolonged interphase.
32 tazoans, an SPB-intrinsic mechanism prevents reduplication early in the cell cycle.
33 ance as coauthor with Bateson to promote the reduplication hypothesis to explain the statistical evid
34 we describe a mechanism to prevent centriole reduplication in Drosophila melanogaster whereby the SCF
35 necessary and sufficient to cause centrosome reduplication in human cells.
36 pes, and active hMps1 accelerates centrosome reduplication in U2OS cells.
37 preventing polyploidization, or aberrant DNA reduplication, in the absence of functional p53.
38 r mitotic fidelity following aberrant genome reduplication, including in diseased states.
39                                   Since endo-reduplication initiates DNA synthesis like normal S phas
40  layer, except for 12.5% with mild segmental reduplication involving 13.7 +/- 10.2% capillary circumf
41                                      How SPB reduplication is prevented early in the cell cycle is al
42  during programmed rounds of papillar genome reduplication known as endocycles.
43 ells underwent microtubule inhibitor-induced reduplication, leading to a polyploidy state.
44 ppeared to be suppressed and chromosome loss/reduplication, leading to uniparental disomy (UPD), repr
45 me, while centriole disengagement provides a reduplication license to allow mother centrioles to dupl
46 the question of how a cell undergoing genome reduplication might regulate chromosome structure to pre
47 of CP110, ultimately resulting in centrosome reduplication, mitotic catastrophe and abrogation of cel
48                                   Chromosome reduplication occurs in many contexts, including: polyte
49 aline (glycoprotein) material and disruption/reduplication of basement membrane.
50 somes where Orc1 prevents Cyclin E-dependent reduplication of both centrioles and centrosomes in a si
51          Overexpression of GFP-mMps1p causes reduplication of centrosomes during S phase arrest.
52 tion, but is essential to prevent subsequent reduplication of DNA and the resulting hyperdiploid stat
53 ication of complex events including loss and reduplication of loci.
54 clin/cyclin-dependent kinases (CDKs) prevent reduplication of the budding yeast centrosome, called a
55 in heterozygous Men1 mice occurs by loss and reduplication of the entire mutant-bearing chromosome.
56 , gamma1 chains) revealed gaps, folding, and reduplication of the epidermo-dermal basement membrane.
57 stancing of the daughter centriole, allowing reduplication of the mother centriole even if the origin
58 ells showed that ORF67 expression results in reduplication of the nuclear membrane.
59 re can be explained by chromosomal loss with reduplication of the remaining chromosome.
60 g that rereplication and the endocycling DNA reduplication program are distinct processes.
61      Moreover, cyclin A-dependent centrosome reduplication requires Mps1, and these stabilizing Mps1
62  human cells during G2 arrests and that this reduplication requires the activity of Polo-like kinase
63                                         Both reduplication responses require the spindle assembly che
64 CDK, evoke two-step system that prevents SPB reduplication throughout the cell cycle.
65 s, a centrosome-intrinsic mechanism prevents reduplication until centriole disengagement.
66 le formation, yet they accelerate centrosome reduplication upon hydroxyurea arrest.
67   We find that mother centrioles can undergo reduplication when original daughter centrioles are only
68 tion of Cetn2 into centrioles and centrosome reduplication, whereas depletion of Cetn3 generates extr
69 mosome separation failure thus causes genome reduplication, which alters mitotic chromosome structure