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1 ocument the role of p53 and Rb in repressing tetraploidization.
2  the extra centrosomes gained at the time of tetraploidization.
3 rmalities, including cytokinesis failure and tetraploidization.
4 n deteriorates cellular fitness by enhancing tetraploidization.
5 more likely reason for furrow regression and tetraploidization.
6 a large number of duplicated genes following tetraploidization.
7 at the additional X. laevis genes arose from tetraploidization.
8 s, and the other that coincided with Xenopus tetraploidization.
9 es may have undergone an additional round of tetraploidization.
10 itial cell line establishment and subsequent tetraploidization.
11 abscission to prevent chromosome breakage or tetraploidization.
12 ytokinesis to prevent chromosome breakage or tetraploidization.
13 y compared to the more pronounced effects of tetraploidization.
14 y landscape that favours tumorigenesis after tetraploidization.
15 rtebrate genome evolution, including an auto-tetraploidization (1R(V)) that predates the early Cambri
16  split, followed by a mid-late Cambrian allo-tetraploidization (2R(JV)) in gnathostomes and a prolong
17 cells reduce supernumerary centrosomes after tetraploidization, a small fraction retains extra centri
18 e screen, and identified mechanisms by which tetraploidization affects genomic stability.
19 lly, we demonstrate that spontaneous somatic tetraploidization after a wide cross between C. oriental
20                                              Tetraploidization, along with large internal duplication
21 Furthermore, polyploidization of wheat (both tetraploidization and hexaploidization) induced revoluti
22 ized by centrosome amplification, chromosome tetraploidization and premature sister chromatid segrega
23 ntrosomes that are typically acquired during tetraploidization are responsible for driving tumorigene
24 ecent studies implicating telomere-dependent tetraploidization as an important mechanism in carcinoge
25 understood but probably include prior genome tetraploidization, centrosome amplification and mitotic
26 ificial increase in centriole number without tetraploidization due to transient overexpression of the
27          By mapping tumor genetic histories, tetraploidization emerged as a key mutational process be
28 elomere damage, we show that telomere-driven tetraploidization enhances the tumorigenic transformatio
29 olved independently since the soybean genome tetraploidization event approximately 13 million years a
30 ding to these results, we hypothesize that a tetraploidization event in A. lyrata allowed the product
31 or was the cytoplasmic donor in the original tetraploidization event, and 2) highland and coastal qui
32 al support for the idea of an ancient genome tetraploidization event.
33 egmental and tandem duplications following a tetraploidization event.
34 nce for an ancient whole-genome duplication (tetraploidization) event that probably occurred just bef
35      Although the ancestor of maize arose by tetraploidization, fewer than half of the genes appear t
36 of centrioles at different time-points after tetraploidization finding that near-tetraploids rapidly
37 at an increase in proliferative activity and tetraploidization had occurred already in mildly dysplas
38                                              Tetraploidization has been proposed as an intermediate s
39 s underlying the phenotypic complexity after tetraploidization in plants.
40 est a general mechanism for the induction of tetraploidization in the early stages of tumorigenesis w
41 n maize arose as a consequence of an ancient tetraploidization in the maize ancestral lineage.
42    These data establish that telomere-driven tetraploidization is induced by critically short telomer
43 from tetraploid precursors, but the cause of tetraploidization is unknown.
44 version event detected for one of the genes, tetraploidization must have occurred before 4.8 Mya, and
45                               We report that tetraploidization occurs in p53-deficient cells experien
46                         Moreover, artificial tetraploidization of diploid cancer cells led to a reduc
47 ies in maize has probably occurred since the tetraploidization of maize, and may contribute to flower
48 ralogous genes that arose as a result of the tetraploidization of the maize genome.
49                                              Tetraploidization, or genome doubling, is a prominent ev
50 and moderate dysplasias, indicating that the tetraploidization precedes the loss or gain of specific
51  cells have an increased rate of spontaneous tetraploidization, suggesting that apoptosis may play an
52 to study whether p75(NTR)-dependent neuronal tetraploidization takes place in the cerebral cortex, gi
53 g, demonstrate the important contribution of tetraploidization to the gene sources for the herbicide
54 aneuploid, although a slight tendency toward tetraploidization was observed.
55   To investigate the fate of its genes after tetraploidization, we analyzed the sequence of five dupl
56 t of the chromosome rearrangements following tetraploidization were centric fusions and did not invol