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1 n in S. cerevisiae meiosis I and to suppress merotelic attachment in S. pombe mitosis, and crosslinki
2 aromyces cerevisiae meiosis I and inhibiting merotelic attachment in Schizosaccharomyces pombe mitosi
3              It predicts that, in metaphase, merotelic attachment is prevented by a kinetochore orien
4 urora B complex are specifically enriched at merotelic attachment sites.
5 ules from both poles of the mitotic spindle (merotelic attachment), and hence aberrant segregation of
6                        These defects promote merotelic attachment, resulting in failure of chromosome
7           Aurora B activity enriches MCAK at merotelic attachments and phosphorylates MCAK on residue
8 nks between spindle forces and correction of merotelic attachments and show that pharmacological mani
9 ora B at the inner centromere, and incorrect merotelic attachments are destabilized by being pulled t
10 eas augmin-nucleated bridging fibers prevent merotelic attachments by creating a nearly parallel and
11 taphase in 10-20 min while keeping erroneous merotelic attachments down to a few percent.
12 pport a preanaphase correction mechanism for merotelic attachments in which correct plus-end attachme
13 during cancer cell divisions frequently have merotelic attachments in which the centromere subdomains
14 uses a significant increase in the number of merotelic attachments per cell.
15 nk multiple kinetochore complexes to prevent merotelic attachments that result in chromosome missegre
16 hores accumulated attachments to both poles (merotelic attachments), congressed (again) to a pseudome
17 n of CKAP2 resulted in a higher incidence of merotelic attachments, anaphase lagging, and polyploidy.
18 table mutants of Hec1 exhibit an increase in merotelic attachments, hyperstretching of centromeres, a
19                      Kinetochores often form merotelic attachments, in which a single kinetochore is
20 lve the defect are specifically localized to merotelic attachments, where their enzymatic activities
21 eads to disrupted MII spindles and increased merotelic attachments.
22 ension at kinetochores, and the frequency of merotelic attachments.
23 s with stretched kinetochores, suggestive of merotelic attachments.
24 ndle microtubules is critical for correcting merotelic attachments.
25 eric substrates at unaligned chromosomes and merotelic attachments.
26 uggest that it has a major role in combating merotelic attachments.
27 nd elevates chromosome missegregation due to merotelic attachments.
28 inetochore separation, rotated bivalents and merotelic attachments.
29 ered geometry helps both prevent and resolve merotelic attachments.
30 aintaining chromosome orientation to prevent merotelic capture.
31 rrelated with rising frequencies of lagging, merotelic chromosomes in anaphase, leading to segregatio
32 ut the mitotic stages, but a small number of merotelic connections, in which a chromatid is connected
33 gulates spindle elongation forces to promote merotelic correction by phosphorylating and inhibiting K
34     The role of spindle elongation motors in merotelic correction is conserved, because partial inhib
35  on the waiting time required to correct the merotelic errors in anaphase and on the roles of chromat
36 ase onset, prevented effective correction of merotelic errors, and increased the threshold of kinetoc
37 le elongation, often permitting inclusion of merotelics in a daughter nucleus.
38 segregating chromosomes, probably because of merotelic kinetochore attachments.
39                                              Merotelic kinetochore orientation is a kinetochore misat
40                                              Merotelic kinetochore orientation is a misattachment in
41                                              Merotelic kinetochore orientation occurs frequently in e
42                                              Merotelic kinetochore orientation, in which a single kin
43 t potential segregation errors deriving from merotelic kinetochore orientation.
44 ensities, the brighter bundle connecting the merotelic kinetochore to the correct pole.
45 ablation to sever microtubules attached to a merotelic kinetochore, which is laterally stretched by o
46 t 'multipolar spindle intermediate' in which merotelic kinetochore-microtubule attachment errors accu
47 ees on the spindle and increased the risk of merotelic kinetochore-microtubule attachments.
48 n in response to spindle forces and avoiding merotelic kinetochore-spindle attachments.
49                        Our study establishes merotelic kinetochores as an experimental model for stud
50                                We found that merotelic kinetochores entering anaphase never lost atta
51 whether and how the mitotic spindle prevents merotelic kinetochores from producing lagging chromosome
52 kinase inhibition increased the frequency of merotelic kinetochores in late metaphase, and the fracti
53                             Chromosomes with merotelic kinetochores often manifest as lagging chromos
54 be an intermediate stage in the formation of merotelic kinetochores.
55 paration, causing mitotic spindle asymmetry, merotelic microtubule-kinetochore attachments, lagging c
56 ize that this polar ejection force minimizes merotelic misattachment by maintaining a constant tensio
57 s, for mammalian cultured cells, kinetochore merotelic orientation is a major mechanism of aneuploidy
58 ay promote the high incidence of kinetochore merotelic orientation that occurs after nocodazole washo
59                                         This merotelic orientation was verified by electron microscop
60 hores by microtubules from both centrosomes (merotelic orientation) is a major cause of aneuploidy.
61                    The kinetochore fibers of merotelics shortened little if any during anaphase, maki
62 re-microtubule attachment defects, including merotelic, syntelic, and combined merotelic-syntelic att
63  including merotelic, syntelic, and combined merotelic-syntelic attachments.
64                            If one fiber of a merotelic was more birefringent than the other, the less