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1 ike kinase 4 (PLK4), the master regulator of centrosome duplication.
2 ivation of CDK2/cyclin E, a key initiator of centrosome duplication.
3 yclin E-NPM/B23 pathway in the regulation of centrosome duplication.
4 lin E-Cdk2 target that is also implicated in centrosome duplication.
5 most completely lost the ability to suppress centrosome duplication.
6 me-binding(-) for their abilities to control centrosome duplication.
7 its transactivation-dependent regulation of centrosome duplication.
8 lytic activity and a biological inhibitor of centrosome duplication.
9 (2)/M checkpoint, the spindle checkpoint and centrosome duplication.
10 B23 has been implicated in the regulation of centrosome duplication.
11 nts, aberrant cell division and dysregulated centrosome duplication.
12 roposed to function as a master regulator of centrosome duplication.
13 icate hamartin and mTOR in the regulation of centrosome duplication.
14 al for regulating microtubule nucleation and centrosome duplication.
15 te that the tumor suppressor, p53, regulates centrosome duplication.
16 Cdk2 activity, both essential for regulating centrosome duplication.
17 t we identified based on its requirement for centrosome duplication.
18 is a key signaling molecule in the events of centrosome duplication.
19 ogate differentiation but also by subverting centrosome duplication.
20 olution of mitotic figures as well as proper centrosome duplication.
21 cells induces abnormal mitotic spindles and centrosome duplication.
22 severe mitotic abnormalities and failures in centrosome duplication.
23 e human Mps1 protein (hMps1) is required for centrosome duplication.
24 but reports conflict regarding their role in centrosome duplication.
25 that this protein plays an essential role in centrosome duplication.
26 uired for an essential step in initiation of centrosome duplication.
27 hat BRCA1 serves as a negative regulator for centrosome duplication.
28 y, a major determinant for the initiation of centrosome duplication.
29 lification are attributed to deregulation of centrosome duplication.
30 illations in the cell cycle may be linked to centrosome duplication.
31 BRCA1) plays an important role in regulating centrosome duplication.
32 ng events, aberrant mitosis and dysregulated centrosome duplication.
33 etween BRCA1 and its interacting proteins in centrosome duplication.
34 ransition, coincident with the initiation of centrosome duplication.
35 vision cycle machinery and the initiation of centrosome duplication.
36 Alms1a has a stem-cell-specific function in centrosome duplication.
37 g (esk, which we designate mMps1p) regulates centrosome duplication.
38 centriole separation that normally precedes centrosome duplication.
39 nd is a direct substrate of CDK2-cyclin E in centrosome duplication.
40 53 is directly involved in the regulation of centrosome duplication.
41 is an effector of p53-mediated regulation of centrosome duplication.
42 age repair, G(2)-M cell-cycle checkpoint and centrosome duplication.
43 abditis elegans is an essential regulator of centrosome duplication.
44 t for the overall p53-mediated regulation of centrosome duplication.
45 n cells, resulting in specific inhibition of centrosome duplication.
46 (NPM/B23) as a substrate of CDK2/cyclin E in centrosome duplication.
47 through S and G2 phases of the cell cycle or centrosome duplication.
48 numbers, HPV-16 E7 rapidly induces abnormal centrosome duplication.
49 mutant NPM/ B23 in cells effectively blocks centrosome duplication.
50 target of CDK2/cyclin E in the initiation of centrosome duplication.
51 entrosome conversion, the execution step for centrosome duplication.
52 ributes to other cellular processes, such as centrosome duplication.
53 ncluding an MVA mutation, leads to excessive centrosome duplication.
54 triole disengagement, the licensing step for centrosome duplication.
55 L52F and D67Y had an intermediate effect on centrosome duplication.
56 ication in a normal cell cycle and regulated centrosome duplication.
57 o centrioles (disengagement) is required for centrosome duplication.
58 hter centriole protein that is essential for centrosome duplication.
59 rgets of CDK2-cyclin E for the initiation of centrosome duplication.
60 which is a critical event for initiation of centrosome duplication.
61 n of ROCK II in respect to the initiation of centrosome duplication.
62 mally localized ROCK II to properly initiate centrosome duplication.
63 th and appropriate number through modulating centrosome duplication.
64 plays an important role in the regulation of centrosome duplication.
65 olo-like kinase 4 (PLK4), a key regulator of centrosome duplication.
66 inase complex critical for the initiation of centrosome duplication.
67 s of Hice1 had minimal effects on interphase centrosome duplication.
68 is elegans, the kinase ZYG-1 is required for centrosome duplication.
69 accumulate at centrosomes or participate in centrosome duplication.
70 uitin-independent proteasomal degradation in centrosome duplication.
71 rosomally localized p53 in the regulation of centrosome duplication.
72 f BRCA1 missense mutations in the control of centrosome duplication, a critical step in the maintenan
74 cent evidence indicates that deregulation of centrosome duplication affects centrosome number and pro
76 In contrast, overexpression of Pin1 drives centrosome duplication and accumulation, resulting in ch
77 lly, inhibitors of Polo-like kinase 4 impair centrosome duplication and cause genomic instability.
80 hoA, as well as RhoC, but not RhoB, promoted centrosome duplication and centrosome amplification.
81 of certain p53 mutants result in deregulated centrosome duplication and centrosome amplification.
82 tion of these dual signals causes precocious centrosome duplication and chromosome mis-segregation, o
83 lation at this site evokes robust defects in centrosome duplication and cohesion as well as arrest of
84 0, a protein that plays an essential role in centrosome duplication and cytokinesis, and have identif
86 s involved in coordinating the initiation of centrosome duplication and DNA replication, suggesting t
89 similarly abrogated HPV E7-induced abnormal centrosome duplication and ectopic expression of CDK2 in
90 event of CDK2-cyclin E for the initiation of centrosome duplication and for the induction of centroso
91 oach demonstrates that hMps1 is required for centrosome duplication and for the normal progression of
92 gly, we also find that SPD-2 is required for centrosome duplication and genetically interacts with ZY
93 ana as an essential protein able to regulate centrosome duplication and genomic stability, by inhibit
94 e actions of BRCA1 and GADD45a in regulating centrosome duplication and in maintaining genetic stabil
95 horylation-specific isomerase Pin1 regulates centrosome duplication and its deregulation can induce c
96 We show that PHD1 function is required for centrosome duplication and maturation through modificati
97 on, indicating that the processes regulating centrosome duplication and microtubule nucleation are di
98 dings demonstrate a novel function of FPC in centrosome duplication and mitotic spindle assembly duri
99 ysis demonstrated that Nde1 is essential for centrosome duplication and mitotic spindle assembly.
100 ) that ensure the coordinated progression of centrosome duplication and other cell cycle events (i.e.
101 osome, suggest a model for the initiation of centrosome duplication and provides a target for licensi
103 e organizing centers in eukaryotic cells and centrosome duplication and separation are linked to the
104 n centrosomes, and shown to be essential for centrosome duplication and separation in Xenopus [13].
105 e formation of these dysfunctional spindles, centrosome duplication and separation, as well as recrui
107 ervations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanis
108 genetic stability through the regulation of centrosome duplication and the G2-M checkpoint and provi
109 r, little is known about the role of Pin1 in centrosome duplication and the significance of Pin1 over
111 protein kinase Mps1 and p53 both function in centrosome duplication and the spindle cell-cycle checkp
113 sm that monitors centrosome integrity before centrosome duplication and ultimately governs the G1 to
114 identified numerous candidate regulators of centrosome duplication and uncovered an unanticipated re
116 ell cycle events, including DNA replication, centrosome duplication, and activation of the E2F transc
117 t genomic stability, disrupt the fidelity of centrosome duplication, and induce cellular transformati
118 logical centrosomal CDK target that promotes centrosome duplication, and its deregulation may contrib
119 , DNA replication, homologous recombination, centrosome duplication, and mitochondrial function, has
120 n overrides the p53-dependent suppression of centrosome duplication, and mortalin-driven centrosome d
122 ut not RhoB, were required for initiation of centrosome duplication, and overactivation of RhoA, as w
123 ndent kinase 2 (CDK2) triggers initiation of centrosome duplication, and p53 is phosphorylated on Ser
124 s with key roles in cell division, including centrosome duplication, and possess four Ca(2+)-binding
126 ays roles in ribosome biogenesis, control of centrosome duplication, and regulation of p53 expression
127 1 functions in modulating G(1)/S transition, centrosome duplication, and repressing tumor formation.
128 s, including ribosome maturation and export, centrosome duplication, and response to stress stimuli.
129 ription regulation, mammalian gametogenesis, centrosome duplication, and suppression of cell prolifer
130 k2-cyclin E is involved in the initiation of centrosome duplication, and that constitutive activation
132 by cyclin A for triggering the initiation of centrosome duplication, and thus the centrosome duplicat
134 ified CP110, a protein that is essential for centrosome duplication, as an interactor and substrate o
135 4 BRCA1 variant proteins were neutral in the centrosome duplication assay, missense mutations of zinc
136 in dividing cells-can arise from defects in centrosome duplication, bipolar spindle formation, kinet
140 e' functions in DNA replication, DNA repair, centrosome duplication, chromosome segregation, and chro
141 ed in either homology-directed DNA repair or centrosome duplication control including the well-known
142 n p53(-/-) cells only partially restored the centrosome duplication control, suggesting that Waf1 com
143 n of centrosomes through deregulation of the centrosome duplication cycle and failure to undergo cyto
144 k2-cyclin E results in the uncoupling of the centrosome duplication cycle and the DNA replication cyc
147 dk2 and Cdk4 deregulate the licensing of the centrosome duplication cycle in p53-null cells by hyperp
149 e determined whether the deregulation of the centrosome duplication cycle is the direct or indirect e
152 between VEGF signaling and regulation of the centrosome duplication cycle, and suggest that endotheli
153 mponent of the yeast centrosome, governs the centrosome duplication cycle, raising the possibility th
160 tants, whereas loss of szy-20 suppresses the centrosome duplication defects in both zyg-1 and spd-2 m
162 l types, and is involved in the induction of centrosome duplication-distribution abnormalities and an
163 various cell cycle checkpoints that monitor centrosome duplication, DNA replication, formation of bi
164 nstrate that Cdk2-E activity is required for centrosome duplication during S phase and suggest a mech
166 s known to regulate both DNA replication and centrosome duplication during the G1-S transition in the
167 Whereas the E7 oncoprotein rapidly drives centrosome duplication errors in cells that appear pheno
168 e 16 (HPV-16) E7 oncoprotein rapidly induces centrosome duplication errors in primary human cells, th
169 olecular mechanism whereby HPV-16 E7 induces centrosome duplication errors is independent of its abil
171 II expression results in the suppression of centrosome duplication, especially delaying the initiati
172 demonstrate that Stat3 plays a vital role in centrosome duplication events, although the downstream t
175 ry subunit for CDK2 that plays a key role in centrosome duplication, frequently is overexpressed in h
176 Here, we show that FGF-2 rapidly uncouples centrosome duplication from the cell division cycle in p
177 omes, suggesting that Cdk2 promotes mMps1p's centrosome duplication function by regulating its stabil
178 ly inhibited, cell division proceeds without centrosome duplication, generating centrosome-less cells
181 se results indicate that normal and abnormal centrosome duplication have significantly different requ
182 ts, expression of HPV-16 E7 induces abnormal centrosome duplication in a cell line that lacks functio
183 ized p53 to participate in the regulation of centrosome duplication in a manner independent of its tr
184 talin remains at centrosomes, and suppresses centrosome duplication in a transactivation function-ind
186 ative version of hMps1 (hMps1KD) can prevent centrosome duplication in a variety of cell types, and a
187 sm observed in these individuals by altering centrosome duplication in addition to DNA replication de
189 having Stat3 adenovirus were able to disrupt centrosome duplication in hydroxyurea-arrested Chinese h
193 o one blastomere of a dividing embryo blocks centrosome duplication in that blastomere; the related c
194 r suppressor protein, by allowing continuous centrosome duplication in the absence of DNA synthesis.
197 2 (Cdk2) is required for multiple rounds of centrosome duplication in Xenopus egg extracts but not f
199 th in vivo and in vitro assays, we show that centrosome duplication in Xenopus laevis embryos require
200 of the ciliopathy gene Cep120, essential for centrosome duplication, in the nephron and collecting du
201 cts with a variety of proteins that regulate centrosome duplication, including BRCA2, CDK2-Cyclin A,
202 he absence of sisterchromatid separation and centrosome duplication, indicating that micronucleation
203 dk2 deficiency completely abrogates aberrant centrosome duplication induced by a viral oncogene.
204 activity is critically involved in abnormal centrosome duplication induced by HPV-16 E7 oncoprotein
205 rosome loss induced by centrinone-a specific centrosome duplication inhibitor-leads to irreversible,
208 We propose that the 'once-only' control of centrosome duplication is achieved by temporally separat
210 ed by amorphous pericentriolar material, and centrosome duplication is controlled by centriole replic
214 We further show that the role of SUN-1 in centrosome duplication is distinct from its role in atta
215 reshold level of hMps1 function required for centrosome duplication is lower than that required for h
219 he cell cycle in early cleavage and regulate centrosome duplication is therefore a major cause of hum
224 tion of centrosome duplication, and thus the centrosome duplication kinetics was not significantly al
225 ation of the regulatory mechanism underlying centrosome duplication leads to centrosome amplification
226 sor protein is involved in the regulation of centrosome duplication: loss of p53 as well as expressio
227 egulation of a number of processes including centrosome duplication, maintenance of genomic integrity
228 hosmin 1 (NPM1) acts in ribosome biogenesis, centrosome duplication, maintenance of genomic stability
229 ow here that CDK2 is not required for normal centrosome duplication, maturation and bipolar mitotic s
232 e, raising the possibility that licensing of centrosome duplication occurs by modulating Sfi1, which
236 on(-)/centrosome-binding(+) mutants suppress centrosome duplication only partially compared with wild
239 es, and p53 is involved in the regulation of centrosome duplication partly through controlling the ac
240 s on its transactivation function to control centrosome duplication, primarily via upregulation of p2
242 in regulates two functions in the control of centrosome duplication: regulation of centrosome number
244 n unclear whether the p53's Waf1-independent centrosome duplication regulatory pathways require its t
245 n localized to centrosomes in late G1 before centrosome duplication, remained at centrosomes during S
247 at different times during M phase to license centrosome duplication, reminiscent of their roles in re
248 We show here that HBXIP is a regulator of centrosome duplication, required for bipolar spindle for
249 centrosome duplication, and mortalin-driven centrosome duplication requires physical interaction bet
250 Recent experiments have established that centrosome duplication requires the activity of cyclin-d
251 berrations can be correlated with defects in centrosome duplication/separation that are known to indu
252 major difference compared to template-driven centrosome duplication that is linked to the nuclear cyc
253 report a new mechanism for the regulation of centrosome duplication that requires USP33, a deubiquiti
254 ee of these proteins have been implicated in centrosome duplication, the nature of the centrosome dys
256 Depletion of Asl or CEP152 caused failure of centrosome duplication; their overexpression led to de n
257 The p53 tumor suppressor protein regulates centrosome duplication through multiple pathways, and p2
258 ate a direct role for PML3 in the control of centrosome duplication through suppression of Aurora A a
259 loss of p15 and p16 provides conditions for centrosome duplication to become deregulated with conseq
260 nce the defect in the mechanism that ensures centrosome duplication to occur once and only once in ea
263 tes the licensing and execution processes of centrosome duplication to prevent centrosome amplificati
266 etic interactions between these genes during centrosome duplication, we generated Brca1(Delta11/Delta
267 )/cyclin E triggers DNA synthesis as well as centrosome duplication, we tested whether Waf1, a CDK in
268 otein kinase II (CaMKII) blocks even initial centrosome duplication, whereas inactivation of Cdk2 doe
269 This phenomenon is caused by defects in centrosome duplication, which in turn affect the formati
270 nstitutively active form of ROCK II promotes centrosome duplication, while down-regulation of ROCK II
271 ound that R175H lost the ability to regulate centrosome duplication, while R249S partially retained i
272 proliferation and transformation, including centrosome duplication, whose defects have been implicat
273 ntains normal centrosome numbers by coupling centrosome duplication with segregation, which is achiev
274 use embryonic fibroblasts drastically delays centrosome duplication without affecting DNA synthesis a