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1 to a specific site to generate a single new centriole.
2 incorporation of both STIL and CPAP into the centriole.
3 ciliogenesis-initiating events at the mother centriole.
4 ed pericentriolar material around the mother centriole.
5 BXW7 strongly associated with HsSAS-6 at the centriole.
6 le wall along the central core region of the centriole.
7 ar material (PCM) to the proximal end of the centriole.
8 n an older "mother" and a younger "daughter" centriole.
9 factors, importantly including supernumerary centrioles.
10 ease gene through an ill-defined function at centrioles.
11 r pathway in association with the two parent centrioles.
12 on the surface and in the vicinity of parent centrioles.
13 iogenesis in cells with manipulated daughter centrioles.
14 at multiple sites, leading to supernumerary centrioles.
15 in over-elongated and structurally aberrant centrioles.
16 estraining HsSAS-6 recruitment to the mother centriole, a molecular mechanism that controls supernume
17 ere, we show that rcd4 mutants exhibit fewer centrioles, aberrant mitoses, and reduced basal bodies i
19 of PC caused an increase in deuterosome and centriole abundance, highlighting the presence of a comp
20 To test whether cells progressively lost centrioles after becoming near-tetraploid, we transientl
22 and E2F4 mutant proteins we demonstrate that centriole amplification is crucially dependent on these
24 previously unsuspected cytoplasmic events of centriole amplification, providing new perspectives for
30 ic surface area-dependent mechanism controls centriole and cilia abundance in multiciliated cells.
31 hnologies have expanded our understanding of centriole and cilium biology, revealing exciting avenues
32 uitment of the ciliary vesicle to the mother centriole and its subsequent maturation, docking, and fu
33 that BCCIP localizes proximal to the mother centriole and participates in microtubule organization a
36 hat FBXW7 is broadly localized on the mother centriole and that its presence is reduced at the site w
37 of two microtubule-derived structures called centrioles and an amorphous mass of pericentriolar mater
38 ts in our understanding of the biogenesis of centrioles and cilia and the regulatory controls that go
45 explain the origin of structurally aberrant centrioles and why centriole numerical and structural de
46 migration, that it localizes to the maternal centriole, and that it forms a complex with many other p
47 lticiliated cells (MCCs), which contain ~150 centrioles, and ionocytes (ICs), which contain two centr
48 ulticiliated cells, originates from parental centrioles, and its cellular position is biased and depe
49 In the absence of F-actin, the sperm DNA, centrioles, and organelles were transported as a unit wi
50 e, where the majority of cenexin, the mother centriole appendage protein and PLK1 binding partner, re
51 tability of microtubule triplets, as well as centriole architectural integrity remain poorly understo
69 ntrates microtubule-nucleators, but also the centriole assembly machinery, promoting biogenesis close
70 rotein 6 (SAS-6) is an essential step in the centriole assembly process and may act as trigger for th
76 glutamylase residues 330-624 and spindle and centriole associated protein 1, residues 549-855 (SPICE1
77 iments, we propose that the establishment of centriole asymmetry in mitosis primes biased interphase
79 and increases its recruitment to the mother centriole at multiple sites, leading to supernumerary ce
80 using this model, we assessed the number of centrioles at different time-points after tetraploidizat
84 an overview of our current understanding of centriole biogenesis and how variations around the same
85 HsSAS-6 for degradation and thereby controls centriole biogenesis by restraining HsSAS-6 recruitment
87 of the growing centriole initiates and times centriole biogenesis to ensure that centrioles grow at t
93 docking of the ciliary vesicle to the mother centriole but prior to axoneme elongation and fusion of
95 old is initially assembled around the mother centriole, but it cannot expand outwards, and centrosome
96 ue homeostasis, are extensions of the mother centriole, but the mechanisms that remodel the centriole
97 as been shown that TTBK2 is recruited to the centriole by distal appendage protein CEP164, little is
98 ese cilia, each MCC produces between 100-600 centrioles by a process termed centriole amplification.
102 utonomously of it-potentially explaining why centrioles can duplicate independently of cell-cycle pro
106 ecular mechanism that controls supernumerary centrioles/centrosomes and the maintenance of bipolar sp
108 Rcd4 is a poorly characterized Drosophila centriole component whose mammalian counterpart, PPP1R35
109 Here we investigate the interaction between centriole components and the PCM by taking advantage of
110 resolution microscopy, and identification of centriole components have accelerated our understanding
111 ed that several ectopically-expressed animal centriole components such as SAS-6 are recruited to the
112 cant progress has been made in understanding centriole composition, we have limited knowledge of how
114 cells either inherit the mother or daughter-centriole-containing centrosome, providing a possible me
115 s of positive selection for cells with extra centrioles, continuous generation of such centrioles, or
116 ocyte to ensure that only the two functional centrioles contributed by the sperm are present in the z
121 he primary cilium is nucleated by the mother centriole-derived basal body (BB) via as yet poorly char
122 support a model in which ANKRD26 initiates a centriole-derived signal to limit cell proliferation in
123 erile, reflecting a requirement for Ana3 for centriole development in the male germ line, rcd4 mutant
125 oles, and ionocytes (ICs), which contain two centrioles, differentiate during the same developmental
127 Centrosome fragmentation and precocious centriole disengagement depend on separase and anaphase-
128 he initiation of centriole licensing through centriole disengagement, at which point the ability to m
130 Using a genome-wide screen, we identify centriole distal appendages as critical for PIDDosome ac
131 and recruit the PIDDosome component PIDD1 to centriole distal appendages, and this interaction is req
133 que opportunity to address this question, as centrioles do not persist at the base of mature cilia.
140 ional splicing factors that are required for centriole duplication interact with WBP11 and are requir
142 onsequences of deregulating Plk4 (the master centriole duplication kinase) activity in Drosophila asy
145 t the USP9X protection of STIL to facilitate centriole duplication underlies roles of both proteins i
146 that SAS-7 functions at the earliest step in centriole duplication yet identified and plays important
148 r protein kinase and the master regulator of centriole duplication, but it may play additional roles
149 licing factors leads to a specific defect in centriole duplication, but the cause of this deficit rem
150 e for CEP131 localization, ciliogenesis, and centriole duplication, it is essential for maintaining t
151 racts with Sak/Plk4, a critical regulator of centriole duplication, more strongly at the GSC mother c
152 of centrosomes due to a failure in daughter centriole duplication, suggesting that Alms1a has a stem
164 e Centrobin (Cnb) accumulate on the daughter centriole during mitosis, thereby generating molecularly
167 erpart, PPP1R35, is suggested to function in centriole elongation and conversion to centrosomes.
174 the first recruited to the site of daughter centriole formation and regulates the centriolar localiz
178 king advantage of fission yeast, which has a centriole-free, PCM-containing centrosome, the SPB.
180 ase impairment with BI-2536 does not protect centrioles from removal in the bat star Patiria miniata.
181 nd times centriole biogenesis to ensure that centrioles grow at the right time and to the right size.
182 k4) and initiates in S-phase when a daughter centriole grows from the side of a pre-existing mother.
185 url-4 transiently associated with the mother centriole in a process that required mother-daughter cen
186 oma brucei is structurally equivalent to the centriole in animals and functions in the nucleation of
188 es at the subdistal appendages of the mother centriole in specific subtypes of neural stem cells, and
189 Although about half of cells with extra centrioles in a population were able to divide, the exte
194 Plk4 oscillation at the base of the growing centriole initiates and times centriole biogenesis to en
195 somes also amplify the appropriate number of centrioles inside a cloud of pericentriolar and fibrogra
196 annot be explained by limited duplication of centrioles, instability of extra centrioles, or by gross
201 f a single new centriole from a pre-existing centriole is strictly controlled to maintain correct cen
202 ioning of PLP to more distal portions of the centriole is sufficient to redistribute PCM and microtub
204 le cilia assembly is absolutely dependent on centrioles, it is not known to what extent they contribu
205 lthough Plk1 localizes around oocyte-derived centrioles, kinase impairment with BI-2536 does not prot
206 onstrating that cell division with amplified centrioles, known to be tolerated in disease states, can
207 Plk1 levels lead to the formation of shorter centrioles lacking a full set of microtubule triplets, i
208 leotide exchange factor (GEF), to the mother centriole, leading to Rab8 activation and cilium growth.
210 itotic progression trigger the initiation of centriole licensing through centriole disengagement, at
211 ver, we uncover that all four oocyte-derived centrioles lose microtubule nucleating activity when ret
212 how yeasts kept this interaction even after centriole loss and showed that the conserved calmodulin-
216 mmalian distal appendages associate with two centriole microtubule triplets via an elaborate filament
217 pendage proteins localize in relation to the centriole microtubules and appendage electron densities.
223 ming of insertion is modulated by changes in centriole number and the accumulation of acetylated MTs.
224 anisms responsible for this return to normal centriole number at the population level in human retina
225 kinase PLK4, human cells return to a normal centriole number during the proliferation of the populat
228 iole duplication cycle normally ensures that centriole number is maintained at two centrioles per G1
232 g SPICE1 phosphorylation results in abnormal centriole number, spindle multipolarity, and chromosome
233 tances can result in an aberrant increase in centriole number-a phenotype that is particularly preval
238 of structurally aberrant centrioles and why centriole numerical and structural defects coexist in tu
240 is achieved through a massive production of centrioles on the surface and in the vicinity of parent
242 ra centrioles, continuous generation of such centrioles, or alleviation of the disadvantageous growth
243 lication of centrioles, instability of extra centrioles, or by grossly asymmetric segregation of extr
245 A structural motif called the G-box in the centriole outer wall protein Sas4 interacts with a short
247 at dysregulation of CEP135 isoforms promotes centriole overduplication and contributes to chromosome
251 Airway progenitor cells contain two parental centrioles (PC) and form structures called deuterosomes
256 ucleation platforms and suggest that massive centriole production in MCCs is a robust process that ca
264 de novo, and thus the longstanding focus on centriole 'replication' may have led us astray from grou
266 We show that centrioles are amplified via centriole rosette formation in both embryonic developmen
268 and had an increased frequency of premature centriole separation, accompanied by reduced density of
270 expansion microscopy to study the origins of centriole structural aberrations in large populations of
274 Here, we show that PLK4 phosphorylates its centriole substrate STIL on a conserved site, S428, to p
278 e the centrosomes, which are composed of two centrioles, surrounded by a protein-rich matrix of elect
279 tions upstream of MSO control, orchestrating centriole symmetry breaking and consequently centrosome
281 thought to form a scaffold around the mother centriole that recruits other components of the mitotic
282 w no evidence of cytoplasmic buds containing centrioles that are produced from the first abortive mei
283 liated cells (MCCs) amplify large numbers of centrioles that convert into basal bodies, which are req
284 we review the structure and functions of the centriole, the centrosome, and the basal body in differe
285 One spindle pole contains the oldest mitotic centriole, the mother centriole, where the majority of c
286 el, we employed a genetic strategy to delete centrioles, the core structural components of the centro
287 ntriole forms at a single site on the mother centriole through a process that includes the hierarchic
290 mary cilium must be disassembled to free its centriole to form the centrosome, a necessary structure
291 ntriole, but the mechanisms that remodel the centriole to promote cilia initiation are poorly underst
293 ipates directly in the mitotic conversion of centrioles to centrosomes, but both are required to load
295 Comparing HCs between utricular regions, centriole trajectories were similar but they migrated to
299 ins the oldest mitotic centriole, the mother centriole, where the majority of cenexin, the mother cen
300 s a component of PCM needed to duplicate the centriole with implications for congenital heart disease