ライフサイエンスコーパス: centrosome

1 ing after ablation-mediated release from the centrosome.

2 ectively detached and depolymerized from the centrosome.

3 pecific location and protein partners at the centrosome.

4 tical microtubule arrays in the absence of a centrosome.

5 omponent of the mitotic spindle pole and the centrosome.

6 ribution of pushing forces that position the centrosome.

7 y into the daughter cell harboring the young centrosome.

8 splacement of both Cep68 and Cep170 from the centrosome.

9 tion of the plasmid cluster toward the young centrosome.

10 results in immediate Nuf dispersal from the centrosome.

11 ically pericentrin and gamma-tubulin, to the centrosome.

12 ach to selectively kill cells with amplified centrosomes.

13 In most species, oocytes lack centrosomes.

14 were observable only in cells with amplified centrosomes.

15 clear envelope breakdown, and duplication of centrosomes.

16 s that were isolated from tumors with excess centrosomes.

17 cells have varied abilities to cluster extra centrosomes.

18 endothelial cells (ECs) acquire excess (>2) centrosomes.

19 riolar proteins that regulate MT assembly at centrosomes.

20 mbles in the absence of centriole-containing centrosomes.

21 increased GSC numbers and mispositioning of centrosomes.

22 relative positioning of mother and daughter centrosomes.

23 pical inheritance of the mother and daughter centrosomes.

24 number of microtubules originating from the centrosomes.

25 val of cancer cells containing supernumerary centrosomes.

26 spindle and an abnormal concentration at the centrosomes.

27 andomizing influence of nucleation away from centrosomes.

28 ustering and survival of cells with multiple centrosomes.

29 d Hsp72 to the poles of cells with amplified centrosomes.

30 ive targeting of cancer cells with amplified centrosomes.

31 nd only a few KMTs directly connected to the centrosomes.

32 detachment and results in HSET depletion at centrosomes, a phenotype also observed in CEP215-deficie

33 Centrosome aberrations (CA) and abnormal mitoses are con

34 Numerical centrosome aberrations underlie certain developmental ab

35 To explore C-NAP1 activities in regulating centrosome activities, we used genome editing to ablate

36 topic, spontaneous microtubule assembly when centrosome activity is defective or absent, which would

37 Strikingly, when centrosome activity was experimentally reduced, the abse

38 ring spermiogenesis and for the formation of centrosomes after fertilization in the zygote.

39 Centrosome amplification (CA) is a hallmark of cancer, o

40 reast cancer cell lines, increased levels of centrosome amplification are accompanied by efficient cl

41 Here, we test the consequence of centrosome amplification by creating mice in which centr

42 Tumors arising from centrosome amplification exhibit frequent mitotic errors

43 this is an important adaptation mechanism to centrosome amplification in cancer.

44 s, we here report that mutant Pik3ca induces centrosome amplification in cultured cells (through a pa

45 Centrosome amplification induced by DNA damage or by PLK

46 Centrosome amplification is a common feature of human tu

47 Centrosome amplification is a common feature of human tu

48 Centrosome amplification is a common feature of many typ

49 e et al. (2017) provide strong evidence that centrosome amplification is sufficient to initiate tumor

50 Genotoxic stresses lead to centrosome amplification, a frequently-observed feature

51 a support a direct causal relationship among centrosome amplification, genomic instability, and tumor

52 polar spindle frequency that correlated with centrosome amplification, while loss of Hsp72 or Nek6 fu

53 on signal led to low CHK1 activation and low centrosome amplification.

54 hosphorylation after irradiation and reduced centrosome amplification.

55 This perturbation of the centrosome-anchoring process ultimately led to an increa

56 s, here we find that Gle1 is enriched at the centrosome and basal body.

57 ruitment sites for proteins destined for the centrosome and cilium.

58 rs involved in microtubule nucleation at the centrosome and coordinates the assembly of protein compl

59 arge scaffolding protein located at both the centrosome and Golgi apparatus.

60 ation of microtubule acetylation, as well as centrosome and Golgi organization and polarization.

61 rough HDAC6 regulation, was shown to control centrosome and Golgi reorientation toward the leading ed

62 Displacement of DVL from the centrosome and its release into the cytoplasm on NEK2 ph

63 th decreased pericentrin localization at the centrosome and microtubule organization defects.

64 optosis (C10orf54, LTA), adhesion (TNXB), or centrosome and microtubule structure/function (KIF9, TUB

65 anding controversy and explain how cells use centrosome and microtubules to maintain directional migr

66 rphase and mitotic MT mechanisms and indeed, centrosome and primary cilia were altered and spindles w

67 -actomyosin coupling steers the direction of centrosome and somal migration, as well as the switch fr

68 lls impairs the spindle assembly checkpoint, centrosome and spindle function, and maintenance of chro

69 r the functions that require movement of the centrosome and the associated nuclear material, dynein n

70 imal cells assemble (nucleate) from both the centrosome and the cis-Golgi cisternae.

71 protein AKAP350A is known to localize to the centrosome and the Golgi, but the molecular details of i

72 otubule-organizing centers (MTOCs; mammalian centrosome and yeast spindle pole body [SPB]) nucleate m

73 our results show that the connection between centrosomes and chromosomes is mediated by an anchoring

74 are small barrel-shaped structures that form centrosomes and cilia [1].

75 s a multifunctional structure that organizes centrosomes and cilia and is important for cell signalin

76 Centrosomes and cilia are organized by a centriole pair

77 rioles are the foundation of two organelles, centrosomes and cilia.

78 e division because of its ability to cluster centrosomes and form bipolar spindles, but it is not req

79 ungal SPBs has advanced our understanding of centrosomes and NE events.

80 r oogenesis, spindle assembly occurs without centrosomes and relies on signals from chromosomes.

81 E1 cells causes a defective recruitment onto centrosomes and satellites.

82 In the absence of both centrosomes and the SAC, brain cells, including neural s

83 nce is the compensatory relationship between centrosomes and the SAC.

84 Two key components are centrosomes and the spindle assembly checkpoint (SAC), a

85 aments, 2) arranged in a radial array by the centrosome, and 3) built into the 9+2 axoneme.

86 simultaneously at adherens junctions and the centrosome, and a membrane-centrosome transport system w

87 d cell cycle checkpoints, aberrations of the centrosome, and failed chromatid cohesion, mirroring fin

88 tructure and functions of the centriole, the centrosome, and the basal body have an impact upon many

89 tructure and functions of the centriole, the centrosome, and the basal body in different tissues and

90 itotic structures, particularly the spindle, centrosomes, and midbody.

91 e, initial proximity between the cluster and centrosomes, and subsequent differential behavior of the

92 d to define the association of AKAP350A with centrosomes, and these studies disclosed that AKAP350A s

93 Centrosomes are a functionally conserved feature of euka

94 s unique in that cancer cells with amplified centrosomes are dependent on the motor for viable divisi

95 Like DNA, centrosomes are duplicated once each cell cycle.

96 gy that can readily be modeled in Drosophila Centrosomes are essential to give organization to the ra

97 Duplicated centrosomes are held together by a proteinaceous linker

98 Centrosomes are microtubule organization centers in cell

99 portantly, we demonstrate that supernumerary centrosomes are sufficient to drive aneuploidy and the d

100 Prior to mitosis, duplicated centrosomes are tethered together, which is thought to p

101 ent assemblies that are critical for mitotic centrosome assembly.

102 ential for centriole duplication and mitotic centrosome assembly.

103 a molecular interaction required for mitotic centrosome assembly.

104 sphorylation of Nuf occurs at prophase, when centrosome-associated Nuf disperses throughout the cytop

105 ts in Nuf underphosphorylation and prolonged centrosome association.

106 However, the strength of microtubule-centrosome attachments is unknown, and the possibility t

107 olog, the centrosomal GABARAP reservoir, and centrosome-autophagosome crosstalk.

108 nisotropic manner to promote the movement of centrosomes away from each other.

109 d its product--PtdIns(4)P--accumulate at the centrosome/basal body in non-ciliated, but not ciliated,

110 iginates from its characterised roles at the centrosome/basal body/cilia network.

111 Third, we find that the initial position of centrosomes, between the male pronucleus and cell cortex

112 ze during sprouting angiogenesis, and excess centrosomes block repolarization and reduce migration an

113 l life, existing not only as the core of the centrosome but also as the basal body, the structure tha

114 affold that recruits proteins to the mitotic centrosome, but how Cnn assembles into a scaffold is unc

115 icrotubule-organizing activity (MTOC) at the centrosome, but the mechanisms regulating this transitio

116 Although excess centrosomes can lead to aneuploidy and chromosome instab

117 INPP5E localizes to centrosomes, chromosomes, and kinetochores in early mito

118 coordinated by PIPKIgamma and INPP5E at the centrosome/ciliary base, is vital for ciliogenesis by re

119 cer cells frequently possess extra amplified centrosomes clustered into two poles whose pseudo-bipola

120 Centrosome clustering is a process frequently used by ca

121 However, mechanisms of centrosome clustering remain poorly understood.

122 Inhibition of centrosome clustering triggers multipolar spindle format

123 function, highlighting a biphasic model for centrosome clustering.

124 related kinase 6 (Nek6) and Hsp72 to promote centrosome clustering.

125 When sDAPs and centrosome cohesion are disrupted, cilia surface to the

126 d for pericentrosomal Golgi localization and centrosome cohesion, independent of its localization to,

127 Furthermore, centrosome compromise revealed that this organelle is re

128 For most of the cell cycle, centrosomes consist of two centrioles embedded in the pr

129 steric interactions between microtubules and centrosomes contribute to robust onset of nuclear dynein

130 Rusan investigates how centrosomes control cell behavior and differentiation du

131 cues should not be seen as direct driver of centrosome decentering and cell polarization but instead

132 Centrosome decentering is often considered to result fro

133 Unlike some centrosome declustering agents, blocking Hsp72 or Nek6 f

134 and identify patients who might benefit from centrosome declustering agents.

135 cts in microtubule renucleation from mitotic centrosomes, decreased kinetochore-fiber integrity, incr

136 onstrate that miR-26a induces aneuploidy and centrosome defects and enhances tumorigenesis.

137 Here we show that centrosome defines the rear instead of the front, using

138 Although the mother centriole mediates most centrosome-dependent processes, the role of the daughter

139 Mitotic progression is restored upon centrosome depletion by the Polo-like kinase 4 inhibitor

140 s with excess centrosomes initially had more centrosome-derived microtubules but, paradoxically, fewe

141 domain of CEP215 in vertebrate cells causes centrosome detachment and results in HSET depletion at c

142 However, the conventional view that centrosome determines cell's front, based on its often-o

143 The non-membrane-bound nature of the centrosome dictates that protein-protein interactions dr

144 The two centrioles of the centrosome differ in age and function.

145 inhibits, delays, or reverses cardiomyocyte centrosome disassembly and binucleation.

146 cal resection rather transiently accelerates centrosome disassembly as well as the rate of binucleati

147 entiation, characterized by binucleation and centrosome disassembly, rendering the heart unable to re

148 or role in driving mitotic events, including centrosome disjunction and separation, and is frequently

149 Centrosome disruption by chemical prevention of centriol

150 rosome loss induced by centrinone-a specific centrosome duplication inhibitor-leads to irreversible,

151 he cell cycle in early cleavage and regulate centrosome duplication is therefore a major cause of hum

152 olo-like kinase 4 (PLK4), a key regulator of centrosome duplication.

153 To survive, cancer cells cluster extra centrosomes during mitosis, avoiding the detrimental eff

154 rates most of the force required to separate centrosomes during spindle assembly.

155 Concomitant with mother centrosome elongation, GSCs form asymmetric spindle, whe

156 es atypical spindles assembled in absence of centrosomes entail poorly understood mechanisms of chrom

157 ation network to the spindle pole body (SPB, centrosome equivalent) to control mitotic exit events.

158 delay, there is a time-dependent increase in centrosome fragmentation and centriole disengagement.

159 Centrosome fragmentation and precocious centriole diseng

160 using microsurgery to alter the distance of centrosomes from cells' ends, we show that centrosomal p

161 ibility that mechanical force might regulate centrosome function has scarcely been explored.

162 ocalized mRNA metabolism required for proper centrosome function.

163 ay be important in tumorigenesis and mitotic centrosome function.

164 cortical layers, abnormal positioning of the centrosome-Golgi complex, and aberrant length/orientatio

165 ECs with excess centrosomes had elevated Rac1 activity, and repolarizati

166 ins that localize to the mitotic spindle and centrosomes have been implicated in the pathogenicity of

167 Removal of centrosome impairs directional cell migration, whereas t

168 They then aggregate around the centrosome in a specialized nuclear cleft that we identi

169 The importance of centrosome in directional cell migration has long been r

170 earward, resulting in the orientation of the centrosome in the direction of migration.

171 Here, we discover that HMMR acts at centrosomes in a PLK1-dependent pathway that locates act

172 Fizzy-related (Fzr or Cdh1) is localized at centrosomes in animal cells.

173 otubule-organizing centers (MTOCs), known as centrosomes in animals and spindle pole bodies (SPBs) in

174 e a131's ability to de-cluster supernumerary centrosomes in cancer cells eliminates Ras-activated cel

175 Excess centrosomes in ECs were associated with p53 phosphorylat

176 results in abnormal elongation of the mother centrosomes in GSCs, suggesting the existence of a stem

177 l ultrastructure are the origin of the first centrosomes in the zygote [2-4].

178 Primary ECs with excess centrosomes in vascular sprouts also had elevated Ser33

179 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essen

180 on after centrosome removal, suggesting that centrosome-independent proliferation is not conferred so

181 Excess centrosomes induce p53-dependent senescence without DNA

182 te neurogenesis, abnormalities in asymmetric centrosome inheritance leading to neuronal migration del

183 ECs with excess centrosomes initially had more centrosome-derived microt

184 ure in the partial NE breakdown required for centrosome insertion into the NE, a step analogous to ma

185 Of importance, these alterations in centrosome integrity do not result from loss of mRNA exp

186 We found that centrosome is always located proximal to the future rear

187 -10, and MCP1 secretion, suggesting that the centrosome is critical for cytokine production.

188 myosin-mediated abscission, during which the centrosome is retained while apical/ciliary membranes ar

189 The centrosome is the major microtubule-organizing centre of

190 Duplication of the centrosomes is a tightly regulated process.

191 lls, how untransformed ECs respond to excess centrosomes is poorly understood.

192 dynamically localized to nuclear envelopes, centrosomes, kinetochores, and midbodies.

193 In single-celled organisms such as fungi, centrosomes [known as spindle pole bodies (SPBs)] are es

194 f ninein, a protein that attaches MTs to the centrosome, leads to greater numbers of centrosome-unatt

195 Ndel1's kinetochore attachment, but not its centrosome localization, during mitosis.

196 Centrosome-localized mitotic Aurora kinase A (AURKA) fac

197 In normal human cells, centrosome loss induced by centrinone-a specific centros

198 We therefore propose that centrosome loss or a prolonged mitosis activate a common

199 ism by which p53 is activated in response to centrosome loss remains unknown.

200 In nontransformed cells, centrosome loss triggers a p53-dependent surveillance pa

201 t conferred solely by the inability to sense centrosome loss.

202 t suppressed mitotic defects associated with centrosome loss.

203 chizosaccharomyces pombe SPB is analogous to centrosomes, making it an ideal model to study MTOC asse

204 se microtubule assembly pathways, defined by centrosome maturation and nuclear envelope breakdown, pl

205 y regulator of critical mitotic events, like centrosome maturation and spindle formation.

206 Intriguingly, centrosome maturation occurs during interphase in an MLK

207 Our data suggest a novel function for centrosome maturation that determines the contribution o

208 ic bridge coincides with the location of the centrosome meiotic-vegetal organizing center.

209 e the bipolar spindle, predominantly the old centrosome migrated away, biasing the partition of the p

210 ucidate the hitherto unexplored mechanism of centrosome migration and show that it is driven by the i

211 Their assembly is primed by centrosome migration to the apical surface, yet surprisi

212 To gain insight into the mechanisms driving centrosome migration, we exploited the reproducibility o

213 involved in the cytoskeleton remodeling and centrosome migration, whereas intraflagellar transport 8

214 ction participate in concert to drive apical centrosome migration.

215 d Cdc42 activity at the PM displayed altered centrosome morphology, suggesting that centrosome regula

216 reorganization of the MT network, fostering centrosome motion to the cell periphery.

217 In all conditions, centrosomes moved from their off-centered position next

218 Cortical contractility restricts centrosome movement at a minimal distance required for H

219 rs, including but by no means limited to the centrosome, MTs undergo rapid transitions through phases

220 ting that the link between the Golgi and the centrosomes must be dissolved to reach metaphase.

221 ctionality alterations and perturbed nucleus-centrosome (N-C) coupling.

222 e and super-resolution imaging, we uncover a centrosome-nucleated wheel-like microtubule configuratio

223 ated whether extracellular cues can regulate centrosome-nucleus positioning and cell migration.

224 results provide important insight as to how centrosome number and chromosomal stability can be affec

225 some amplification by creating mice in which centrosome number can be chronically increased in the ab

226 We show that increasing centrosome number elevated tumor initiation in a mouse m

227 nalysis revealed that Aire was important for centrosome number regulation and spindle pole integrity

228 some positioning, chromosomal alignment, and centrosome number.

229 Centrosome numbers are tightly regulated during the cell

230 Abnormal centrosome numbers can impair cell division and cause ch

231 nished phosphorylation of PLK4 and in excess centrosome numbers in cells.

232 est, thus ensuring the maintenance of normal centrosome numbers.

233 t of the ATG8 family member GABARAP from the centrosome occurs during starvation-induced autophagosom

234 Centrosomes, or spindle pole bodies (SPBs) in yeast, are

235 metric spindle, wherein the elongated mother centrosome organizes considerably larger half spindle th

236 equired for rearward nuclear movement during centrosome orientation in migrating fibroblasts.

237 n-dependent rearward nuclear movement during centrosome orientation.

238 n a manner associated with radiation-induced centrosome overduplication and mitotic cell death.

239 , which suggests that pathologic outcomes of centrosome overduplication depend on the transformation

240 virus (MCV) small T (sT) oncoprotein induces centrosome overduplication, aneuploidy, chromosome break

241 - radial arrays of microtubules organized by centrosomes - play a fundamental role in the spatial coo

242 erall our work reveals that accurate initial centrosome position, together with steric interactions,

243 ion with morphological changes, we monitored centrosome positioning during EMT in vivo, in developing

244 n this regard, cenexin was required for both centrosome positioning in interphase cells and proper sp

245 These results suggest that centrosome positioning is set by the last mitotic oogoni

246 bility, thus having a crucial role in proper centrosome positioning, chromosomal alignment, and centr

247 efocusing and phosphorylation of the mitotic centrosome protein CEP215 at serine-613.

248 n, mediated by signals concentrated near the centrosome, recapitulates all the experimental observati

249 ing along cell edges and pivoting around the centrosome regulate MT rearrangement and thereby direct

250 tered centrosome morphology, suggesting that centrosome regulation may be mediated by active Cdc42 at

251 esting the existence of a stem cell-specific centrosome regulation program.

252 By using Leapfrog, we identify key centrosome-related genes and homeodomain classes previou

253 the molecular details of its function at the centrosome remain elusive.

254 e elongation, and both chemical and physical centrosome removal demonstrate that astral microtubules

255 ts exhibited compromised proliferation after centrosome removal, suggesting that centrosome-independe

256 tion of microtubule dynamics, confirmed that centrosome repositioning was responsible for further cel

257 Centrosome separation along the surface of the nucleus a

258 ysical change, cell confinement, can trigger centrosome separation and increase spindle steady-state

259 Eg5, the mechanism by which Kif15 generates centrosome separation forces is unknown.

260 usly unrecognised link between p53, PLK1 and centrosome separation that has therapeutic implications

261 ed kinesin-14 motor, in preventing premature centrosome separation through a microtubule-dependent pa

262 sensitivity to PLK1 inhibitors by permitting centrosome separation to occur, allowing cells to traver

263 uclear envelope is known to be important for centrosome separation, but it is unclear how nuclear dyn

264 Premitotic destruction of PLK1 disrupts centrosome separation, causing mitotic spindle asymmetry

265 e to robust onset of nuclear dynein-mediated centrosome separation.

266 anating from neighboring scaffolds shows how centrosomes/SPBs can integrate inputs from multiple path

267 that Shp2 is distributed to the kinetochore, centrosome, spindle midzone, and midbody, all of which a

268 Therefore, stabilization of the centrosome-spindle pole interface by the CEP215-HSET com

269 erization implicated three of these genes in centrosome/spindle pole body, centromere, and cohesion f

270 As the two centrosomes split to assemble the bipolar spindle, predo

271 we developed a signature, "CA20", comprising centrosome structural genes and genes whose dysregulatio

272 To uncover how centrosomes sustain and regulate force, we purified SPBs

273 Centrosome-targeted Neurl-4 was sufficient to restore ci

274 annel 3, but although this is sufficient for centrosome targeting of Mps1, it is not necessary becaus

275 ransformed ECs respond differently to excess centrosomes than do most tumor cells-they undergo senesc

276 The central MTOC is the centrosome that duplicates during the cell cycle and ass

277 a cell cycle-regulated concentration at the centrosome that is accompanied by dramatic changes in it

278 idence of an accumulation of paxillin at the centrosome that is dependent on focal adhesion kinase (F

279 he first cell of an animal (zygote) requires centrosomes that are assembled from paternally inherited

280 in the regulation of the disjunction of the centrosome, the assembly of the mitotic spindle, the fun

281 C is established as essential for functional centrosomes, the major MTOCs in animal cells.

282 They are needed for the correct formation of centrosomes, the organelles at the poles of the spindle

283 for cell division to occur in the absence of centrosomes, these divisions typically result in defects

284 cell cycles can take place in the absence of centrosomes, this is an error-prone process that opens u

285 ization of nuclear dynein forces to separate centrosomes, thus ensuring robust bipolar spindle assemb

286 precursor components first localize with the centrosome to the cytoplasm adjacent to the telomere clu

287 s frequently used by cancer cells with extra centrosomes to avoid multipolar divisions.

288 Microtubule-organizing centers move from centrosomes to the nuclear envelope during muscle develo

289 subsequent differential behavior of the two centrosomes together bias the partition of plasmid DNA d

290 Centrosomes together with the mitotic spindle ensure the

291 clustering of mechanical forces to push the centrosome toward the cell apical pole.

292 -microtubule configuration through which the centrosome translocates.

293 junctions and the centrosome, and a membrane-centrosome transport system was revealed.

294 the centrosome, leads to greater numbers of centrosome-unattached MTs as well as greater sliding of

295 the propagation of cells carrying amplified centrosomes via p53 stabilisation and p21-mediated cell-

296 e frequency of primary human ECs with excess centrosomes was quickly reduced in a p53-dependent manne

297 how that microtubules are nucleated from the centrosomes, we find only a few KMTs directly connected

298 h cell spreading and the polarization of the centrosome were unaffected, T-cell receptor (TCR)-mediat

299 of spindle poles and the generation of extra centrosomes, which is similar phenotype to USP7-knockdow

300 zes asymmetrically to the younger (daughter) centrosome, yet it is not required for the asymmetric di