ライフサイエンスコーパス: Aurora-B

1 Aurora B also executes important functions in interphase

2 Aurora B facilitates KT-MT dynamics by phosphorylating k

3 Aurora B inactivation disrupts cytokinesis and causes de

4 Aurora B is a serine/threonine kinase that has been impl

5 Aurora B is overexpressed in human tumors although wheth

6 Aurora B is overexpressed in many cancers but, surprisin

7 Aurora B kinase controls kinetochore assembly by phospho

8 Aurora B kinase elicits a cascade of events starting wit

9 Aurora B kinase has a critical role in regulating attach

10 Aurora B kinase is essential for faithful chromosome seg

11 Aurora B kinase phosphorylates kinetochore substrates to

12 Aurora B kinase plays essential roles in mitosis.

13 Aurora B kinase regulates the proper biorientation of si

14 Aurora B kinase was more commonly overexpressed than AAK

15 Aurora B kinase, a key regulator of cell division, local

16 Aurora B kinase, which is essential for several aspects

17 Aurora B knockdown inhibited Mad2 phosphorylation in mit

18 Aurora B localizes prominently to inner centromeres, and

19 Aurora B phosphorylates both Ska1 and Ska3 to inhibit th

20 Aurora B phosphorylates PLK1 on Thr210 to activate its k

21 Aurora B phosphorylation of Dam1p C terminus weakens dir

22 Aurora B promotes this process in a manner that is codep

23 Aurora B recruitment accompanies histone H3 threonine-3

24 Aurora B regulates cytokinesis timing and plays a centra

25 Aurora B-orchestrated PLK1 kinase activity was examined

26 elay key events in anaphase, including AIR-2/Aurora B relocalization to the microtubules, in response

27 ociated with delayed activation of Aurora A, Aurora B, and cyclin-dependent kinase 1 (CDK1).

28 Analysis of AAK, Aurora B kinase, MYC, BCL-2, phosphatidylinositol 3-kina

29 f Haspin and Bub1 activities fully abolished Aurora B accumulation at centromeres.

30 NP is responsible for binding and activating Aurora B kinase.

31 In addition, Aurora B and RepoMan independently promote cancer cell p

32 rrent spatial models for how tension affects Aurora B-dependent kinetochore phosphorylation.

33 ription and that the cell cycle arrest after Aurora B inhibition depends on p53 and pRB tumor suppres

34 on the new H3 is significantly reduced after Aurora B inhibition, suggesting a cross-talk between H3S

35 ould act as a flexible "dog leash," allowing Aurora B to phosphorylate dynamic substrates localized i

36 Although Aurora B is regarded as the "master regulator" of kineto

37 of the outer kinetochore protein KKIP5 in an Aurora B kinase- and kinetochore-dependent, but ATM/ATR-

38 -Cdk1 localized at the spindle midzone in an Aurora B-dependent manner, with incompletely separated c

39 Cyclin B1 degradation and mitotic exit in an Aurora B-dependent manner.

40 re, we describe a novel pathway involving an Aurora B-PLK1 axis for regulation of MCAK activity in mi

41 in SCCRO-deficient cells with addition of an Aurora B inhibitor at the midbody stage suggests that Au

42 We propose that bistability of an Aurora B-phosphatase system underlies formation of spati

43 Thus, an Aurora B gradient appears to mediate a surveillance mech

44 s exhibit overexpression of Mad2, BubR1, and Aurora B, but only overexpression of Aurora B phenocopie

45 er, depletion of the ESCRT-III component and Aurora B substrate CHMP4C enables abscission, bypassing

46 d by mutations in kinetochore components and Aurora B kinase Ipl1.

47 omere triggers dissociation of condensin and Aurora B from the centromere, thereby stabilizing the bi

48 romotes the colocalization of EWSR1/FLI1 and Aurora B on the chromosomes during prophase and metaphas

49 evated expression of Ki67, p-histone H3, and Aurora B confirmed by immunocytochemistry compared with

50 of the checkpoint depends both on Haspin and Aurora B.

51 tromere-associated kinesin localization, and Aurora B T-loop phosphorylation at kinetochores.

52 alization of CENP-A(Cse4), CENP-C(Mif2), and Aurora B(Ipl1) When the RNA interference system was intr

53 ivation of Polo kinetochore targets Mps1 and Aurora B.

54 we delineated the contributions of PLK1 and Aurora B to RhoA activation and cytokinesis initiation i

55 both phosphorylated histone H3-positive, and Aurora B-positive cardiomyocytes in the post-LVAD hearts

56 n defects in CPC chromosomal recruitment and Aurora B-dependent spindle assembly, but not in spindle

57 The co-up-regulation of RepoMan and Aurora B in tumors is inversely correlated with patient

58 Hence, the co-up-regulation of RepoMan and Aurora B is associated with tumor aggressiveness but als

59 f Ndc80, including a 27-residue sequence and Aurora B phosphorylation sites, is both necessary and su

60 ver of regulatory phosphorylation on another Aurora B substrate MKlp1 was observed, suggesting that P

61 This de-phosphorylation antagonizes Aurora B kinase to modify the functions and interactions

62 in cis by recruiting mitotic kinases such as Aurora B kinase.

63 A midzone-associated Aurora B gradient was found to monitor chromosome positi

64 -294 hearts analyzed by Ki67, pH3, and AurB (Aurora B kinase) expression parallel to increased small

65 ora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serine/threon

66 romeric histone H2A, attenuation of KT-based Aurora B kinase activity, and lethal chromosome congress

67 esponsible for reciprocal activation between Aurora B kinase (AURKB) and MYC.

68 in line with an inverse correlation between Aurora B and p21(Cip1) expression in human leukemias.

69 lization contributes to CPC functions beyond Aurora B activation.

70 revious work has shown KIF4A is activated by Aurora B at the anaphase central spindle.

71 uploidy and the stress pathways activated by Aurora B inhibition and also support the use of Aurora B

72 is dynamic regulation of Mad1 association by Aurora B is only uncovered when CENP-I is depleted, cons

73 ignaling and EMT that could be attenuated by Aurora B kinase inhibitor treatment.

74 The duration of this block is controlled by Aurora B kinase.

75 bule and kinetochore binding is curtailed by Aurora B is the spindle and kinetochore-associated (Ska)

76 ule attachments that are not destabilized by Aurora B.

77 cyclin B1-associated CDK1, and indirectly by Aurora B, and is antagonized by PP1-mediated dephosphory

78 on force and kinetochore phosphorylation by Aurora B kinase.

79 amatically increases Dsn1 phosphorylation by Aurora B.

80 is12C by Dsn1 impedes its phosphorylation by Aurora B.

81 ntly, the antagonistic regulation of Polo by Aurora B and Map205 in cytokinesis reveals that interdom

82 Here we show that phosphorylation of Polo by Aurora B is required for cytokinesis.

83 two holoenzymes are dynamically regulated by Aurora B kinase during mitosis.

84 ion, each component of which is regulated by Aurora B kinase.

85 ore-microtubule coupling and is regulated by Aurora B kinase.

86 's affinity for microtubules is regulated by Aurora B phosphorylation on its N-terminal tail [12-15],

87 ty of kinetochore attachment is regulated by Aurora B/Ipl1 kinase and this regulation is conserved fr

88 Ska complex regulates, and is regulated by, Aurora B [13].

89 ctivity that accompanies anaphase and causes Aurora B translocation away from centromeres [7-12] and

90 lly interacts with the checkpoint components Aurora B and ANCHR, and the abscission delay upon checkp

91 The chromosomal passenger complex containing Aurora B can be found on a subset of spindle microtubule

92 l passenger protein complex (CPC) containing Aurora B kinase, borealin, INCENP, and survivin, which o

93 egulated by the same mechanisms that control Aurora B, including FOXM1-regulated expression and prote

94 , how Haspin and Bub1 collaborate to control Aurora B activity at centromeres remains unclear.

95 Conversely, Aurora B knock down by short-hairpin RNAs (shRNAs) suppr

96 tricted negative feedback loop counteracting Aurora B in anaphase.

97 show that protein phosphatase 1 counteracts Aurora B activity to enable Ska kinetochore accumulation

98 ETAA1, but not TOPBP1, results in decreased Aurora B kinase activity during mitosis.

99 we identified a small, Bub1 kinase-dependent Aurora B pool that supported faithful chromosome segrega

100 However, chemical inhibition of either Aurora B or survivin does not target CPC specifically du

101 Mechanistically, we show that elevated Aurora B expression in breast cancer cells activates AKT

102 uld be recognized as erroneous, would elicit Aurora B-dependent destabilization of kinetochore-microt

103 g chemically induced dimerization to enhance Aurora B activity at metaphase kinetochores.

104 end-tracking protein, is required to enrich Aurora B at inner centromeres in a microtubule-dependent

105 ediated primarily by the centromere-enriched Aurora B kinase (ABK), typically occurs near spindle pol

106 increases Dsn1 phosphorylation by enriching Aurora B at inner kinetochores, close to CENP-C.

107 d trans-phosphorylation that is critical for Aurora B activation.

108 Moreover, ULP-4 is necessary for Aurora B(AIR-2) extraction from chromatin and relocation

109 strate of Aurora B, but is also required for Aurora B activity.

110 zes to kinetochores and is also required for Aurora B-serine 331 phosphorylation in nocodazole or unp

111 Thus, in meiosis, the requirements for Aurora B are distinct at centromeres and telomeres, illu

112 tinct molecular pathways are responsible for Aurora B recruitment to centromeres and kinetochores.

113 Here, we describe a new role for Aurora B in telomere dispersion and disjunction during f

114 e spindle midzone, making it unavailable for Aurora B at the equatorial cortex.

115 This work reveals a role for Aurora-B in removing chromatin-associated RNAs during pr

116 atus, we reveal a spatially defined role for Aurora-B kinase in retarding the end-on conversion proce

117 Finally, we uncover a novel role for Aurora-B regulated Astrin-SKAP complex in ensuring the c

118 8] and moving Aurora B substrates away from Aurora-B-localizing sites at centromeres (spatial separa

119 an essential CPC component required for full Aurora B activity.

120 ger complex (CPC), without abolishing global Aurora B function.

121 How Aurora B is recruited to and evicted from these regions

122 Very little is however known about how Aurora B levels are regulated in interphase.

123 However, whether and how Aurora B governs telomere separation during meiosis has

124 It has long been debated how Aurora B halts this action when bi-orientation is establ

125 Our results give important insight into how Aurora B disrupts kinetochore-microtubule interaction in

126 To understand how Aurora-B activity is counteracted, we compare the roles

127 n distinguishing human Aurora A versus human Aurora B kinase in vivo.

128 kinetochores during metaphase hyperactivates Aurora B via PP2A inhibition, and thereby rescues the fe

129 Thus, we identify Aurora-B as a key upstream regulator of end-on conversio

130 In meiosis II, Aurora B controls KT-MT attachment but appears dispensab

131 Importantly, Aurora B-dependent Ndc80 phosphorylation, a mark that ha

132 This decrease in Aurora B results in diminished binding of the chromokine

133 with corresponding significant decreases in Aurora B phosphorylation of Ndc80/Hec1.

134 ad in cancers, which causes an impairment in Aurora B activity.

135 inally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitot

136 about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression

137 This phosphorylation invokes a switch in Aurora B specificity, with increased phosphorylation of

138 s tension across the centromeres inactivates Aurora B kinase, and PP2A phosphatase dephosphorylates t

139 tance-dependent manner, thereby inactivating Aurora B in metaphase.

140 The Sli15/Ipl1(INCENP/Aurora-B) core-CPC interacted with COMA in vitro through

141 Interestingly, increased Aurora B activity also leads to problems with chromosome

142 a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of t

143 The inhibitor furthermore does not induce Aurora B specific effects in cells.

144 ntial target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer includ

145 tability, which is not rescued by inhibiting Aurora-B, an attachment destabiliser, but is reversed by

146 also present evidence that USP13 instigates Aurora B deubiquitination and/or protect it from degrada

147 of Sgo1, suggesting that Sgo1 can integrate Aurora B and PP2A activities to modulate Aurora B substr

148 fore anaphase onset by a mechanism involving Aurora B kinase, a key regulator of mitosis in a wide ra

149 dle association is important for active Ipl1/Aurora B complexes to preferentially destabilize misatta

150 show that this activity is regulated by Ipl1/Aurora B phosphorylation during cell cycle progression.

151 Dsn1 phosphorylation by Ipl1/Aurora B relieves this autoinhibition, enabling MIND to

152 omere and provides the binding site for Ipl1/Aurora B.

153 itment of the tension checkpoint kinase Ipl1/Aurora B to inner centromeres in metaphase but is not re

154 CENP scaffold and the catalytic subunit Ipl1/Aurora B.

155 The Ipl1/Aurora B kinase corrects improper attachments by phospho

156 gulated by the conserved protein kinase Ipl1/Aurora-B and promotes the subsequent assembly of a kinet

157 Central to this regulation is Aurora B kinase, which phosphorylates kinetochore substr

158 er complex (CPC), whose enzymatic subunit is Aurora B kinase, promotes chromosome biorientation by de

159 A key regulator of abscission timing is Aurora B kinase activity, which inhibits abscission and

160 In one mechanism, the centromeric kinase Aurora B phosphorylates Mis12C and strengthens its bindi

161 ger complex (CPC), containing mitotic kinase Aurora B as a catalytic subunit, ensures faithful chromo

162 The mitotic kinase Aurora B is concentrated at the anaphase central spindle

163 ntribute to activation of the mitotic kinase Aurora B.

164 Inhibition of the kinase Aurora B does not change the distribution despite signif

165 (INCENP), Survivin, Borealin, and the kinase Aurora B, contributes to the activation of the mitotic c

166 ger complex (CPC), which includes the kinase Aurora B, is a master regulator of meiotic and mitotic p

167 ssembly depends on multiple mitotic kinases (Aurora B, Mps1, and Plx1) and is suppressed by protein p

168 0 and histone H3 phospho-Thr3) that localize Aurora B.

169 n this pathway and is sufficient to localize Aurora B to microtubules prior to anaphase.

170 reveal co-existence of distinct high and low Aurora B activity states, sustained by a two-component k

171 lation site (T343) responsible for mediating Aurora B-induced AKT/GSK3beta/Snail1 signaling and EMT t

172 During (pro)metaphase, Aurora B is concentrated at the inner centromere by the

173 ation during anaphase, assisted by a midzone Aurora B phosphorylation gradient - the 'ruler' model.

174 ate Aurora B and PP2A activities to modulate Aurora B substrate phosphorylation.

175 ing the outer kinetochores [7, 8] and moving Aurora B substrates away from Aurora-B-localizing sites

176 expression of a phosphomimetic S331E mutant Aurora B rescued chromosome alignment or segregation in

177 We conclude that the dual activities of Aurora B and CENP-I generate a molecular switch that mai

178 er is diminished recruitment and activity of Aurora B kinase on chromosome arms.

179 ation also depends on the kinase activity of Aurora B, the catalytic subunit of the chromosomal passe

180 We propose that the coincidence of Aurora B and CENP-C at inner kinetochores ensures the fi

181 nger complex (CPC) in animals, consisting of Aurora B kinase and three evolutionarily conserved prote

182 ine 3 (H3T3ph) promotes proper deposition of Aurora B at the inner centromere to ensure faithful chro

183 y, suggesting that kinetochore enrichment of Aurora B promotes the phosphorylation of other kinetocho

184 Expression of Aurora B S227A phenocopies inhibition of PKCepsilon in b

185 implications for the different functions of Aurora B, which promote the proper interaction between s

186 RZZ dissociation functions independently of Aurora B, which regulates their association.

187 induction of p21 by p53 after inhibition of Aurora B is dependent on the p38 MAPK, which promotes tr

188 CDK11(p58) kinase activity or inhibition of Aurora B kinase activity.

189 We also demonstrate that inhibition of Aurora B results in down-regulation of E2F-mediated tran

190 Inhibition of Aurora B results in stabilization of p53 and induction o

191 in a p38-dependent manner upon inhibition of Aurora B.

192 Moreover, inhibition of Aurora B/C kinases results in Kif4 mislocalization and c

193 eated with Hesperadin, a potent inhibitor of Aurora B/C kinases.

194 aneuploid cells synergize with inhibitors of Aurora B to inhibit colony formation and oncogenic trans

195 Lack of Aurora B kinase function results in the inability to cor

196 nd, in addition, impairs the localization of Aurora B during anaphase, leading to induction of aneupl

197 While localization of Aurora B is essential for faithful cell division, it is

198 that EWSR1/FLI1 impairs the localization of Aurora B kinase to the midzone (the midline structure lo

199 reased incidence of aberrant localization of Aurora B, and greater levels of aneuploidy, compared wit

200 on the spindle, indicating misregulation of Aurora B.

201 This modification triggers mobilization of Aurora B kinase from inner centromeres to kinetochore pr

202 Abnormal modulation of Aurora B in interphase leads to cell cycle defects often

203 Overexpression of Aurora B also results in a reduced DNA damage response a

204 ccount for the balanced co-overexpression of Aurora B and RepoMan in many cancers, which limits chrom

205 Overexpression of Aurora B in cultured cells induces defective chromosome

206 Long-term overexpression of Aurora B in vivo results in aneuploidy and the developme

207 Thus, overexpression of Aurora B may contribute to tumor formation not only by i

208 R1, and Aurora B, but only overexpression of Aurora B phenocopies mitotic defects observed in ARF(-/-

209 ocess involves PKCepsilon phosphorylation of Aurora B S227.

210 stablishing a kinetochore-associated pool of Aurora B kinase, a chromosomal passenger complex (CPC) s

211 This pool of Aurora B phosphorylates substrates including the kinesin

212 sphorylated by centromere-localized pools of Aurora B, and calls for a reevaluation of the current sp

213 ied and investigated discrete populations of Aurora B at the centromere/kinetochore region.

214 re independently dictates the recruitment of Aurora B kinase, kinase activity on a kinetochore substr

215 explanation for the common up-regulation of Aurora B in human cancers.

216 theoretical model for spatial regulation of Aurora B phosphorylation.

217 These studies reveal a novel role of Aurora B in maintaining genomic integrity by promoting t

218 we show that Ska is not only a substrate of Aurora B, but is also required for Aurora B activity.

219 A critical target of Aurora B is the N-terminal "tail" domain of Hec1, which

220 It is a key target of Aurora B kinase, which destabilizes erroneous attachment

221 Ubiquitination-promoted turnover of Aurora B at the midbody was deficient in SCCRO- and KLHL

222 ucidated, yet signaling pathways upstream of Aurora B in this context remain poorly understood.

223 ntegrates this and other signals upstream of Aurora B to regulate when the final step in the physical

224 ora B inhibition and also support the use of Aurora B inhibitors in combination therapy for treatment

225 rotubule attachment in a manner dependent on Aurora B.

226 midzone and PLK1, while the other depends on Aurora B activity and centralspindlin at the equatorial

227 for USP13 to exert its stabilizing effect on Aurora B, their association is promoted by the Aurora B-

228 a genome protection mechanism that relies on Aurora B and the ESCRT-III subunit CHMP4C to delay absci

229 gest that CDK11(p58) kinase activity opposes Aurora B activity to enable abscission to proceed and re

230 ma and -epsilon play a general role opposing Aurora B at the central spindle.

231 The 'NoCut', or Aurora B abscission checkpoint can be activated if DNA i

232 To promote bi-orientation, Aurora B kinase disrupts aberrant kinetochore-microtubul

233 the conserved CTD SUMOylation sites perturbs Aurora B recruitment and checkpoint activation.

234 Pharmacologic Aurora B inhibition might be a potential effective treat

235 as does expression of a non-phosphorylatable Aurora B S227A mutant.

236 that Chk2 stabilizes Mps1 and phosphorylates Aurora B-serine 331 to prevent mitotic exit when most ki

237 ent abscission checkpoint by phosphorylating Aurora B at S227.

238 Assessing if this PKCepsilon-Aurora B module provides a more widely exploited genome-

239 bles abscission, bypassing the PKCvarepsilon-Aurora B exit pathway.

240 ts microtubule-binding capability to promote Aurora B activity in cells and stimulates Aurora B catal

241 We propose that Ska promotes Aurora B activity to limit its own microtubule and kinet

242 of the chromosome passenger complex proteins Aurora B kinase (AURKB) and Survivin in early mitosis.

243 in or Bub1 activity is sufficient to recruit Aurora B to a distinct chromosomal locus.

244 ta indicate that SUMOylated Topo II recruits Aurora B to ectopic sites, constituting the molecular tr

245 In cells with reduced Aurora B activity, there is a decrease in the frequency

246 at centromeric SET/TAF1 on Sgo2 up-regulates Aurora B kinase activity via PP2A inhibition in prometap

247 elays of nuclear envelope reassembly require Aurora B kinase activity.

248 Restoring Aurora B to near-normal levels rescues mitotic phenotype

249 Thus, we propose that SET, Aurora B and Bub1 form a distance-dependent positive fee

250 otective control for the cell cycle, we show Aurora B phosphorylation at S227 by PKCepsilon also occu

251 nd that USP13-associates with and stabilizes Aurora B in cells, especially before their entry into mi

252 te Aurora B activity in cells and stimulates Aurora B catalytic activity in vitro.

253 R is activated at centromeres, it stimulates Aurora B through Chk1, preventing formation of lagging c

254 res in early mitosis to activate its subunit Aurora B kinase.

255 t PP2A-B56gamma can dephosphorylate the T799 Aurora B site on KIF4A and thereby counteract the Aurora

256 Importantly, targeting Aurora B to microtubules by UBASH3B is necessary for the

257 way during epithelial polarization and that Aurora B has a role in the formation of the apical surfa

258 Our results demonstrate that Aurora B inhibits both direct interaction with the micro

259 ted Ndc80 degradation, and demonstrates that Aurora B-dependent regulation of kinetochores extends be

260 Here, we found that Aurora B phosphorylates PKM2, but not PKM1, at T45; this

261 Molecular dynamics indicates that Aurora B S227 phosphorylation induces conformational cha

262 This raised the possibility that Aurora B localization at centromeres is dispensable for

263 This model predicts that Aurora B localization at centromeres is required for bi-

264 Here we show that Aurora B and Bub1 at the centromere/kinetochore regulate

265 Here we show that Aurora B expression is elevated in basal-like breast can

266 inhibitor at the midbody stage suggests that Aurora B is the target of SCCRO-promoted Cul3(KLHL21) ac

267 Recent evidence suggests that Aurora B kinase ensures proper chromosome segregation du

268 This suggests that Aurora B substrates at the kinetochore are not phosphory

269 These findings support that Aurora B induces EMT to promote breast cancer metastasis

270 d RNAs during prophase and demonstrates that Aurora-B-dependent relocalization of SAF-A during cell d

271 Here the authors show that Aurora-B regulates end-on conversion in human cells and

272 The Aurora B abscission checkpoint delays cytokinesis until

273 The Aurora B chromosomal passenger complex (CPC) is a conser

274 The Aurora B kinase coordinates kinetochore-microtubule atta

275 kinases, the Polo-like kinase TbPLK and the Aurora B kinase TbAUK1, and a cohort of trypanosome-spec

276 sting of Borealin, Survivin, INCENP, and the Aurora B kinase) is essential to achieve error-free chro

277 rora B, their association is promoted by the Aurora B-mediated phosphorylation of USP13 at Serine 114

278 l of shugoshin-2 from chromosome arms by the Aurora B/C kinase, an event crucial for the efficient re

279 a B site on KIF4A and thereby counteract the Aurora B- and microtubule-stimulated ATPase activity of

280 is more complicated than predicted from the Aurora B phosphorylation gradient model.

281 ow that PKCvarepsilon directly modulates the Aurora B-dependent abscission checkpoint by phosphorylat

282 ity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers

283 , we found that local kinase activity of the Aurora B kinase (AURKB) subunit of the CPC caused disass

284 c checkpoint, nor the phosphorylation of the Aurora B kinetochore substrates Hec1, Dsn1, and Knl1.

285 We reason that the Aurora B-PLK1 signaling at the kinetochore orchestrates

286 While the Aurora B protein kinase destabilizes low-tension attachm

287 mitosis is antagonistically regulated by the Aurora-B kinase and RepoMan (recruits PP1 onto mitotic c

288 monstrate that PKCvarepsilon signals through Aurora B to exit the abscission checkpoint and complete

289 is evicted from prophase chromosomes through Aurora-B-dependent phosphorylation of the SAF-A DNA-bind

290 bule attachments (K fibers) epistatically to Aurora B, the other major error-correcting kinase.

291 igh RepoMan levels sensitize cancer cells to Aurora-B inhibitors.

292 al telomere deprotection, regulated by TRF2, Aurora B and ATM.

293 UBASH3B interacts with ubiquitylated Aurora B, one of the main kinases regulating chromosome

294 romosome segregation depends critically upon Aurora B phosphorylation of Ndc80/Hec1.

295 ecular and cellular connections of the USP13-Aurora B axis, which potentially participates in the rew

296 the CPC becomes particularly important when Aurora B phosphorylates kinetochore targets to eliminate

297 y exchanging centromere Borealin pool, while Aurora B and Mps1 play minimal roles in maintaining CPC

298 control the assembly of these pathways, with Aurora B kinase promoting KMN network recruitment to CEN

299 Here, we show that fission yeast Aurora B localizes at telomeres during meiosis I and pro

300 survivin), which recruits Ipl1-Sli15 (yeast Aurora B-INCENP) to centromeres, can become dispensable